iLib08 - Citavi Abe, Toshiaki; Saigo, Yoko; Hojo, Masayoshi; Kano, Tetsuya; Wakusawa, Ryosuke; Tokita, Yumi; Tamai

, Makoto (2006): Protection of photoreceptor cells from phototoxicity by transplanted retinal pigment epithelial cells expressing different neurotrophic factors. In: Cell transplantation, Jg. 14, H. 10, S. 799–808. Transplantation of cells or tissues and the intravitreal injection of neurotrophic Abstract factors are two methods that have been used to treat retinal diseases. The purpose of this study was to examine the effects of combining both methods: the transplantation of retinal pigment epithelial (RPE) cells expressing different neurotrophic factors. The neutrophic factors were Axokine, brain derivedneurotrophic factor (BDNF), and basic fibroblast growth factor (bFGF). The enhanced green fluorescence protein (eGFP) gene was used as a reporter gene. These genes were transduced into RPE cells by lipofection, selected by antibiotics, and transplanted into the subretinal space of 108 rats. The rats were examined at 1 week and 3 months after the transplantation to determine whether the transduced cells were present, were expressing the protein, and were able to protect photoreceptors against phototoxicity. The survival of the transplanted cells was monitored by the presence of eGFP. The degree of protection was determined by the thickness of the outer nuclear layer. Our results showed that the degree of photoreceptor protection was different for the different types of neurotrophic factors at 1 week. After 3 months, the number of surviving transplanted cell was markedly reduced, and protection was observed only with the BDNF-transduced RPE cells. A significant degree of rescue was also observed by BDNF-transduced RPE cells in the nontransplanted area of the retina at both the early and late times. Lymphocytic infiltration was not detected in the vitreous, retina, and choroid at any time. We conclude that the transplantation of BDNF-transduced RPE cells can reduce the photoreceptor damage induced by phototoxicity in the transplanted area and weakly in the nontransplanted area. Schlagwörter Animals; Brain-Derived Neurotrophic Factorbiosynthesisgeneticsphysiology; Cell Survival; Cell Transplantation; Ciliary Neurotrophic Factorbiosynthesisgeneticsphysiology; Dermatitis, Phototoxicpathologyphysiopathologyprevention & control; Fibroblast Growth Factor 2biosynthesisgeneticsphysiology; Gene Expression Regulation; Genes, Reporter; Green Fluorescent Proteinsanalysisgenetics; Lightadverse effects; Nerve Growth Factorsbiosynthesisgeneticsphysiology; Pigment Epithelium of Eyechemistrycytologymetabolismtransplantation; Rats; Rats, Long-Evans; Rats, Sprague-Dawley; Retinal Rod Photoreceptor Cellscytologyphysiology; Transduction, Genetic Albrecht-Buehler, G. (1977): Phagokinetic tracks of 3T3 cells: parallels between the orientation of track segments and of cellular structures which contain actin or tubulin. In: Cell, Jg. 12, H. 2, S. 333–339. Abstract Phagokinetic tracks were used to determine the current direction of migration in 3T3 cells. Comparing this direction with the orientation of actin or tubulin-containing cellular structures by indirect immunofluorescence, the following results were obtained. First, the main actin-containing bundles were located at the bottom and tail end of 3T3 cells and ran parallel to the current or preceding direction of migration. Second, the 3 micrometer long rod-like structure (primary cilium), which contains tubulin and which has been observed by other investigators in transmission electron microscopy (Barnes, 1961; Sorokin, 1962; Wheatley, 1969) and in indirect immunofluorescence (Osborn and Weber, 1976), was oriented predominantly parallel to the substrate and to the current movement direction. It seems possible that the primary cilium has a role in the directional control of a migrating 3T3 cell, and that the main actin containing bundles act as substrateattached rails along which the nucleus and bulk cytoplasm slide during displacement of the cells. Schlagwörter Actins; Cell Line; Cell Movement; Cilia; Fluorescent Antibody Technique; Glycoproteins; Microtubules; Tubulin

iLib08 - Citavi Albrecht-Buehler, G. (1997): Autofluorescence of live purple bacteria in the near infrared. In: Experimental cell research, Jg. 236, H. 1, S. 43–50. Online verfügbar unter doi:10.1006/excr.1996.3688. We have developed a novel microscope with which to study the fluorescence of Abstract cells in the near-infrared region (lambda = 750-2500 nm). For one of its first applications we report on the autofluorescence of live purple bacteria, Rhodospirillum rubrum, and suggest that the autofluorescent component is bacteriochlorophyll. The rapid fading of the autofluorescence of fixed bacteria and of purified bacteriochlorophyll suggests that the live bacteria are able to regenerate their pigment with a time constant of approximately 20 s. Schlagwörter Bacteriochlorophylls; Infrared Rays; Microscopy, Fluorescence; Rhodospirillum rubrum; Time Factors Allen, Karen Miller (1983): Artificial lighting and health. A selected bibliography. Monticello Ill.: Vance Bibliographies (Architecture series--bibliography, A-1087). Schlagwörter Fluorescent lighting; Physiological effect; Bibliography.; Health aspects; Electric lighting Amick, Charles L. (1947): Fluorescent lighting manual. 2nd ed. Fluorescent lighting (Hg.). New York: McGrawHill. Schlagwörter Fluorescent lighting. Arai, Takao; Tani, Satoshi; Isoshima, Akira; Nagashima, Hiroyasu; Joki, Tatsuhiro; Takahashi-Fujigasaki, Junko; Abe, Toshiaki (2006): [Intraoperative photodynamic diagnosis for spinal ependymoma using 5-aminolevulinic acid: technical note]. In: No shinkei geka. Neurological surgery, Jg. 34, H. 8, S. 811–817. OBJECTIVE: The fluorescence-guided resection using 5-aminolevulinic acid (5Abstract ALA) is a well established method for the treatment of brain tumor, especially malignant glioma. However, there is no report on photodynamic diagnosis (PDD) for spinal tumor. In the present study, we evaluated the usefulness of PDD for spinal ependymoma using 5-ALA. METHODS: Three patients with spinal ependymoma received oral doses of 5-ALA (20 mg/kg body weight) 2 hours before anesthesia induction. Intraoperatively, fluorescence was observed with a 420 nm sharp cut filter after excitation with a violet semiconductor laser (405 nm) and was verified by analysis of fluorescent spectra. Residual fluorescent samples taken from the tumor cavity were examined histologically RESULTS: Fluorescence peaked at 636nm in the removed tumors in all cases. Fluorescent tissue tended to exist at the cranial and caudal portion in the tumor cavity or around the anterior median fissure. The residual fluorescent tissue was not detected after removal of the tumor in case 1. The residual fluorescent tissue was composed of tumor cells and ependymal lining in case 2 or the infiltrated inflammatory cells and vascular endothelial cells in case 3. Postoperative magnetic resonance (MR) imaging showed no residual tumor in any of the cases. CONCLUSION: The results of this study indicate the usefulness of 5-ALA-induced tumor fluorescence in guiding resection of spinal ependymoma. 5-ALA-induced porphyrin fluorescence may label spinal ependymomas easily and clearly enough to enhance the completeness of tumor removal. Schlagwörter Adult; Aminolevulinic Acid; Ependymoma; Female; Fluorescence; Humans; Intraoperative Period; Lighting; Magnetic Resonance Imaging; Male; Middle Aged; Photosensitizing Agents; Porphyrins; Sensitivity and Specificity; Spinal Cord Neoplasms Atkinson, Arthur Dinham Stephen (1944): Fluorescent lighting. Dealing with the principles and practice of fluorescent lighting, for electrical engineers, illuminating engineers and architects. London: Newnes. Schlagwörter Fluorescent lighting. Atkinson, Arthur Dinham Stephen (1946): Fluorescent lighting. Brooklyn N.Y.: Chemical publishing co. inc. Schlagwörter Fluorescent lighting.

iLib08 - Citavi Atkinson, Arthur Dinham Stephen (1951): Modern fluorescent lighting. Dealing with the principles and practice of fluorescent lighting, for electrical engineers, illuminating engineers, and architects. London: Newnes. Schlagwörter Fluorescent lighting. Atkinson, Arthur Dinham Stephen (1955): Modern fluorescent lighting. Dealing with the principles and practice of fluorescent lighting, for electrical engineers, illuminating engineers, and architects. 2d ed. London: Newnes. Schlagwörter Fluorescent lighting. Ben-Hur, E.; Elkind, M. M. (1972): Survival response of asynchronous and synchronous Chinese hamster cells exposed to fluorescent light following 5-bromodeoxyuridine incorporation. In: Mutation research, Jg. 14, H. 2, S. 237–245. Schlagwörter Animals; Bromodeoxyuridinemetabolismpharmacology; Cell Line; Cell Survivaldrug effectsradiation effects; Cells, Culturedradiation effects; Cricetinae; Cysteaminepharmacology; DNAradiation effects; DNA Replication; Fibroblastsdrug effectsradiation effects; Fluorescence; Light; Mercaptoethylaminespharmacology; Photic Stimulation; Radiation Dosage; Radiation Effects; Radiation-Protective Agents; Radiation-Sensitizing Agents; Time Factors Ben-Hur, E.; Elkind, M. M. (1972): Damage and repair of DNA in 5-bromodeoxyuridine-labeled Chinese hamster cells exposed to fluorescent light. In: Biophysical journal, Jg. 12, H. 6, S. 636–647. Online verfügbar unter doi:10.1016/S0006-3495(72)86109-5. Schlagwörter Animals; Bromodeoxyuridinemetabolism; Cell Line; Centrifugation, Density Gradient; Cricetinae; Cysteaminepharmacology; DNAbiosynthesisradiation effects; DNA Repair; Fibroblastsdrug effectsmetabolismradiation effects; Fluorescence; Isotope Labeling; Kinetics; Light; Molecular Weight; Radiation Effects; RadiationProtective Agents; Thymidinemetabolism; Tritium Ben-Hur, E.; Elkind, M. M. (1974): Letter: Damage and repair of DNA in 5-bromodeoxyuridine-labeled Chinese hamster cells exposed to fluorescent light. In: Biophysical journal, Jg. 13, H. 12, S. 1342. Online verfügbar unter doi:10.1016/S0006-3495(73)86067-9. Schlagwörter Animals; Bromodeoxyuridine; Cell Line; Centrifugation, Density Gradient; Cricetinae; DNA Repair; DNA, Single-Strandedbiosynthesis; Fluorescence; Molecular Weight Beral, V.; Evans, S.; Shaw, H.; Milton, G. (1982): Malignant melanoma and exposure to fluorescent lighting at work. In: Lancet, Jg. 2, H. 8293, S. 290–293. In a study of 274 women with malignant melanoma, aged 18--54 years, and 549 Abstract matched controls in New South Wales, Australia, reported exposure to fluorescent light at work was associated with a doubling of melanoma risk (relative risk [RR] = 2.1; 95% confidence limits 1.32--3.32). The risk grew with increasing duration of exposure to fluorescent light and was higher in women who had worked mainly in offices (RR = 2.6) than in women whose main place of work was indoors but not in offices (RR = 1.8). The findings could not be explained by the differences in histories of sunlight exposure, in skin or hair colour, or in any other factor. There was a relative excess of lesions on the trunk in the group exposed to fluorescent light at work. 27 men with melanoma and 35 similarly aged controls were studied, and a significant increase in risk was also found: the RB in those exposed for greater than or equal to 10 years compared with those exposed for less than 10 years was 4.4 (95% confidence limits 1.1--17.5). Such an association has not been reported before, but it is plausible and could explain many of the paradoxical features of the epidemiology of melanoma. Until more data accumulate it must, however, be viewed cautiously. Schlagwörter Adolescent; Adult; Age Factors; Female; Fluorescence; Humans; Lightadverse effects; Lighting; Melanomaetiology; Middle Aged; Occupational Diseasesetiology; Risk; Sex Factors; Skin Neoplasmsetiology

iLib08 - Citavi Boatright, Jeffrey H.; Moring, Anisha G.; McElroy, Clinton; Phillips, Michael J.; Do, Vi T.; Chang, Bo et al. (2007): Tool from ancient pharmacopoeia prevents vision loss. In: Molecular vision, Jg. 12, S. 1706–1714. PURPOSE: Bear bile has been used in Asia for over 3,000 years to treat visual Abstract disorders, yet its therapeutic potential remains unexplored in Western vision research. The purpose of this study was to test whether treatment of mice undergoing retinal degeneration with tauroursodeoxycholic acid (TUDCA), a primary constituent of bear bile, alters the course of degeneration. METHODS: Two retinal degeneration models were tested: the rd10 mouse, which has a point mutation in the gene encoding the beta subunit of rod phosphodiesterase, and light induced retinal damage (LIRD). For LIRD studies, albino Balb/C adult mice were subcutaneously injected with TUDCA (500 mg/kg body weight) or vehicle (0.15 M NaHCO(3)). Sixteen h later, each mouse received repeat injections. Half of each treatment group was then placed in bright light (10,000 lux) or dim light (200 lux) for seven h. At the end of exposure, animals were transferred to their regular housing. Electroretinograms (ERGs) were assessed 24 h later, mice sacrificed, eyes embedded in paraffin and sectioned, and retina sections assayed for morphology and apoptosis by TUNEL and anti-active caspase-3 immunoreactivity via fluorescent confocal microscopy. A subset of mice were sacrificed 8 and 15 days after exposure and retina sections analyzed for morphology and apoptosis. For rd10 studies, mice were injected subcutaneously with TUDCA or vehicle at postnatal (P) days 6, 9, 12, and 15. At p18, ERGs were recorded, mice were euthanized and eyes were harvested, fixed, and processed. Retinal sections were stained (toluidine blue), and retinal cell layers morphometrically analyzed by light microscopy. Consecutive sections were analyzed for apopotosis as above. RESULTS: By every measure, TUDCA greatly slowed retinal degeneration in LIRD and rd10 mice. ERG a-wave and b-wave amplitudes were greater in mice treated with TUDCA compared to those treated with vehicle. Retinas of TUDCA-treated mice had thicker outer nuclear layers, more photoreceptor cells, and more fully-developed photoreceptor outer segments. Finally, TUDCA treatments dramatically suppressed signs of apoptosis in both models. CONCLUSIONS: Systemic injection of TUDCA, a primary constituent of bear bile, profoundly suppressed apoptosis and preserved function and morphology of photoreceptor cells in two disparate mouse models of retinal degeneration. It may be that bear bile has endured so long in Asian pharmacopeias due to efficacy resulting from this anti-apoptotic and neuroprotective activity of TUDCA. These results also indicate that a systematic, clinical assessment of TUDCA may be warranted. Schlagwörter Animals; Apoptosisdrug effects; Bilechemistry; Blindnessetiologyprevention & control; Cyclic Nucleotide Phosphodiesterases, Type 6; Disease Models, Animal; Electroretinography; Injections, Subcutaneous; Light; Medicine, East Asian Traditional; Mice; Mice, Mutant Strains; Phosphoric Diester Hydrolasesgenetics; Photoreceptor Cells, Vertebratedrug effectspathology; Retinal Degenerationcomplicationsetiologygeneticsphysiopathology; Taurochenodeoxycholic Acidadministration & dosagechemical synthesispharmacology; Ursidae Brondon, Philip; Stadler, Istvan; Lanzafame, Raymond J. (2005): A study of the effects of phototherapy dose interval on photobiomodulation of cell cultures. In: Lasers in surgery and medicine, Jg. 36, H. 5, S. 409–413. Online verfügbar unter doi:10.1002/lsm.20183. Abstract BACKGROUND AND OBJECTIVES: Dosimetry and treatment frequency are controversial phototherapy issues. Efficacy of dose fractionation on photobiomodulation was evaluated in vitro. STUDY DESIGN/MATERIALS AND METHODS: Human HEP-2 and murine L-929 cell lines were cultured in complete DMEM media. Photoradiation (670 nm, 5 J/cm2/treatment, 50 J/cm2 total energy delivery), was performed varying treatments per 24 hour period: Group I (Controls)0, Group II-1/d, Group III-2/d, Group IV-4/d. Cell proliferation was measured using

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Cyquant (fluorescent DNA content) and MTT (3-(4, 5-dimethylthiazol-2-yl)-2, 5diphenyl tetrasolium bromide) assays for 240 hours post therapy. A proliferation index: PI = (#Cells Experimental(t) / #Cells Control(t)) was computed. RESULTS: MTT assay results demonstrated maximal response in Group III (P < 0.05, n = 3). Cyquant maxima occurred in HEP-2 Groups II and III (P < 0.045) and L-929 Group III (P < 0.091). CONCLUSIONS: Cellular response to dose frequency varies. More frequent treatments (2/24 hours) increased metabolism and proliferation in both cell lines. Further investigation of dose fractionation in phototherapy is warranted. Animals; Cell Line; Cell Proliferation; Coloring Agents; Connective Tissue Cells; Dose Fractionation; Epithelial Cells; Humans; Mice; Phototherapy; Tetrazolium Salts; Thiazoles; Time Factors

Bulina, Maria E.; Lukyanov, Konstantin A.; Britanova, Olga V.; Onichtchouk, Daria; Lukyanov, Sergey; Chudakov, Dmitriy M. (2006): Chromophore-assisted light inactivation (CALI) using the phototoxic fluorescent protein KillerRed. In: Nature protocols, Jg. 1, H. 2, S. 947–953. Online verfügbar unter doi:10.1038/nprot.2006.89. The phototoxic red fluorescent GFP-like protein KillerRed has recently been Abstract described. The phototoxicity of KillerRed exceeds that of EGFP by at least 1,000fold, making it the first fully genetically encoded photosensitizer. KillerRed opens up new possibilities for precise light-induced cell killing and target protein inactivation. Because KillerRed is encoded by a gene, it can be expressed in a spatially and temporally regulated manner, under a chosen promoter, and fused with the desired protein of interest or localization signal. Here we provide a protocol for target protein inactivation in cell culture using KillerRed. As KillerRed is a new tool, the protocol focuses on aspects that will allow users to maximize the potential of this protein, guiding the design of chimeric constructs, recommended control experiments and preferred illumination parameters. The protocol, which describes target protein visualization and subsequent inactivation, is a 2- or 3-d procedure. Schlagwörter Bacteria; Epithelial Cells; Gene Expression Regulation; Green Fluorescent Proteins; Hela Cells; Humans; Light; Luminescent Agents; Protein Binding Chaloupka, R.; Sureau, F.; Kocisova, E.; Petrich, J. W. (1998): Hypocrellin A photosensitization involves an intracellular pH decrease in 3T3 cells. In: Photochemistry and photobiology, Jg. 68, H. 1, S. 44–50. The fluorescent pH probe carboxy-seminaphtorhodafluor-1 (C-Snarf-1) has been Abstract used for laser microspectro-fluorometric assays of intracellular pH in 3T3 mouse fibroblasts treated with hypocrellin A. These results are compared to those previously obtained with the structurally related hydroxylated polycyclic quinone, hypericin (Sureau et al., J. Am. Chem. Soc. 118, 9484-9487, 1996). A mean local intracellular pH drop of 0.6 units has been observed in the presence of 1 microM hypocrellin A after 90 s of exposure to 0.1 microW of laser irradiation at 514.5 nm. The time evolution of the cytoplasm acidification for hypocrellin A-treated cells is faster than that for cells treated by hypericin. Thus, release of protons from an excited state of hypocrellin A appears to be more efficient than that from hypericin. In addition, the pH dependence of the quenching of C-Snarf-1 fluorescence in 3T3 cells under continuous irradiation has been observed. It is shown here that under continuous illumination, a pH decrease is able to induce a modification of the intracellular binding equilibrium of C-Snarf-1 that results in an increase of C-Snarf-1 fluorescence intensity. This latter observation suggests that the protons generated upon the photoexcitation of hypericin or its analogs may be involved in the production of other photoreactive species. Finally, we suggest that, just as for hypericin, this pH drop may be involved in the antiviral and antitumor activity of hypocrellin A. Schlagwörter 3T3 Cells; Animals; Benzopyrans; Fluorescent Dyes; Hydrogen-Ion Concentration; Intracellular Fluid; Lasers; Mice; Naphthols; Perylene; Photobiology; Photosensitizing Agents; Quinones; Rhodamines

iLib08 - Citavi Duncan, T. E.; O'Steen, W. K. (1986): The diurnal susceptibility of rat retinal photoreceptors to light-induced damage. In: Experimental eye research, Jg. 41, H. 4, S. 497–507. Abstract Exposure of albino rats to high intensity light results in rapid, graded loss of photoreceptors. The hormonal status and age of an animal at the time of exposure affect the severity of light-induced retinal damage. The adrenal axis and pituitary hormones (prolactin) have been demonstrated previously to affect the degree of cell death in the retina. Because circadian rhythms for adrenal and pituitary secretion have been demonstrated in the rat, a series of experiments was undertaken to determine if a diurnal pattern of retinal susceptibility to light damage exists which might be related to endogenous endocrine rhythms. Male Sprague-Dawley rats were exposed to 4 hr of high intensity fluorescent light for 8 consecutive days during different phases of the 14:10 hr light: dark animal room light cycle. Morphometric analysis performed at the light microscopic level 2 weeks after exposure demonstrated a differential susceptibility to light-induced cell death depending upon the period during the light-dark cycle when animals received their daily light exposure. Neuronal cell death was confined to the outer nuclear layer as previously described. The retinas of animals exposed during the middle of the dark period or during the first 5 hr of the light period were significantly more damaged than the retinas of animals exposed during the last 9 hr of the light period. Control groups for the relative amounts of dark-adaptation between groups suggested that the diurnal susceptibility to light damage was not solely dependent upon the degree of dark adaptation. These results demonstrate a diurnal susceptibility of photoreceptors to light-induced cell death. Schlagwörter Animals; Cell Survivalradiation effects; Circadian Rhythm; Dark Adaptation; Light; Male; Photometry; Photoreceptor Cellsradiation effects; Rats; Rats, Inbred Strains; Time Factors Elenbaas, W. (1959): Fluorescent lamps and lighting. New York: Macmillan (Phillips' technical library). Schlagwörter Fluorescent lighting.; Fluorescent lamps. Elenbaas, W. (1971): Fluorescent lamps. 2nd ed. London: Macmillan (Philips technical library). Schlagwörter Fluorescent lighting.; Fluorescent lamps. Federal Construction Council; Task Group T-58 (1968): High-frequency lighting. United States. (Hg.). Washington: National Academy of Sciences (National Academy of Sciences. Publication 1610., no. 53). Schlagwörter Fluorescent lighting. Forsythe, William Elmer; Adams, Elliot Quincy (1948): Fluorescent and other gaseous discharge lamps. New York: Technical Division Murray Hill Books. Schlagwörter Fluorescent lighting.; Electric discharge lighting. Gaillard, E. R.; Atherton, S. J.; Eldred, G.; Dillon, J. (1995): Photophysical studies on human retinal lipofuscin. In: Photochemistry and photobiology, Jg. 61, H. 5, S. 448–453. Abstract Fluorescent material generated in the human retina accumulates within lipofuscin granules of the retinal pigment epithelium (RPE) during aging. Its presence has been suggested to contributed to various diseases including age-related macular degeneration. Because this material absorbs light at wave lengths as long as 550 nm, photophysical studies were performed to determine whether lipofuscin could contribute to light damage and to determine if its composition is similar to a synthetically prepared lipofuscin. Time-resolved experiments were performed to monitor (1) fluorescence decay, (2) the UV-visible absorption of longer-lived excited states and (3) the formation and decay of singlet oxygen at 1270 nm. Steady-state and time-resolved fluorescence studies indicate that human and synthetic lipofuscin have fluorophores in common. Time-resolved absorption experiments on human retinal lipofuscin and synthetic lipofuscin showed the presence of at least two transient species, one absorbing at 430 nm (lifetime ca 7 microseconds) and a

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second absorbing at 580 nm, which decays via second order kinetics. In addition, there is a third absorbing species stable to several hundred milliseconds. The transient species at 430 nm is quenched by oxygen, suggesting that it is a triplet state. Subsequent studies showed the formation of singlet oxygen, which was monitored by its phosphorescence decay at 1270 nm. These studies demonstrate that lipofuscin can act as a sensitizer for the generation of reactive oxygen species that may contribute to the age-related decline of RPE function and blue light damage. Adult; Humans; Kinetics; Lipofuscinchemistryisolation & purification; Photochemistry; Photolysis; Pigment Epithelium of Eyemetabolism; Protein Conformation; Quantum Theory; Spectrometry, Fluorescence; Spectrophotometry

Gantt, R.; Parshad, R.; Ewig, R. A.; Sanford, K. K.; Jones, G. M.; Tarone, R. E.; Kohn, K. W. (1978): Fluorescent light-induced DNA crosslinkage and chromatid breaks in mouse cells in culture. In: Proceedings of the National Academy of Sciences of the United States of America, Jg. 75, H. 8, S. 3809–3812. A single 20-hr exposure of mouse cells derived from embryonic or lung tissue to Abstract cool-white fluorescent light (4.6 W/m2) causes both DNA damage and chromosome aberrations including chromatid breaks, exchanges, and minutes. In Kohn's alkaline elution technique, the DNA from exposed cells elutes more slowly than that from shielded cells. Because larger molecular weight DNA elutes slower than smaller, we interpret these results to mean that the DNA in cells exposed to light is crosslinked. The estimated frequency of crosslinks is sufficient to account for the number of chromatid breaks observed. The types of chromosome aberrations produced by light indicate that the primary lesion results in chromatid rather than chromosome breaks, and the results suggest an influence of cell density in that cells in densely populated cultures showed few or no chromatid breaks after irradiation. The present results, together with observations from the literature, suggest that the DNA crosslinkage and the chromosome aberrations produced by light may be related. Schlagwörter Cells, Cultured; Chromatidsradiation effects; Chromosome Aberrations; DNAradiation effects; Fluorescence; Lightadverse effects; Time Factors Gordon, William C.; Casey, Douglas M.; Lukiw, Walter J.; Bazan, Nicolas G. (2002): DNA damage and repair in light-induced photoreceptor degeneration. In: Investigative ophthalmology & visual science, Jg. 43, H. 11, S. 3511–3521. Abstract PURPOSE: Intense light causes photoreceptor death that is greatest in the superior central retina. Short-duration treatment in a light-damage model results in TUNELpositive photoreceptor nuclei within this region. However, cells lost 10 days after light treatment are fewer than the TUNEL-labeled cells observed earlier. Therefore, this study was undertaken to monitor DNA fragmentation and cell death to explain the discrepancy. METHODS: Eyes of dark-adapted rats were light damaged for 4 or 5 hours. DNA fragmentation was measured by TUNEL, laddering, and highly repetitive short interspersed nuclear element (SINE) analysis in dark-adapted, nondamaged control (dark-control) retinas and in retinas collected at 6-hour intervals after light treatment. TUNEL-positive photoreceptor nuclei were counted in these samples along a superior-to-inferior meridian and compared with control and damaged 10-day retinas. Monocytes and DNA polymerase beta were monitored by immunohistochemistry. RESULTS: TUNEL-positive staining of photoreceptors was centered around the superior central retina. At 10 days, photoreceptor loss had occurred in this region. In graphs of 6-hour-interval data, two DNA-fragmentation peaks, 24 hours apart, were evident. Monocytes appeared after nuclear damage. Total TUNEL-positive cells under both peaks exceeded the number of photoreceptors lost. The DNA-repair enzyme, polymerase beta, was induced in the superior central retina, within photoreceptor inner segments, 24 hours after light treatment, but declined thereafter. CONCLUSIONS: One population of damaged cells may mend DNA until the repair mechanism is exceeded and then revert to apoptosis, or, alternatively, two populations may undergo DNA fragmentation 24

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hours apart. Either DNA fragmentation is masked at midpoint by temporary repair, or two waves of damage occur, but repair rescues the first set, not the second. Photoreceptors lost are fewer than TUNEL-positive cells. Thus, both possibilities suggest photoreceptor DNA repair. The transient appearance of DNA polymerase beta in photoreceptors under these experimental conditions further suggests nuclear repair. Thus, maintenance of in-house DNA-repair mechanisms may provide an alternate approach for the rescue of photoreceptors, as well as other neurons with stress-induced damage. These events may provide useful drug targets to promote photoreceptor survival in various forms of retinal degeneration. Animals; Blotting, Western; DNAanalysis; DNA Damageradiation effects; DNA Fragmentation; DNA Polymerase betametabolism; DNA Repair; Fluorescent Antibody Technique, Indirect; In Situ Nick-End Labeling; Light; Male; Photoreceptor Cells, Vertebratepathologyradiation effects; Proliferating Cell Nuclear Antigenmetabolism; Radiation Injuries, Experimentalgeneticsmetabolismpathology; Rats; Rats, Sprague-Dawley; Retinal Degenerationgeneticsmetabolismpathology; Time Factors; Up-Regulation

Heeke, D. S.; White, M. P.; Mele, G. D.; Hanifin, J. P.; Brainard, G. C.; Rollag, M. D. et al. (1999): Light-emitting diodes and cool white fluorescent light similarly suppress pineal gland melatonin and maintain retinal function and morphology in the rat. In: Laboratory animal science, Jg. 49, H. 3, S. 297–304. BACKGROUND AND PURPOSE: A novel light-emitting diode (LED) light source for Abstract use in animal-habitat lighting was evaluated. METHODS: The LED was evaluated by comparing its effectiveness with that of cool white fluorescent light (CWF) in suppressing pineal gland melatonin content and maintaining normal retinal physiology, as evaluated by use of electroretinography (ERG), and morphology. RESULTS: Pineal melatonin concentration was equally suppressed by LED and CWF light at five light illuminances (100, 40, 10, 1, and 0.1 lux). There were no significant differences in melatonin suppression between LED and CWF light, compared with values for unexposed controls. There were no differences in ERG awave implicit times and amplitudes or b-wave implicit times and amplitudes between 100-lux LED-exposed rats and 100-lux CWF-exposed rats. Results of retinal histologic examination indicated no differences in retinal thickness, rod outer segment length, and number of rod nuclei between rats exposed to 100-lux LED and 100-lux CWF for 14 days. Furthermore, in all eyes, the retinal pigmented epithelium was intact and not vacuolated, whereas rod outer segments were of normal thickness. CONCLUSION: LED light does not cause retinal damage and can suppress pineal melatonin content at intensities similar to CWF light intensities. Schlagwörter Animals; Electroretinographyradiation effects; Lightadverse effects; Male; Melatoninmetabolism; Pineal Glandmetabolismradiation effects; Radioimmunoassay; Rats; Rats, Sprague-Dawley; Retinaphysiologyradiation effects Kasperowski, Walther (195?): Mehr Licht durch Leuchtstofflampen. Technik und Anwendung der Fluoreszenzbeleuchtung. Wien: A. Göschl. Schlagwörter Fluorescent lighting. Katz, M. L.; Eldred, G. E. (1989): Retinal light damage reduces autofluorescent pigment deposition in the retinal pigment epithelium. In: Investigative ophthalmology & visual science, Jg. 30, H. 1, S. 37–43. Abstract Lipofuscin in the retinal pigment epithelium (RPE) is thought to be derived from phagocytosed photoreceptor outer segment disc membranes. Based on this hypothesis, one would predict that the rate of lipofuscin deposition in the RPE would be proportional to the density of photoreceptor cells in the retina. In previous studies it was demonstrated that specific loss of photoreceptor cells due to a genetic defect resulted in a substantial decrease in the rate of age-related lipofuscin accumulation in the RPE. In order to confirm that this decreased RPE lipofuscin deposition was directly related to reduced photoreceptor cell density, experiments were conducted

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to determine whether light-induced photoreceptor cell destruction affected RPE lipofuscin content. The effects of retinal light damage on RPE autofluorescent pigment accumulation resulting from both normal aging and vitamin E deficiency were examined. Starting immediately after weaning, albino Fisher 344 rats were fed diets either containing or lacking vitamin E. All animals were maintained on a 12 hr/12 hr light/dark cycle. During the light phases of the cycles, the cage illuminance for one-half the animals in each dietary group was 750 lux, while the remaining rats were exposed to a light level of 15 lux. Illumination was provided by 40 watt coolwhite fluorescent lamps. After 17 weeks, rats in both dietary groups that were maintained under the higher light intensity had substantially reduced photoreceptor cell densities relative to animals in the same dietary group maintained under dim light conditions.(ABSTRACT TRUNCATED AT 250 WORDS) Agingmetabolism; Animals; Chromatography, Thin Layer; Fluorescence; Lightadverse effects; Lipofuscinmetabolism; Male; Pigment Epithelium of Eyemetabolism; Rats; Rats, Inbred F344; Retinainjuries; Retinal Pigmentsmetabolism; Vitamin E Deficiencymetabolism

Kehat, Rinat; Zemel, Esther; Cuenca, Nicolas; Evron, Tama; Toiber, Debra; Loewenstein, Anat et al. (2007): A novel isoform of acetylcholinesterase exacerbates photoreceptors death after photic stress. In: Investigative ophthalmology & visual science, Jg. 48, H. 3, S. 1290–1297. Online verfügbar unter doi:10.1167/iovs.06-0847. Abstract PURPOSE: To study the involvement of stress-induced acetylcholinesterase (AChE) expression in light-induced retinal damage in albino rats. METHODS: Adult albino rats were exposed for 24 hours to bright, damaging light. AChE expression was monitored by in situ hybridization, by histochemistry for AChE activity, and by immunocytochemistry. An orphan antisense agent (Monarsen; Ester Neurosciences, Ltd., Herzlia Pituach, Israel) was administered intraperitoneally to minimize light-induced AChE expression. The electroretinogram (ERG) was recorded to assess retinal function. RESULTS: Twenty-four-hour exposure to bright light caused severe reduction in the ERG responses and augmented expression of mRNA for the "read-through" variant of AChE (AChE-R) in photoreceptor inner segments (IS), bipolar cells, and ganglion cells. AChE activity increased in IS. The expressed AChE protein was a novel variant, characterized by an extended N terminus (N-AChE). Systemic administration of the orphan antisense agent, Monarsen, reduced the photic induction of mRNA for AChE-R, and of the N-AChE protein. Rats exposed to bright, damaging light and treated daily with Monarsen exhibited larger ERG responses, relatively thicker outer nuclear layer (ONL), and more ONL nuclei than did rats exposed to the same damaging light but treated daily with saline. CONCLUSIONS: The findings indicate that the photic-induced novel variant of AChE (N-AChE-R) may be causally involved with retinal light damage and suggest the use of RNA targeting for limiting such damage. Schlagwörter Acetylcholinesterasegeneticsmetabolism; Animals; Cell Death; DNA, Antisensepharmacology; Electroretinographyradiation effects; Fluorescent Antibody Technique, Indirect; Gene Expression Regulation, Enzymologicphysiology; In Situ Hybridization; Isoenzymesmetabolism; Light; Male; Microscopy, Confocal; Photoreceptor Cells, Vertebratepathology; RNA, Messengermetabolism; Radiation Injuries, Experimentalenzymology; Rats; Rats, Sprague-Dawley; Retinaradiation effects; Retinal Degenerationenzymologypathology Kennedy, A. R.; Ritter, M. A.; Little, J. B. (1980): Fluorescent light induces malignant transformation in mouse embryo cell cultures. In: Science (New York, N.Y.), Jg. 207, H. 4436, S. 1209–1211. Abstract Fluorescent light induced a dose-dependent malignant transformation in mouse C3H10T1/2 cells. A plateau in the dose-response curve for transformation was correlated with that observed with ultraviolet light exposure. The similarity in the two dose-response patterns suggests that similar molecular processes may be involved in the induction of malignant transformation by the two types of radiation. Schlagwörter Animals; Cell Survivalradiation effects; Cell Transformation, Neoplasticradiation

iLib08 - Citavi effects; Cells, Cultured; DNAradiation effects; Dose-Response Relationship, Radiation; Embryo, Mammalianradiation effects; Fluorescence; Light; Mice; Pyrimidine Dimersradiation effects; Ultraviolet Rays Koide, R.; Ueda, T. N.; Dawson, W. W.; Hope, G. M.; Ellis, A.; Somuelson, D. et al. (2001): [Retinal hazard from blue light emitting diode]. In: Nippon Ganka Gakkai zasshi, Jg. 105, H. 10, S. 687–695. PURPOSE: To compare the effect of exposure time from a blue(460 nm) light Abstract emitting diode(LED) on the morphology of the outer retina and determine conditions where damage occurs. MATERIALS AND METHODS: Young adult rhesus monkeys were anesthetized, and received blue LED exposure from a modified slitlamp. A 3 mm beam of 0.85 mW was imaged onto the retina through a lens positioned before the cornea and exposure damage was determined at time intervals for 12 to 90 min. Fundus photography, fluorescein angiography(FAG), retinal tomography(HRT), and s-cone electororetinogram(S-ERG) were recorded at baseline, 2, and 30 days. RESULTS: Two days after 40 min exposure, there was a grey, discolored region, which was over-fluorescent in FAG, and an incresse in HRT and S-ERG corresponding to the site which was exposed to LED light. In histological examination at 30 days, the LED had caused produced a marked disruption of the disks of photoreceptor cells, damaged retinal pigment epithelium(RPE) apical villi, and a loss of RPE melanin after 90 min exposure. CONCLUSION: A threshold level was found around 40 min. This morphological damage may impair function and continuous exposure to blue light is potentially dangerous to vision. Schlagwörter Animals; Lightadverse effects; Macaca mulatta; Male; Pigment Epithelium of Eyeradiation effectsultrastructure; Radiation Injuries, Experimentalpathology; Retinapathologyradiation effects Laabich, Aicha; Vissvesvaran, Ganesh P.; Lieu, Kuo L.; Murata, Kyoko; McGinn, Tim E.; Manmoto, Corinne C. et al. (2006): Protective effect of crocin against blue light- and white light-mediated photoreceptor cell death in bovine and primate retinal primary cell culture. In: Investigative ophthalmology & visual science, Jg. 47, H. 7, S. 3156–3163. Online verfügbar unter doi:10.1167/iovs.05-1621. Abstract PURPOSE: The present study was performed to investigate the effect of crocin on blue light- and white light-induced rod and cone death in primary retinal cell cultures. METHODS: Primary retinal cell cultures were prepared from primate and bovine retinas. Fifteen-day-old cultures were exposed to blue actinic light or to white fluorescent light for 24 hours. Cultures were treated by the addition of different concentrations of crocin for 24 hours before light exposure or for 8 hours after light exposure. Cultures kept in the dark were used as controls. Green nucleic acid stain assay was used to evaluate cell death. Rods and cones were immunolabeled with specific antibodies and counted. TUNEL labeling was used to detect fragmented DNA in fixed cells after light exposure. RESULTS: Primary retinal cell cultures contained a mixture of retinal cells enriched in photoreceptors, bipolar cells, and Müller cells. Twenty-four-hour exposure to blue and white light induced death in 70% to 80% of the photoreceptors in bovine and primate retinal cell cultures. Crocin protected the photoreceptors against blue light- or white light-mediated damage in a concentration-dependent manner with an EC50 of approximately 30 microM. TUNEL assays confirmed that crocin protected photoreceptors from light damage. CONCLUSIONS: These results show that blue and white light selectively induce rod and cone cell death in an in vitro model. Crocin protects retinal photoreceptors against light-induced cell death. Schlagwörter Animals; Carotenoidspharmacology; Cattle; Cell Count; Cell Culture Techniques; Cell Deathdrug effectsradiation effects; Crocus; Dose-Response Relationship, Drug; Flowers; Fluorescent Antibody Technique, Indirect; In Situ Nick-End Labeling; Lightadverse effects; Macaca fascicularis; Photoreceptor Cells, Vertebratedrug effectsradiation effects; Plant Extractspharmacology; Radiation Injuries, Experimentaletiologyprevention & control; Retinal Degenerationetiologyprevention

iLib08 - Citavi & control Lam, R. W.; Buchanan, A.; Clark, C. M.; Remick, R. A. (1991): Ultraviolet versus non-ultraviolet light therapy for seasonal affective disorder. In: The Journal of clinical psychiatry, Jg. 52, H. 5, S. 213–216. Although light therapy has been shown to be effective in the treatment of seasonal Abstract affective disorder (SAD), little research has been done to determine which light wavelengths affect treatment outcome. In this triple crossover study the authors compared 1 week of light therapy in which bright (2500 lux), full-spectrum fluorescent light, with and without blockade of the ultraviolet (UV) spectrum, was used with a dim (500 lux) light control in 11 SAD patients. The dim light condition had no significant antidepressant effects as measured by the Hamilton Rating Scale for Depression (HAM-D), the Beck Depression Inventory (BDI), and an atypical depressive symptom (ATYP) score. The UV-light condition significantly reduced HAM-D, BDI, and ATYP scores, whereas the UV-blocked condition significantly reduced only the ATYP score. These results suggest that the UV-spectrum in light therapy may have a differential effect on typical and atypical symptoms in SAD. Schlagwörter Depressive Disorderpsychologytherapy; Evaluation Studies as Topic; Female; Humans; Light; Male; Personality Inventory; Phototherapymethods; Psychiatric Status Rating Scales; Research Design; Seasons; Ultraviolet Rays; Ultraviolet Therapy Lee, F. L.; Yu, D. Y.; Tso, M. O. (1990): Effect of continuous versus multiple intermittent light exposures on rat retina. In: Current eye research, Jg. 9, H. 1, S. 11–21. The damaging effects of continuous light exposure to the albino rat retina have Abstract been well documented. However, the cumulative effects of multiple light exposures are not well defined. We therefore compared the retinal injury induced by a single 24 hour light exposure with that caused by three intermittent exposures of 8 hours each. Eight dark-adapted albino Lewis rats were exposed for 24 hours to green fluorescent light (490-580 nm) at an illuminance level of 175 foot-candles. A second group of 8 rats was exposed under similar conditions in three split doses of 8 hours each at intervals of 7 days between each exposure. Recovery was allowed in total darkness, and the animals were sacrificed 2 weeks following the last exposure. Retinal damage was assessed by morphometry and light and electron microscopy. Mild cumulative retinal injury, mostly in photoreceptor cells with relative sparing of the retinal pigment epithelium, was seen in the split dose group, while extensive damage involving photoreceptor cells and retinal pigment epithelium was noted in the group exposed continuously for 24 hours. Schlagwörter Animals; Lightadverse effects; Male; Periodicity; Photoreceptor Cellsradiation effectsultrastructure; Pigment Epithelium of Eyeradiation effectsultrastructure; Rats; Rats, Inbred Lew; Retinaradiation effectsultrastructure McColl, S. L.; Veitch, J. A. (2001): Full-spectrum fluorescent lighting: a review of its effects on physiology and health. In: Psychological medicine, Jg. 31, H. 6, S. 949–964. Abstract BACKGROUND: Full-spectrum fluorescent lighting (FSFL) has been credited with causing dramatic beneficial effects on a wide variety of behaviours, mental health outcomes and physical health effects, as compared to other fluorescent lamp types. These effects are hypothesized to occur because of similarity between FSFL emissions and daylight, which is said to have evolutionary superiority over other light sources. METHOD: This review, covering the period 1941-1999, critically considers the evidence for direct effects of FSFL through skin absorption as well as indirect effects on hormonal and neural processes. CONCLUSIONS: Overall, the evidence does not show dramatic effects of fluorescent lamp type on behaviour or health, neither does it support the evolutionary hypothesis. Schlagwörter Arousalphysiology; Brainphysiology; Calciummetabolism; Evolution; Female; Fluorescence; Health Status; Humans; Hydrocortisoneurine; Hyperbilirubinemiatherapy; Light; Male; Melatoninurine; Phototherapy; Psychomotor

iLib08 - Citavi Performancephysiology; Seasonal Affective Disordertherapy; Skinradiation effects; Stress, Psychologicalmetabolism; Sympathetic Nervous Systemphysiology; Vitamin Dmetabolism Miller, Henry Arthur (1947): Luminous tube lighting. Including high voltage fluorescent lighting. 2d ed. London: Newnes. Schlagwörter Electric discharge lighting. Miller, Henry Arthur (1949): Cold cathode fluorescent lighting. London: Technical Press. Schlagwörter Fluorescent lighting. Nell, Walter (1952): Beleuchtungstechnik mit Leuchtstofflampen und Leuchtröhren. Leipzig: Fachbuchverlag. Schlagwörter Fluorescent lighting. Noell, W. K.; Albrecht, R. (1971): Irreversible effects on visible light on the retina: role of vitamin A. In: Science (New York, N.Y.), Jg. 172, H. 978, S. 76–79. Diffuse retinal irradiation by visible light produces in the rat the death of visual cells Abstract and pigment epithelium. Typically, cage illumination of 1500 lux from fluorescent light through a green filter leads to severe damage when continued for 40 hours. Vitamin A deficiency protects against this damage but experiments show that retinol released by light from rhodopsin is probably not the toxic agent. Protection against light damage depends on a long-range state of cell adaptation to light itself. The normal diurnal cycle of light and dark seems to be the essential factor in controlling visual cell viability and susceptibility. Schlagwörter Animals; Electrocardiography; Eye Diseasesetiology; Lightadverse effects; Rats; Retina; Retinal Pigmentsmetabolism; Time Factors; Vitamin Ametabolismphysiology; Vitamin A Deficiencymetabolism Okuno, Tsutomu; Saito, Hiroyuki; Ojima, Jun (2002): Evaluation of blue-light hazards from various light sources. In: Developments in ophthalmology, Jg. 35, S. 104–112. Abstract Visible light of short wavelength (blue light) may cause a photochemical injury to the retina, called photoretinitis or blue-light hazard. In this study, various light sources were evaluated for blue-light hazard. These sources include the sun, the arc associated with arc welding and plasma cutting, molten steel, iron and glass, the interior of furnaces, the arc or envelope of discharge lamps, the filament or envelope of incandescent lamps, the envelope of fluorescent lamps and lightemitting diodes. The spectral radiance of each light source was measured, and blue-light effective radiance and the corresponding permissible exposure time per day were calculated in accordance with the ACGIH (American Conference of Governmental Industrial Hygienists) standard. The sun, arc welding, plasma cutting and the arc of discharge lamps were found to have extremely high effective radiances with corresponding permissible exposure times of only 0.6-40 s, suggesting that viewing these light sources is very hazardous to the retina. Other light sources were found to have low effective radiances under the study conditions and would pose no hazard, at least for short exposure times. Schlagwörter Dose-Response Relationship, Radiation; Humans; Light; Maximum Allowable Concentration; Radiation Injuries; Radiation Monitoring; Radiometry; Retina; Retinitis Paddock, S. W.; Albrecht-Buehler, G. (1988): Rigidity of the nucleus during nuclear rotation in 3T3 cells. In: Experimental cell research, Jg. 175, H. 2, S. 409–413. Abstract Using near infrared microscopy and ultraviolet fluorescence microscopy of living 3T3 cells stained with the fluorochrome Hoechst 33342, we have demonstrated that the nucleoli and Hoechst 33342-stained chromocenters in the nucleus maintain a fixed pattern during nuclear rotation. We conclude that the term "nuclear rotation" refers to rotation of the entire nucleus in the cytoplasm of interphase cells, and that

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nuclear rotation is not an expression of karyoplasmic streaming. In conjunction with earlier results on nuclear rotation the data imply that the interface of nuclear rotation is located either between the two nuclear membranes or in the adjacent cytoplasm. Benzimidazoles; Cell Nucleus; Fluorescent Dyes; Interphase; Microscopy, Fluorescence; Microscopy, Ultraviolet; Rotation; Video Recording

Parshad, R.; Sanford, K. K.; Jones, G. M. (1985): Chromatid damage induced by fluorescent light during G2 phase in normal and Gardner syndrome fibroblasts. Interpretation in terms of deficient DNA repair. In: Mutation research, Jg. 151, H. 1, S. 57–63. Abstract Skin fibroblasts from Gardner syndrome (GS) compared with those from normal donors showed a significantly higher incidence of chromatid gaps and breaks following exposure to low-intensity, cool-white fluorescent light during G2 phase of the cell cycle. Considerable evidence supports the concept that chromatid gaps and breaks seen directly after exposure to DNA-damaging agents represent unrepaired DNA single- and double-strand breaks respectively. The changes in incidence of chromatid aberrations with time after light exposure are consistent with the sequence of events known to follow DNA damage and repair. Initially, the incidence of light-induced chromatid gaps was equivalent in GS and normal fibroblasts. In the normal cells, the chromatid gaps disappeared by 1 h post-exposure, presumably as a result of efficient repair of DNA single-strand breaks. In contrast, the incidence of gaps increased in GS cells by 0.5 h followed by a decrease at 1 h and concomitant increase in chromatid breaks. It appears from these findings that the increased incidence of chromatid damage in GS fibroblasts results from deficient repair of DNA single-strand breaks which arise from incomplete nucleotide excision of DNA damage during G2 phase. Schlagwörter Cells, Cultured; Chromatidsradiation effects; DNA Repair; Dose-Response Relationship, Radiation; Gardner Syndromegenetics; Humans; Interphase; Light Parshad, R.; Sanford, K. K.; Jones, G. M.; Tarone, R. E. (1978): Fluorescent light-induced chromosome damage and its prevention in mouse cells in culture. In: Proceedings of the National Academy of Sciences of the United States of America, Jg. 75, H. 4, S. 1830–1833. Abstract Twenty-hour-exposure to fluorescent light produces chromatid breaks in a line of adult mouse lung cells grown in Dulbecco-Vogt medium supplemented with fetal bovine serum. The light-induced damage appears to be enhanced by increasing the concentration of oxygen in the gas phase of the culture. The effective wavelength(s) of light is in the visible range between 400 and 450 nm andis probably the mercury emission peak at 405 or 436 nm. Addition of catalase or glutathione with ascorbic acid to the culture medium reduced the number of chromatid breaks to a level not significantly different from that in the shielded cultures. It thus appears that the production of H2O2 in the culture medium or in the cell is responsible for the chromatid breaks. Most of the chromosomal abnormalities observed in long-term culture of mouse cells may result from exposure of cells or medium to fluorescent room lights in the presence of atmospheric oxygen. These genetic abnormalities can be minimized by shielding cells and medium from light, lowering the PO2 of the medium, and including reducing agents such as glutathione and ascorbic acid in the medium formulation. Schlagwörter Ascorbic Acidpharmacology; Catalasemetabolism; Cells, Cultureddrug effectsradiation effects; Chromosome Aberrations; Culture Media; Glutathionepharmacology; Hydrogen Peroxide; Light; Oxygen; Spectrum Analysis; Superoxide Dismutasemetabolism Parshad, R.; Sanford, K. K.; Jones, G. M.; Tarone, R. E.; Hoffman, H. A.; Grier, A. H. (1981): Susceptibility to fluorescent light-induced chromatid breaks associated with DNA repair deficiency and malignant transformation in culture. In: Cancer research, Jg. 40, H. 12, S. 4415–4419. Abstract The increased susceptibility of mouse cells to fluorescent light-induced chromatid damage following their spontaneous malignant transformation in culture could result

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from loss or inactivation of catalase that decomposes the photoproduct H2O2 or from impaired capacities to repair DNA damage. No consistent change in catalase activity with respect to neoplastic state could be established. To interpret the cytogenetic damage in terms of DNA strand breaks, we determined the incidence of chromatid breaks induced by light exposure during the G1 and late S-G2 phases of the cell cycle in normal and malignant derivatives of a C3H mouse cell line. Chromatid breaks at metaphase following light exposure during G1 would result from DNA strand breaks, cross-links, or base damage, whereas breaks following exposure during late S-G2 would result from single-or double-strand breaks. Both G1 and late S-G2 were susceptible in malignant cells but only G1 in normal. Since caffeine inhibits DNA repair, we compared its effects on light-induced chromatid damage in the normal and malignant cells to assess their DNA repair capacities. Treatment of normal cells with caffeine (50 microgram/ml) directly following five hr of light exposure in G1 increased the chromatid damage to that in malignant cells exposed with or without caffeine. Similarly, treatment of normal cells with caffeine during late S-G2 exposure increased chromatid damage to a level not significantly different from that in malignant cells exposed without caffeine. Caffeine had little influence on chromatid damage in malignant cells. The increased susceptibility of malignant mouse cells to fluorescent light-induced chromatid breaks thus appears to result from impaired capacities to repair DNA damage. Animals; Caffeinepharmacology; Catalasemetabolism; Cell Cycle; Cell Line; Cell Transformation, Neoplasticmetabolism; Chromatidsradiation effects; Chromosome Aberrations; DNA Repair; Interphase; Light; Mice

Parshad, R.; Sanford, K. K.; Tarone, R. E.; Jones, G. M.; Baeck, A. E. (1979): Increased susceptibility of mouse cells to fluorescent light-induced chromosome damage after long-term culture and malignant transformation. In: Cancer research, Jg. 39, H. 3, S. 929–933. Abstract Exposure of mouse cells in culture to fluorescent light has been shown to produce chromatid breaks and exchanges. Hydrogen peroxide formed in the cell during illumination has been implicated as the causative agent. The present results indicate that susceptibility to light-induced chromosome damage increases with time in culture and seems to be associated with or requisite for the spontaneous malignant transformation of mouse cells. All three cell lines followed during longterm culture that either became tumorigenic or showed cytological evidence of neoplastic transformation developed a concomitant increase in susceptibility. In three additional cell lines, susceptibility to light-induced chromatid damage was significantly increased in the spontaneously transformed malignant cells as compared with their nonneoplastic precursors. The increased susceptibility is not simply the result of long-term culture, since three other nonneoplastic cell lines after prolonged culture were significantly less susceptible than their malignant counterparts. Increased susceptibility to light-induced chromatid damage could result from impaired DNA repair or from the loss of defense mechanisms for destroying H2O2 or scavenging free radicals. Schlagwörter Animals; Cell Line; Cell Transformation, Neoplastic; Chromosome Aberrations; Crossing Over, Geneticradiation effects; DNAmetabolism; Hydrogen Peroxidemetabolism; Lightadverse effects; Mice; Time Factors Parshad, R.; Sanford, K. K.; Taylor, W. G.; Tarone, R. E.; Jones, G. M.; Baeck, A. E. (1980): Effect of intensity and wavelength of fluorescent light on chromosome damage in cultured mouse cells. In: Photochemistry and photobiology, Jg. 29, H. 5, S. 971–975. Schlagwörter Animals; Catalasemetabolism; Cell Line; Chromatidsmetabolism; Chromosomesradiation effects; Fluorescence; Hydrogen Peroxidemetabolism; Light; Mice Pitts, D. G.; Bergmanson, J. P.; Chu, L. W. (1984): Rabbit eye exposure to broad-spectrum fluorescent light. In: Acta ophthalmologica. Supplementum, Jg. 159, S. 1–54.

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Two F40CW fluorescent lamps mounted in an EYS-2404 fixture and 300 nm, 5 nm waveband UV radiation were used to expose pigmented rabbit eyes. The results of the exposures to the eye were evaluated with the biomicroscope, ophthalmoscope, light microscope and electron microscope. The following conclusions were reached: The adverse ocular responses to fluorescent radiation exposure were due to longduration, broadband radiation. These reactions were more generalized for fluorescent exposures when the cornea and lens are compared to UV exposures. The differences between the levels of threshold exposure needed to cause damage for the fluorescent source and UV radiation were attributed to exposure duration and the rate of delivery of the radiation. Corneal and lenticular damage was mild when compared with UV 300 nm exposures, and the threshold occurred after 8 h to 12 h of exposure. The effect of the radiation was to interfere with the normal functions of the cell while changes to the inert materials in the tissues was secondary to injury to the cell. The damage was mild in the corneal epithelium, somewhat more severe in the corneal endothelium, but minimal in the corneal stroma. Early retinal changes were found after 8 h of exposure to the fluorescent source. These induced changes were evident in the neural retina as spaces and were assumed to represent oedema. The retinal oedema was initially found only in the receptor cell, outer nuclear and nerve fibre layers. Many vacuoles or spaces were located in the junctional area between the ganglion cell and nerve fibre layers while smaller spacing occurred also within the nerve fibre layer. Twelve h of exposure to the fluorescent source produced a further increase in the oedema in the retina. The outer segments of the receptor cells appear to disintegrate and significant open spaces are evident among the inner and outer segments of the receptors. The inner plexiform layer shows an increased number of spaces within and among the neural elements, and the mitochondria appeared to be undergoing changes. The 20-h and longer exposure induced severe changes affecting all layers of the retina. These changes include massive retinal oedema with degenerative signs in all retinal neurons. A sympathetic reaction of the unexposed, contralateral eye occurred as the result of the damage to the exposed eye. Minimal sympathetic responses to the cornea and the lens began at exposure durations at or above 12 h, while the retina showed the sympathetic reaction beginning at 8 h.(ABSTRACT TRUNCATED AT 400 WORDS) Animals; Cornearadiation effectsultrastructure; Eyeradiation effectsultrastructure; Fluorescence; Lens, Crystallineradiation effectsultrastructure; Lightadverse effects; Rabbits; Radiation Dosage; Time Factors; Ultraviolet Raysadverse effects

Reese, C. T.; Ntam, C.; Martin, T. V.; Carrington, S.; Leotaub, J.; Cox, L. et al. (2007): Internalization of nearinfrared fluorescent dyes within isolated macrophage populations. In: Cellular and molecular biology (Noisy-leGrand, France), Jg. 53, H. 3, S. 27–33. Abstract The development and application of microsensor technology has enhanced the ability of scientists to further understand various biological activities, such as changes in the intracellular environment after injury or toxic exposure. NIR microsensor technology may be useful in detecting the cellular injuries or adverse changes during the early onset period, allowing for the administration of therapies to initiate recovery. The development and use of Infrared (IR) and near infrared (NIR) dyes as biological micro-sensors due to their advanced spectral characteristics may be helpful. Three of the more useful NIR dye characteristics include the ability to minimize background interference by extraneous biological matrices, the ability to exhibit optimal molar absorptivity and quantum yields, and the ability to maintain normal cellular activity. Thus, the current study was designed to investigate the ability of selected NIR micro-sensor dyes to undergo cellular internalization, demonstrate intracellular NIR fluorescent signaling, and maintain normal cellular activity. The results demonstrate that the selected NIR micro-sensor dyes undergo cellular internalization. The presence of the dyes within the cells did not affect cell viability. In addition, these dyes demonstrate changes in absorbance and

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fluorescence after the immune cells were challenged with a stimulant. Moreover, critical cellular functions, such as tumor necrosis factor release and superoxide production were not compromised by the internalization of the fluorescent dyes. These data suggest that selected NIR micro-sensor dyes can undergo intracellular internalization within isolated macrophages without adversely affecting various parameters of normal cellular activity. Analysis of Variance; Biological Transport; Biosensing Techniques; Chemotaxis; Fluorescent Dyes; Fluorometry; Infrared Rays; Macrophages; Spectrometry, Fluorescence; Superoxides; Tumor Necrosis Factor-alpha

Reinhardt, Harris (1942): The fluorescent lighting handbook. A practical guide to the performance, characteristics and applications of fluorescent lighting. Hygrade Sylvania corporation. (Hg.). Salem Mass.: Hygrade Sylvania Corporation. Schlagwörter Fluorescent lighting. Reszka, K.; Eldred, G. E.; Wang, R. H.; Chignell, C.; Dillon, J. (1996): The photochemistry of human retinal lipofuscin as studied by EPR. In: Photochemistry and photobiology, Jg. 62, H. 6, S. 1005–1008. Abstract Fluorescent material generated in the human retina accumulates within lipofuscin (HLF) granules of the retinal pigment epithelium (RPE) during aging. We have been investigating the possible light-induced contribution of these fluorophores to various diseases including age-related macular degeneration. Our studies have shown that some of the fluorescent components of HLF are products of the reaction of retinaldehyde with ethanolamine and that synthetic mixtures of this reaction can serve as a useful model for photophysical studies. Previous research by us has demonstrated that irradiation of either natural or synthetic lipofuscin resulted in the formation of a triplet state and possibly a free radical. Here EPR studies were performed to verify the formation of that radical. The UV irradiation of either synthetic or natural human retinal lipofuscin extracts in oxygen-free methanol led to the formation of a 5,5-dimethylpyrroline-N-oxide (DMPO) spin-trapped carboncentered radical resulting from either hydrogen atom or electron abstraction from solvent molecules. In the presence of oxygen superoxide was formed, which was observed as a DMPO adduct. It is concluded that certain components of the chloroform-soluble fluorophores of human RPE lipofuscin granules and the fluorescent reaction products of retinaldehyde and ethanolamine are photophysically similar but not the same. Electron or hydrogen abstraction from a substrate by these fluorophores in vivo and the resulting radical products may contribute to the age-related decline of RPE function and blue light damage in the retina. Schlagwörter Adult; Electron Spin Resonance Spectroscopy; Humans; Lipofuscinchemistryisolation & purification; Photochemistry; Pigment Epithelium of Eyechemistrymetabolism Saltarelli, C. G.; Coppola, C. P. (1979): Influence of visible light on organ weights of mice. In: Laboratory animal science, Jg. 29, H. 3, S. 319–322. Abstract Hau:ICR mice separated by sex, were reared for 30 days under various fluorescent lamps: pink, blue, black UV, cool white and full spectrum. Body weights and absolute organ weights were compared. After light exposure, female body weights were not significantly different between any groups; however, a difference in male body weights was observed. Light affected the weights of the pituitary, adrenals, kidneys and prostate in male mice and the adrenals, thyroid and pineal glands in females. The weight of adrenal glands of both males and females were most sensitive to changes in lighting. Schlagwörter Adrenal Glandsradiation effects; Animals; Body Weightradiation effects; Female; Light; Male; Micegrowth & development; Organ Sizeradiation effects; Pineal Glandradiation effects; Pituitary Glandradiation effects; Sex Factors

iLib08 - Citavi Sanford, K. K.; Parshad, R.; Jones, G.; Handleman, S.; Garrison, C.; Price, F. (1980): Role of photosensitization and oxygen in chromosome stability and "spontaneous" malignant transformation in culture. In: Journal of the National Cancer Institute, Jg. 63, H. 5, S. 1245–1255. Visible light and oxygen enhanced both chromosome instability and malignant Abstract transformation of mouse cells in culture. Nine cell lines were initiated from 8 pools of 10- to 13-day C3H embryos. Each cell line was divided into sublines, which were either maintained shielded from light or were exposed for 3 or 24 hours to fluorescent light (approximately 150 foot-candles) two or three times weekly. Cultures of the sublines were also maintained with either a gaseous phase of 0-1% oxygen or atmospheric (18%) oxygen. Each line was monitored for cytologic manifestations of malignant neoplastic transformation, and 8 lines were monitored for chromosome alterations. Seven lines were assayed for tumorigenicity by intraocular implantation into syngeneic hosts. Repeated light exposure and/or high oxygen increased the frequency of minute chromosomes, which result from chromatid breaks, and also increased the rate of shift from diploid to heteroploid state. Four cell lines showed no cytologic changes indicative of neoplastic change during the test period. Two of these were assayed in vivo and failed to grow as tumors. In the remaining 6 lines, cytologically neoplastic colonies appeared earlier or more abundantly in the light-exposed cultures and/or those gassed with high oxygen. In 3 of these lines, tumors developed only from the light-exposed cultures; in the other 2, tumor latency periods were significantly shorter in the cultures exposed to light or gassed with atmospheric oxygen. Schlagwörter Animals; Cell Divisionradiation effects; Cell Line; Cell Survivalradiation effects; Cell Transformation, Neoplastic; Chromosome Aberrations; Embryo, Mammalian; Lightadverse effects; Mice; Mice, Inbred C3H; Neoplasm Transplantation; Neoplasms, Experimentaletiology; Oxygen; Transplantation, Homologous Schmidt, Tiffany M.; Taniguchi, Kenichiro; Kofuji, Paulo (2008): Intrinsic and extrinsic light responses in melanopsin-expressing ganglion cells during mouse development. In: Journal of neurophysiology, Jg. 100, H. 1, S. 371–384. Online verfügbar unter doi:10.1152/jn.00062.2008. Abstract Melanopsin (Opn4) is a photopigment found in a subset of retinal ganglion cells (RGCs) that project to various brain areas. These neurons are intrinsically photosensitive (ipRGCs) and are implicated in nonimage-forming responses to environmental light such as the pupillary light reflex and circadian entrainment. Recent evidence indicates that ipRGCs respond to light at birth, but questions remain as to whether and when they undergo significant functional changes. We used bacterial artificial chromosome transgenesis to engineer a mouse line in which enhanced green fluorescent protein (EGFP) is expressed under the control of the melanopsin promoter. Double immunolabeling for EGFP and melanopsin demonstrates their colocalization in ganglion cells of mutant mouse retinas. Electrophysiological recordings of ipRGCs in neonatal mice (postnatal day 0 [P0] to P7) demonstrated that these cells responded to light with small and sluggish depolarization. However, starting at P11 we observed ipRGCs that responded to light with a larger and faster onset (<1 s) and offset (<1 s) depolarization. These faster, larger depolarizations were observed in most ipRGCs by early adult ages. However, on application of a cocktail of synaptic blockers, we found that all cells responded to light with slow onset (>2.5 s) and offset (>10 s) depolarization, revealing the intrinsic, melanopsin-mediated light responses. The extrinsic, cone/rod influence on ipRGCs correlates with their extensive dendritic stratification in the inner plexiform layer. Collectively, these results demonstrate that ipRGCs make use of melanopsin for phototransduction before eye opening and that these cells further integrate signals derived from the outer retina as the retina matures. Schlagwörter Action Potentialsphysiologyradiation effects; Age Factors; Animals; Animals, Newborn; Chromosomes, Artificial, Bacterialphysiology; Dose-Response Relationship, Radiation; Gene Expression Regulation, Developmentalphysiologyradiation effects; Green Fluorescent

iLib08 - Citavi Proteinsgeneticsmetabolism; Light; Mice; Mice, Transgenic; Patch-Clamp Techniquesmethods; Photic Stimulationmethods; Reaction Time; Retinacytologygrowth & development; Retinal Ganglion Cellsmetabolismradiation effects; Rod Opsinsgeneticsmetabolism Sheng, Hui; Lu, Yi; Qing, Feng-ling (2008): [Blue light-induced damage to human retinal pigmented epithelial cells mediated by A2E]. In: [Zhonghua yan ke za zhi] Chinese journal of ophthalmology, Jg. 43, H. 11, S. 1017–1021. Abstract OBJECTIVE: To observe the internalization of A2E by human retinal pigmented epithelial (hRPE) cells and study whether the lipofuscin fluorophore A2E (Nretinylidene-N-retinylethanolamine) participates in blue light-induced damage to hRPE cells. METHODS: A mixture of all-trans-retinal and ethanolamine was used to produce A2E in one step. A2E granules were delivered to medium of cultured hRPE cells for internalization. Confluent cultures were subsequently exposed to 450 nm (blue) light for 20 minutes with or without A2E (25, 50, 100 micromol/L). The light intensity was 70 mW/mm(2). Phototoxicity was quantified at 12, 24, 36, and 48 h after exposure by CCK-8 of viable cells. Apoptosis of cells was detected by Hoechst 33342 DNA staining and flow cytometry. RESULTS: The reaction of all-trans-retinal (100 mg) and ethanolamine (9.5 mg) produced 53.8 mg A2E in one step. When A2E was delivered to hRPE cells in culture, it accumulated intracellularly. Internalized A2E presented as autofluorescent granules having a perinuclear distribution. As shown by CCK-8 analysis, the A2E-fed hRPE cell viability reduced with duration after 450 nm light exposure. Conversely, blue light-exposed hRPE cells that did not contain A2E showed less loss of cell viability. The percentage of hRPE cell apoptosis with 25 micromol/L A2E 12, 24, 36 and 48 h after blue light exposure was (12.11 +/- 2.32)%, (31.21 +/- 3.72)%, (64.23 +/- 3.53)% and (58.71 +/- 3.48)% respectively. Conversely, the apoptosis was less than 5% in other hRPE cells. CONCLUSIONS: A2E is essential to blue light-induced hRPE cell damage. Only blue light exposure and without A2E lead to little cell injury. hRPE cells in old people which contain much lipofuscin are sensitive to blue light injury. Siopes, T. D. (1984): The effect of full-spectrum fluorescent lighting on reproductive traits of caged turkey hens. In: Poultry science, Jg. 63, H. 6, S. 1122–1128. Large White turkey breeder hens were exposed to either incandescent or fullAbstract spectrum (FS) fluorescent lighting during two 20-week reproductive cycles in closed confinement. Data were recorded for body weights, feed intake, and reproductive traits. Body weights and feed intake were similar between treatments in both egg laying cycles. In addition, there were no significant differences in egg production, fertility, hatchability, or poult weight between the incandescent and FS fluorescent light treatment in either the first or second year egg laying cycle. It was concluded that exposure of breeder turkey hens to FS fluorescent light in closed confinement results in reproductive performance similar to that obtained with incandescent lighting. Schlagwörter Animals; Body Weight; Eating; Female; Fluorescence; Housing, Animal; Light; Oviposition; Reproduction; Turkeysphysiology Society for Visual Education. (Hg.) (1970): "Cool" light from electricity (Filmstrip). n.p.: Society for Visual Education. Schlagwörter Electric currents.; Neon lamps.; Fluorescent lighting. Spreadbury, F. G. (1946): Electric discharge lighting. London: Sir I. Pitman & sons ltd. Schlagwörter Electric lighting, Mercury vapor.; Electric lighting, Sodium vapor.; Fluorescent lighting. Stark, W. S.; Carlson, S. D. (1985): Blue and ultraviolet light induced damage to the Drosophila retina: ultrastructure. In: Current eye research, Jg. 3, H. 12, S. 1441–1454.

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Intense ultraviolet (UV) and blue stimulation photolyses rhodopsin through a fluorescent metarhodopsin (M') in the predominant photoreceptor type, R1-6, of the compound eye of white eyed Drosophila melanogaster. We investigated the associated retinal degeneration using High Voltage Electron Microscopy (HVEM). The threshold for UV induced damage was about 19 log quanta/cm2 while for blue, the threshold was about 20. These intensities are toward the upper level of the dynamic range for rhodopsin photolysis. Thus, there is a sensitization for near UV induced degeneration as had been found for photolysis of the visual pigment. Vitamin A deprivation protects against light elicited retinal degeneration, particularly in the UV. Since vitamin A deprivation eliminates the blue absorbing rhodopsin and a UV sensitizing pigment in R1-6, the degeneration is likely mediated through quantal absorption through these photoexcitation pigments. Intense light converts the microvilli of the rhabdomeres (the photopigment containing organelles) into dense strands and the cytoplasm fills with a dense reticulum. Such damage is elicited shortly after stimulation and is permanent. Under most conditions, the second order interneurons are spared. These results are discussed in the context of other animal models of intense light retinal degeneration. Animals; Dose-Response Relationship, Radiation; Drosophila melanogaster; Interneuronsradiation effects; Microscopy, Electron; Neurogliaradiation effects; Neuronsradiation effects; Photoreceptor Cellsradiation effects; Radiation Injuries, Experimentaletiologypathology; Retinapathologyradiation effects; Retinal Degenerationetiologypathology; Synapsesradiation effects; Ultraviolet Raysadverse effects

Stark, W. S.; Walker, K. D.; Eidel, J. M. (1985): Ultraviolet and blue light induced damage to the Drosophila retina: microspectrophotometry and electrophysiology. In: Current eye research, Jg. 4, H. 10, S. 1059–1075. Abstract Intense ultraviolet (UV) and blue stimulation decreases visual pigment concentration and increases long wavelength fluorescent emission in R1-6 photoreceptors in the white eyed fruit fly Drosophila melanogaster. We used microspectrophotometry to show that the threshold for visual pigment decrease is about 1 log unit lower for UV than for blue light (18.7 vs approximately 19.9 log quanta/cm2 respectively). UV and blue stimuli about 0.2 log units brighter had been shown to cause structural degeneration. Above the threshold for structural damage, visual pigment is decreased permanently while below this level, a recovery of visual pigment was achieved within several hours. Microspectrofluorometric data are partially consistent with the hypothesis that the visual pigment is converted into a fluorescent product which had been named M'. M' had been proposed to be a new form of metarhodopsin which absorbs chiefly in the yellow and which has a fluorescent emission in the red; long wavelength stimulation had been reported to regenerate the native visual pigment from M'. Our data suggest that the situation is significantly more complex than this simple model. For instance, we report that long wavelength stimulation regenerates only a small fraction of the visual pigment which had been decreased by UV or blue stimulation. Furthermore, several lines of evidence suggest that other fluorescent products are also created by intense UV and blue stimulation. We were particularly interested in the lower damage threshold for UV light because of the hypothesis that UV visual sensitivity is mediated by a sensitizing pigment which absorbs UV light and transfers its energy to the blue absorbing rhodopsin. Our data suggest that the UV light decreases the rhodopsin without preferentially decreasing the sensitizing pigment. Schlagwörter Animals; Drosophila melanogasterradiation effects; Electrophysiology; Electroretinography; Fluorometry; Lightadverse effects; Retinaradiation effects; Retinal Pigmentsbiosynthesismetabolismradiation effects; Spectrophotometrymethods; Time Factors; Ultraviolet Raysadverse effects Stenkamp, Deborah L.; Satterfield, Rosanna; Muhunthan, Kalyani; Sherpa, Tshering; Vihtelic, Thomas S.; Cameron, David A. (2008): Age-related cone abnormalities in zebrafish with genetic lesions in sonic hedgehog.

iLib08 - Citavi In: Investigative ophthalmology & visual science, Jg. 49, H. 10, S. 4631–4640. Online verfügbar unter doi:10.1167/iovs.07-1224. Abstract PURPOSE: Sonic hedgehog (Shh) signaling is essential for photoreceptor differentiation and retinal cell survival in embryonic zebrafish. The study was conducted to determine whether adult heterozygous carriers of mutant alleles for the shh gene display retinal abnormalities. METHODS: Retinal cryosections from young, middle-aged, and senescent wild-type and sonic-you(+/-) (syu(+/-)) zebrafish were probed with retinal cell type-specific markers. Contralateral retinal flatmounts from these fish, and from adult albino zebrafish subjected to light-induced photoreceptor damage followed by regeneration, were hybridized with blue cone opsin cRNA for quantitative analysis of the blue cone pattern. Retinal expression of shh mRNA was measured by quantitative RT-PCR. RESULTS: Regions of cone loss and abnormal cone morphology were observed in the oldest syu(+/-) zebrafish, although no other retinal cell type was affected. This phenotype was age-related and genotype-specific. Cone distribution in the oldest syu(+/-) zebrafish was predominantly random, as assessed by measuring the short-range pattern, whereas that of wild-type fish and the younger syu(+/-) zebrafish was statistically regular. A measure of long-range pattern revealed atypical cone aggregation in the oldest syu(+/-) zebrafish. The light-treated albino zebrafish displayed random cone patterns immediately after light toxicity, but showed cone aggregation on regeneration. Retinas from the syu(+/-) fish showed reduced expression of shh mRNA compared with those of wild-type siblings. CONCLUSIONS: The syu(+/-) zebrafish presents a model for the study of hereditary age-related cone abnormalities. The syu(+/-) retinas most likely experience progressive cone photoreceptor loss, accompanied by cone regeneration. Shh signaling may be required to maintain cone viability throughout life. Schlagwörter Agingphysiology; Alleles; Animals; Cell Death; Cell Proliferation; Fluorescent Antibody Technique, Indirect; Gene Expressionphysiology; Hedgehog Proteinsgenetics; In Situ Hybridization; In Situ Nick-End Labeling; Light; Microscopy, Fluorescence; Mutation; RNA, Messengermetabolism; Radiation Injuries, Experimentaletiologygeneticspathology; Retinaradiation effects; Retinal Cone Photoreceptor Cellsmetabolismpathology; Retinal Degenerationetiologygeneticspathology; Reverse Transcriptase Polymerase Chain Reaction; Rod Opsinsmetabolism; Zebrafishgenetics; Zebrafish Proteinsgenetics Stoutemyer, Vernon Theodore; Close, Albert William (1945): Plant propagation under fluorescent light. United States. (Hg.). Beltsville Md. Schlagwörter Plant propagation.; Fluorescent lighting. Strum, Carl Heinz (1952): Vorschaltgeräte und Schaltungen für Leuchtstofflampen. Brown, Boveri &. Cie A. -G (Hg.). Mannheim: Brown Boveri & Cie. Schlagwörter Fluorescent lighting. Taniguchi, Yukinori; Ikehara, Tatsuya; Kamo, Naoki; Watanabe, Yasutaka; Yamasaki, Hiroshi; Toyoshima, Yoshinori (2007): Application of fluorescence resonance energy transfer (FRET) to investigation of light-induced conformational changes of the phoborhodopsin/transducer complex. In: Photochemistry and photobiology, Jg. 83, H. 2, S. 311–316. Online verfügbar unter doi:10.1562/2006-06-15-RA-922. Abstract The photoreceptor phoborhodopsin (ppR; also called sensory rhodopsin II) forms a complex with its cognate the Halobacterial transducer II (pHtrII) in the membrane, through which changes in the environmental light conditions are transmitted to the cytoplasm in Natronomonas pharaonis to evoke negative phototaxis. We have applied a fluorescence resonance energy transfer (FRET)-based method for investigation of the light-induced conformational changes of the ppR/pHtrII complex. Several far-red dyes were examined as possible fluorescence donors or acceptors because of the absence of the spectral overlap of these dyes with all the photointermediates of ppR. The flash-induced changes of distances between the

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donor and an acceptor linked to cysteine residues which were genetically introduced at given positions in pHtrII(1-159) and ppR were determined from FRET efficiency changes. The dye-labeled complex was studied as solubilized in 0.1% ndodecyl-beta-D-maltoside (DDM). The FRET-derived changes in distances from V78 and A79 in pHtrII to V185 in ppR were consistent with the crystal structure data (Moukhametzianov, R. et al. [2006] Nature, 440, 115-119). The distance from D102 in pHtrII linker region to V185 in ppR increased by 0.33 angstroms upon the flash excitation. These changes arose within 70 ms (the dead time of instrument) and decayed with a rate of 1.1 +/- 0.2 s. Thus, sub-angstrom-scale distance changes in the ppR/pHtrII complex were detected with this FRET-based method using far-red fluorescent dyes; this method should be a valuable tool to investigate conformation changes in the transducer, in particular its dynamics. Archaeal Proteins; Fluorescence Resonance Energy Transfer; Halobacteriaceae; Halorhodopsins; Multiprotein Complexes; Photochemistry; Protein Conformation; Recombinant Proteins; Sensory Rhodopsins

Tanito, Masaki; Kaidzu, Sachiko; Anderson, Robert E. (2006): Protective effects of soft acrylic yellow filter against blue light-induced retinal damage in rats. In: Experimental eye research, Jg. 83, H. 6, S. 1493–1504. Online verfügbar unter doi:10.1016/j.exer.2006.08.006. Abstract Recently, a yellow intraocular lens (IOL) was developed for the purpose of reducing potential blue light-induced retinal damage after cataract surgery. However, the effect of yellow filters on retinal protection remains to be clarified. To test the protective effects of yellow filters on blue light-induced retinal damage, a yellow and a clear soft acrylic filter were attached to the right and left eyes, respectively, of albino rats and exposed to 4.5 k lux blue fluorescent lights with peak wavelength at 420 nm (ranging 380-500 nm; short blue) or 446 nm (ranging 400-540 nm; long blue) for 6h. To assess retinal damage, the electroretinogram (ERG) was recorded at 7 days, outer nuclear layer (ONL) thickness and area were measured at 7 days, apoptosis was analyzed by TUNEL staining at 24 h, and the level of lipid peroxidation in retinas was assessed by Western dot blots using specific antibodies against 4-hydroxynonenal (4-HNE)- and carboxyethylpyrrole (CEP)-modified proteins immediately after light exposure. After short blue light exposure, a- and bwave ERG amplitudes and the ONL thickness at 1-2.5 mm inferior and 0.5-2.5 mm superior to optic nerve head (ONH) were significantly reduced. TUNEL staining in the ONL at 0-2 mm inferior and 1-2 mm superior to the ONH, and retinal levels of 4HNE- and CEP-modified proteins were significantly increased in the clear filtercovered eyes compared to yellow filter-covered eyes. After long blue light exposure, the only difference seen was a greater ONL thickness at 1.5 mm superior to the ONH in yellow filter-covered eye. Transmission of light through the yellow filter was 58% for short blue and 89% for long blue compared to the clear filter. The ONL area was not different between clear filter-covered and -uncovered eyes after exposure to short or long blue light. Given the results, yellow IOL material protects the retina against acute shorter wavelength blue light exposure more effectively than the clear IOL material. Schlagwörter Animals; Apoptosisradiation effects; Color; Electroretinography; Eye Proteinsmetabolism; Filtrationinstrumentation; Lens, Crystallinephysiologyradiation effects; Lightadverse effects; Lipid Peroxidation; Photoreceptor Cells, Vertebrateradiation effects; Radiation Injuries, Experimentalprevention & control; Rats; Rats, Sprague-Dawley; Retinametabolismphysiopathologyradiation effects; Retinal Degenerationpathologyprevention & control; Scattering, Radiation; Ultraviolet Rays Veitch, J. A.; McColl, S. L. (2001): A critical examination of perceptual and cognitive effects attributed to fullspectrum fluorescent lighting. In: Ergonomics, Jg. 44, H. 3, S. 255–279. Abstract Full-spectrum fluorescent lighting (FSFL) has been credited with causing dramatic improvements in vision, perception and cognitive performance as compared with

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other fluorescent lamp types. These effects are hypothesized to occur because of similarity between FSFL emissions and daylight, which is said to have evolutionary superiority over other light sources. This review, covering 1945-98, critically considers the evidence for these claims. In general, poor-quality research has resulted in an absence of simple deterministic effects that can be confidently attributed to fluorescent lamp type. Promising avenues for lighting behaviour research include investigations of cognitive mediators of lighting-behaviour relationships, and flicker rates and colour rendering effects on visual processing, appearance judgements and affect. Good lighting solutions are more complex than lamp type specification. Cognition; Humans; Job Satisfaction; Lighting; Task Performance and Analysis; Visual Perception; Workplace

Wyse, J. P. (1980): Renewal of rod outer segments following light-induced damage of the retina. In: Canadian journal of ophthalmology. Journal canadien d'ophtalmologie, Jg. 15, H. 1, S. 15–19. Fluorescent lighting was used to induce severe but reversible damage of the rod Abstract outer segments of the retinas of albino rats. The animals were then kept in continuous darkness for up to 12 days. Pairs of animals were killed after 1, 3, 5, 7, 9 and 12 days of continuous darkness. Light microscopic examination of the retinas demonstrated a sharp demarcation between the light-damaged distal ends of the rod outer segments and the newly formed proximal ends. Measurement of the proximal ends demonstrated proximo-distal renewal of the rod outer segments during the first 9 days of continuous darkness. Parametric statistical analysis of the data revealed that the renewal occurred linearly, at an average rate of 2.66 micron/d, which is similar to the rate of renewal of the rod outer segments in the undamaged retina of the rat. Schlagwörter Animals; Dark Adaptation; Lightadverse effects; Photoreceptor Cellsphysiologyradiation effects; Rats; Regeneration Xu, Xiaoyang; Zhao, Xiufeng; Liu, Timon Cheng-Yi; Pan, Hongying (2008): Low-Intensity Laser Irradiation Improves the Mitochondrial Dysfunction of C2C12 Induced by Electrical Stimulation. In: Photomedicine and laser surgery. Online verfügbar unter doi:10.1089/pho.2007.2125. Abstract Abstract Objective: We investigated the effects of electrical stimulation and lowintensity laser (LIL) energy on the mitochondrial function of cultured C2C12 myotubes in order to find a dosage that could be used to improve the function of mitochondria, and then rehabilitate exercise-induced damage and fatigue. Background Data: Many other studies in the past demonstrated that LIL had a cytoprotective effect, and a recent study also found that LIL could reduce muscular fatigue during tetanic contractions in rats. Methods: Cultured C2C12 myotubes were subjected to electrical stimulation or/and LIL irradiation at various intensities. Reactive oxygen species (ROS) were detected with a fluorescent probe (DCFH-DA) and mitochondrial function was assessed with an MTT assay. Results: The results showed that electrical stimulation at 20 ms, 5 Hz, and 45 V for 75 min can induce mitochondrial dysfunction in cultured C2C12 myotubes. Electrical stimulationinduced mitochondrial dysfunction was improved, but degeneration occurred with LIL at doses of 0.33-8.22 and 11.22-14.16 J/cm(2), respectively, and these changes were markedly increased with LIL at 0.33 and 1.34 J/cm(2), respectively. Conclusions: We conclude that treatment of myotubes with the proper dosage of LIL irradiation significantly diminished production of ROS and restored mitochondrial function, and this may provide a foundation for the use of photobiomodulation to treat exercise-induced mitochondrial dysfunction or skeletal muscular fatigue. Yu, Xiaoping; Chen, Ka; Wei, Na; Zhang, Qianyong; Liu, Jihuan; Mi, Mantian (2007): Dietary taurine reduces retinal damage produced by photochemical stress via antioxidant and anti-apoptotic mechanisms in SpragueDawley rats. In: The British journal of nutrition, Jg. 98, H. 4, S. 711–719. Online verfügbar unter

iLib08 - Citavi doi:10.1017/S0007114507744409. Abstract Taurine has been shown to be tissue protective in many models of oxidant-induced injury. However, its protective role against retinal damage induced by photochemical stress is less well known. The purpose of the present study was to investigate whether dietary taurine reduced retinal photochemical damage in Sprague-Dawley rats and to further explore the underlying molecular mechanisms of this action. Twenty rats fed AIN-93 formulation and maintained in the dark for 48 h were used as controls (n 20). Another forty rats were randomly divided into two groups and then treated with (n 20) or without 4 % taurine (n 20) for 15 d respectively. After treatment, these two groups were exposed to fluorescent light (3000 +/- 200 lux and 25 degrees C), and the protective effects of dietary taurine were then evaluated. The present results showed that dietary taurine effectively prevented retinal photochemical damage as assessed by changes of morphology. Also, the supplementation caused an increase of taurine in the retina, a decrease of malondialdehyde (P < 0.01), and elevation of superoxide dismutase (P < 0.01) and glutathione peroxidase activities in the retina (P < 0.01). Moreover, dietary taurine inhibited activator protein-1 (AP-1) (c-fos/c-jun subunits) expression (P < 0.05), up regulated NF-kappaB (p65) expression (P < 0.05), and decreased caspase-1 expression (P < 0.05) so as to reduce the apoptosis of photoreceptors in the retina (P < 0.05). These results suggest that dietary taurine reduced retinal damage produced by photochemical stress via antioxidant and anti-AP-1-NF-kappaBcaspase-1 apoptotic mechanisms in rats. Schlagwörter Animals; Antioxidantsphysiology; Apoptosisdrug effects; Diet; Oxidants, Photochemicalpharmacology; Random Allocation; Rats; Rats, Sprague-Dawley; Retinal Diseaseschemically inducedprevention & control; Taurineadministration & dosagepharmacology; Treatment Outcome Zand, M. S.; Albrecht-Buehler, G. (1989): Long-term observation of cultured cells by interference-reflection microscopy: near-infrared illumination and Y-contrast image processing. In: Cell motility and the cytoskeleton, Jg. 13, H. 2, S. 94–103. Online verfügbar unter doi:10.1002/cm.970130204. Abstract Interference-reflection microscopy (IRM) is the only method presently available with which to visualize cell-substratum adhesions in living tissue culture cells continuously for long periods of time without the use of fluorescent markers (Curtis: J. Cell Biol. 20:199-215, 1964; Izzard and Lochner: J. Cell Sci. 21:129-159, 1976). This method utilizes approximately 1% of the incident illumination to produce the IRM image (Verschueren: J. Cell Sci. 75:279-301, 1985) and so far has required the use of high-intensity light sources in the visible spectral range (400-800 nm). Unfortunately, visible light of this intensity and spectral range induces marked changes in the behavior and morphology of motile fibroblasts, including cessation of locomotion. In contrast, the present paper reports that continuous observations of live cells in IRM for periods of up to 8 hours are possible if the illuminating light is in the red to near-infrared range (650-950 nm) and without any observable change in normal cell morphology or behavior. In addition, we describe how the technique of Y-contrast image processing can be applied to IRM images to create a threedimensional image of the ventral cell surface topography. Schlagwörter Animals; Cell Line; Cell Movement; Cells, Cultured; Fibroblasts; Infrared Rays; Mice; Microscopy, Interference Zwikker, C. (1952): Fluorescent lighting. A review of the scientific and technical fundamentals and of the applications of the fluorescent lamp and its accessories. London: distributors for United Kingdom; Cleaver Hume Press; distributors for U.S.A.: Elsevier Press Houston (Philips technical library). Schlagwörter Fluorescent lighting.