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Home > April 2010 Vol. 2 Issue 4 > L-Carnosine's Effects on Cataract Development

L-Carnosine's Effects on Cataract Development [1]

Cataract is the opacification of the ocular lens or capsule.

By Tina Kaczor, ND, FABNO

Abstract

Cataracts are the leading cause of blindness worldwide. With an aging population, the
incidence and prevalence of cataract-induced blindness is expected to rise
considerably. L-carnosine (β-alanyl-L-histidine) is an endogenous dipeptide compound
in vertebrates that has been designated an “antiaging” molecule due to its ability to
delay senescence of cells. L-carnosine and N-acetyl-L-carnosine have demonstrated a
reduction in opacification of the lens when used as a direct instillation to the eye. These
compounds represent a promising new means of addressing cataracts.

Introduction

Cataract is the opacification of the ocular lens or capsule. According to the World
Health Organization, in the year 2002, the last year that statistics were estimated,
cataracts caused nearly half of the 37 million cases of blindness worldwide.1 In the
United States, 20.5 million Americans over the age of 40 are affected in at least one
eye, with an estimated increase to over 30 million Americans by the year 2020.2
Surgery is the only treatment option available and, while highly successful at restoring
sight, it is not feasible in many developing countries that lack the infrastructure for
adequate access to care.3 Ultimately, an easily disseminated medication that is
economical and convenient could have a profound impact on the prevalence of the
disease.4 Currently no agent is approved for use in preventing or delaying the onset of
cataracts. There is evidence, however, that the natural agent L-carnosine (β-alanyl-L-
histidine) effectively delays cataract development. The uniformity of benefit from
preliminary evidence on carnosine and lens health, combined with a low toxicity profile
make this endogenous dipeptide an intriguing candidate for prevention of cataract
formation.
Background

Lens fiber cells are long, transparent cells continually produced by epithelial cells in the
anterior portion of the lens and growing around the periphery (like longitudinal lines on a
globe) to reach the posterior aspect. This process begins embryologically with the first
lens fiber cells essentially providing the nexus upon which fetal and then adult lens
fibers are built. Anatomically, these cells accumulate like layers in an onion, with the
center becoming the nuclear region, outside of which is the cortical region. Aptly
named, the subcapsular region is found between the cortical region and capsule that
encompasses the lens.

Of note, all mature lens fiber cells lack nuclei or organelles, necessitating diffusion of
many molecules, including nutrients, into the cells. The lack of intracellular structures
and complete solubility of proteins, predominantly proteins called crystallins, within the
lens cells is necessary for light rays to penetrate to the back of the eye.

Cataracts are classified into 3 types, depending on the region of the eye in
which they originate.

Cataracts are classified into 3 types, depending on the region of the eye in which they
originate. Nuclear cataracts begin at the center of the lens and affect distant vision in
particular. These are the most common type of cataract and are thought to occur due to
the aging process—thus the common term “age-related” or “senile” cataracts. Cortical
cataracts are also called “diabetic cataracts”; they begin in the periphery of the lens and
progress inward in a spoke-like fashion. Subcapsular cataracts usually begin at the
back of the lens (posterior subcapsular cataracts) and are found in patients with a
history of diabetes, steroid use, retinitis pigmentosa, or severe nearsightedness.

While symptomology varies between type and degree of cataract, the main symptoms
of cloudy vision and sensitivity to glare is common to all forms at some stage of
development. Double vision or multiple images in one eye can also occur. Unique to the
development of nuclear cataracts, there may be a period of “second sight,” when the
focus of near objects improves. This ability to see close objects more clearly is short
lived, however, as the lens becomes more opaque and cloudy vision more severe.
Cortical cataracts affect both distant and near vision and, while blurring occurs,
sensitivity to glare and loss of contrast are more significant in this type of cataract.
Subcapsular cataracts usually occur concomitantly with nuclear or cortical, and this type
is marked by a more rapid progression.

Before any agents, synthetic or natural, are considered it is prudent to address known
risk factors for cataract development. Risk factors include aging, diabetes, obesity,
exposure to UVB radiation, smoking, previous eye surgery, prolonged use of some
drugs (eg, corticosteroids, some diuretics, antipsychotics), and previous eye injury or
inflammation. While many of these can be actively addressed through lifestyle
modifications, others such as aging and eye injury clearly cannot be controlled. In
addition to these established risk factors, epidemiological data suggests dietary intake
of several nutrients can be protective. Nutrients such as taurine, carotenoiods,
tocopherol, and acsorbate have shown a protective role from the development of some
types of cataracts.5,6

Carnosine is an endogenous dipeptide synthesized by carnosine synthase in an ATP-

dependent reaction that links amino acid substrates histidine and β-alanine. A high
concentration is found in skeletal muscle fibers. As such, L-carnosine is also obtained
from meat in the diet, although it appears to undergo rapid degradation by serum
carnosinase. L-carnosine is also found in neural tissue, with a larger concentration in
the olfactory bulb. Its biological role is not known conclusively, but the higher
concentrations in these long-living cells is in keeping with its putative role as an
antisenescence molecule.7

The presence of endogenous carnosine in the lens of the eye suggests it is needed in
normal physiological processes.8 Of note, there is no evidence that the eye contains
carnosine synthase. Therefore carnosine, like many other nutrients, must be derived
from systemic circulation, diffusing into the aqueous humor then subsequently into the
lens cells themselves. Carnosinase, the enzyme that degrades carnosine into its
component amino acids, is found in the eye. The presence of carnosinase may result in
rapid degradation of carnosine into its component amino acids.

L- Carnosine versus N-acetylcarnosine

Currently, N-acetylcarnosine (NAC), not L-carnosine, eye drops are commercially

available. NAC was found to be a prodrug of L-carnosine within the eye, as it
undergoes deacetylation to release carnosine into the aqueous humor.9 Since
carnosine is thought to be rapidly degraded by resident carnosinase in the lens, and
NAC appears to be protected from this enzyme, the instillation of NAC was proposed as
a means of achieving a more effective delivery of L-carnosine to the lens. Furthermore,
NAC is a less hydrophobic molecule, so it may more readily pass through the
membrane lipid bilayer of lens cells. While the data on these compounds is certainly not
interchangeable, when considering the compounds as an instillation directly into the
eye, the molecular effects of L-carnosine can be extrapolated to include that seen with
NAC as well, since the latter compound is completely deacetylated in situ to render L-
carnosine.

Overview of Cataractogenesis and Carnosine

The development of cataracts, or cataractogenesis, is marked by many of the same

processes that are involved in the senescence of cells. Namely, reactive oxygen
species (ROS), advanced glycation end products (AGEs), and deleterious aldehydes
and thiols accumulate intracellularly. In excess, these incendiary molecules lead to
changes in lipid and protein structures that are the hallmark of aging cells. Two
morphological changes that directly result in increasing opacification are peroxidation of
the lipid bilayer of cellular membranes of the lens and crosslinking of otherwise soluble
crystallin proteins forming insoluble aggregates within the lens fiber cells. Each of these
macromolecular changes leads to disruption in the passage of light through the lens by
scattering light rays, and with adequate accumulation, this eventually can obscure light
passage completely.

The ability of L-carnosine to attenuate the products of lipid peroxidation within the
ocular lens was first suggested by Dr. Alan Babizhayev and colleagues in 1987.10
Indeed, much research has since confirmed that carnosine reduces the formation of
lipid peroxides within the lens.11,12,13

In addition to directly attenuating membrane structure damage through lessening

peroxidation of lipids, reduction of lipid peroxides also reduces the formation of its
highly reactive metabolite, malondialdehyde (MDA). MDA interacts with amino acid
moieties on crystallin proteins within the lens to cause crosslinking of these proteins,
resulting in insoluble aggregate molecules.14

In cataracts, many enzymes that normally provide defense against ROS

overproduction, including superoxide dismutase and catalase, are depleted.15
Exacerbating this effect, the nuclear region of the lens is normally dependent on the
production and subsequent diffusion of glutathione from the cortical region, but this
diffusion process becomes less efficient as we age.16 Carnosine has been shown to
preserve levels of these enzymes in cataract lenses, thus improving their antioxidative
capacity.17 There is also postulation that carnosine lessens ROS damage through its
ability to chelate free metal ions, which are required to generate O2-.18

Separately, carnosine has been shown to act as an alternative target for glycation, a
“sacrificial transglycation,” that effectively binds sugars to itself rendering them
unavailable to bind proteins. This leads to a measurable decrease in AGEs and may be
responsible for much of carnosine’s antisenescence action apart from its antioxidant
capacity.19

Another mechanism by which carnosine is able to reduce protein adducts is by directly

binding to carbonyl groups on proteins. Carbonyl groups increase in high oxidation and
glycation environments; thus they often coincide with aging of cells. Carnosine’s binding
to reactive carbonyls, a process called “carnosinylation,” prevents proteins from binding
to one another and forming adducts.20

Remarkably, L-carnosine has been shown capable of deaggregating the crystalline lens
proteins that directly result in opacity. Methylglyoxal-induced glycation of α-crystallin
aggregates was reversed with the addition of carnosine to the media.21 The ability of
carnosine to denatured protein aggregates was also demonstrated in an in vitro study of
rat lenses. Both L- and D-carnosine had a “disassembling” effect on α-crystallin fibrils
and restored the transparency of cataractous lenses. This was accompanied by a
reduction in the average size of the proteins, confirming that disassembly did take
place.22

A dominant pathway of cataractogenesis in diabetic patients, in addition to those

discussed above, is the polyol pathway. This is the sequential transformation of glucose
into sorbitol and subsequently fructose within the lens by the enzymes aldose reductase
and sorbitol dehydrogenase, respectively.23 Aldose reductase inhibitors have been
found to prevent sugar-induced cataracts, thus confirming the integral role of this
pathway on cataract formation.24 The fructose molecule is highly reactive and, together
with oxidized proteins and a direct reduction of esterase activity, leads to AGEs.
Carnosine has been shown to directly inhibit aldehyde reductase, thus lowering the
concentration of fructose and AGEs.25 Further, the addition of carnosine to lens media
abrogated fructose induced deactivation of esterase activity.26

In Vivo Studies

In one study using rats with streptozocin-induced diabetes, cataract development was
shown to progress in a biphasic manner, with a slow progression in the first 8 weeks
followed by a rapid increase in the next 5 weeks. Carnosine delayed the onset of lens
opacification in the early stages of cataract development, reaching statistical
significance at week 4 (P<0.05), but failed to affect later progression of the disease.
This rodent study also demonstrated a reduction in the levels of AGEs in treated eyes
versus untreated, which was concordant with better preservation of glutathione and
catalase levels in the treated groups.27

NAC may not only act as a progdrug but may itself be involved in the antiaggregation
effects observed with NAC-containing eye drops. A rodent study using UV-induced
cataractogenesis supported this finding and suggested that a mixture of D-pantethine
and NAC is even more effective than NAC alone in its antiaggregate effects.28

A recent study using rats with streptozocin-induced diabetes showed a delay in the
development of cataracts using an instillation of aspirin (1%), L-carnosine (1%), or an
alternating combination of the 2. Both single agent interventions delayed cataracts while
the combination was more effective than either agent alone. In addition, there was an
increase in the levels of soluble protein in the lenses of the treated groups versus
controls.29

In a small study, 30 dogs of various breeds with existing lens opacities were
administered a combination product containing 2% NAC. Additional ingredients in the
proprietary formula include glutathione, cysteine ascorbate, L-taurine, and riboflavin
(Ocluvet™, by Practivet, Arizona, USA). 58 eyes of 30 dogs were evaluated, 22 with
mature cataract, 13 with immature cataract, 9 with cataract associated with eye
inflammation, and 14 with nuclear sclerosis. Images of the lenses were taken at weeks
2, 4, and 8. Objective measurement of lens opacification was determined by a lens
opacification index (LOI) using computerized integration of the grayscale level of each
pixel across the lens image. There was a reduction in the level of LOI in all groups,
although this was only statistically significant in the immature cataract and nuclear
sclerosis groups. Subjectively, owners perceived improvement in 80% of the dogs
studied. The greater benefit in early cataract development supports in vitro data that
suggests later stages of cataract development appear to overwhelm the benefits of
antioxidant support.30

Another canine study using 1.0% NAC in its patented formulation (Can-C®, Innovative
Vision Products, Delaware, USA) used 30 dogs in the treatment group, 15 dogs in
placebo-controlled group, and 10 dogs without treatment. All dogs had cataracts at the
start and all eyes were assessed. Placebo consisted of all ingredients in the drops
except NAC. After 6 months of treatment, 96% of eyes in the treatment group showed
improvement in the slit image and retroillumination photographs. No mention is given in
the publication of the statistical analysis or of the results of the 2 nontreatment
groups.31

Babizhayev and colleagues have shown beneficial effects of 1.0% NAC instillation in
the eyes in several small human clinical trials. In a randomized study of 49 subjects with
senile cataracts (76 affected eyes), 26 (41 affected eyes) were given NAC (1.0%)
eyedrops twice daily. There were 2 control groups: a placebo group of 13 patients (21
affected eyes) who received an eye drop formulation containing all ingredients but NAC
and an untreated group of 10 patients (14 eyes) who did not receive any eye drops. For
statistical analysis, the control groups were pooled. The 6-month outcome showed 90%
of patients in the treated group had improved visual acuity and 89% showed improved
glare sensitivity. Image analysis of the cataracts at 6 months showed a statistically
significant difference (P<.0001) using an in-house imaging that included slit-lamp
assessment and retroillumination of the lenes to assess.32

In a continuation of the above study, the participants were assessed every 6 months for
a total of 24 months. At 24 months no one in the treatment group had declining visual
acuity, while overall there was a decline in the control group. Overall, reductions in glare
sensitivity and visual acuity were sustained for the 24 month duration of the study; this
difference was statistically significant (P< .0001).33

In another trial by the same group, 65 older drivers with 1 or both eyes affected by
cataract and 72 older adult controls without cataract were recruited to participate in a
double-blind, placebo-controlled trial. Assessment of glare sensitivity (halos) at red and
green targets was made using an in-house test. At 4 months participants receiving NAC
had a statistically significant improvement in visual acuity and glare sensitivity
(P<0.001).34

In 2009 another trial of 75 patients with cataracts and 72 without, 1.0% NAC was
instilled daily for 9 months. In both groups visual acuity and reduction in glare sensitivity
reached statistical significance (P<0.001) at 9 months.35

Discussion

A growing body of evidence suggests that L-carnosine attenuates aging processes,

ultimately culminating in delayed senescence of the organism as a whole, as suggested
in Drosophila and mouse models.36 Mechanisms of carnosine’s antiaging effects
include its role as an antioxidant, antiglycating agent, metal chelating agent, aldehyde
scavenger, carbonyl scavenger, and stimulator of nitric oxide synthase.37 Many of these
are relevant to the development of cataracts, and it is a reasonable assumption that
carnosine’s beneficial effects in the lens are largely due to these mechanisms of cellular
self-preservation. For a thorough review of carnosine’s biological effects throughout the
body, the reader is referred to a recent publication by Alan Hipkiss.38

Much of the clinical research demonstrating the efficacy of carnosine in preventing or

treating cataracts in humans has been done by Dr. Babizhayev of Innovative Vision
Products (IVP), Delaware, USA. His group proposed the use of NAC as a prodrug for L-
carnosine in 1996.39 Since then, IVP has manufactured a patented formula called Can-
C (private label, Nu-Eyes) which consists of deionized water, glycerin (1.0%), NAC
(1.0%), carboxymethylcellulose (0.3%), benzyl alcohol (0.3%), and potassium borate
and bicarbonate buffers.40 Babizhayev’s group proposes this particular formulation
obtains superior absorption through the cornea and that acetylation of carnosine
optimizes the delivery of carnosine into the lens in several ways: protection from
degradation by carnosinase in the aqueous humor, a more lipophilic molecule that
allows for easier penetration into the lens, and, due to the pharmacokinetics of
deacetylation, “timed release” of the carnosine molecule.41,42

Babizhayev and colleagues reported that instillation of non-acetylated L-carnosine (1%)

to rabbit eyes did not lead to an increase of L-carnosine concentration in the anterior
compartment versus placebo, an effect they speculate is due to carnosinase
degradation of the dipeptide.43 While this is in keeping with the assumption that
carnosinases in the eye rapidly degrade L-carnosine, there is recent evidence of L-
carnosine accumulation in the eyes of rabbits using a 5.0% instillation.44 Further,
Babisheyev asserts that not only is L-carnosine less effective than NAC, but that there
may be risk of harm to the eye due to the byproduct of histamine that ultimately results
from the degradation of carnosine. These predictions are disputed, at least in part, by
data in animals that demonstrates reduced cataractogenesis with the use of L-
carnosine eye drops.45 There is no in vivo data that directly compares the efficacy of L-
carnosine versus NAC eyedrops. More definite studies are needed to unequivicably
conclude whether NAC is superior to L-carnosine.

While there is no data on dietary consumption of carnosine and cataract development,

serum carnosine levels do decrease with age.46 Given carnosine’s multiple
antisenescent actions, this correlation may be part of the aging process itself.
Carnosine levels can be increased through the consumption of meat, and a carnivorous
diet has been postulated to have possible antiaging effects.47 Strict vegetarian diets are
devoid of the peptide, so a diet high in carnosine precursors histidine and alanine, with
emphasis on the more rate-limiting alanine, may be the closest simulation. Oral
supplementation of carnosine or its substrates has not been studied in regard to eye
health. There is also no data to suggest a diet high in carnosine will effectively diminish
cataract formation.

Conclusion

The endogenous dipeptide carnosine (β-alanyl-L-histidine) is recognized as an

antiaging molecule at both cellular and whole animal levels. Overall, the state of the
evidence on carnosine’s role in delaying or treating cataractogenesis is preliminary.
However, the role of carnosine as a universal antiaging molecule is fairly well
established. This larger body of evidence, along with the uniformity of beneficial effects
on cataractous lenses in the limited studies that have been published, provide rationale
for consideration of this nontoxic agent in delay of cataract development, particularly in
early stage cataracts.

About the Author

Tina Kaczor, ND, FABNO, is editor-in-chief of Natural Medicine Journal and a

naturopathic physician, board certified in naturopathic oncology. She received her
naturopathic doctorate from National University of Natural Medicine, and completed her
residency in naturopathic oncology at Cancer Treatment Centers of America, Tulsa,
Oklahoma. Kaczor received undergraduate degrees from the State University of New
York at Buffalo. She is the past president and treasurer of the Oncology Association of
Naturopathic Physicians and secretary of the American Board of Naturopathic
Oncology. She has been published in several peer-reviewed journals. Kaczor is based
in Portland, Oregon.

References

1 Resnikoff S, Pascolini D, Etya’ale D, et al. Global data on visual impairment in the

year 2002. Bulletin of the World Health Organization. 2004;82:844-851.
2 Congdon N, Vingerling JR, Klein BE, et al. Prevalence of cataract and
pseudophakia/aphakia among adults in the United States. Arch Ophthalmol. Apr
2004;122(4):487-494.
3 Chang M, Congdon N, Baker S, Bloem M, Savage H, Sommer A. The surgical
management of cataract: barriers, best practices and outcomes. International
Ophthalmology. 2008;28(4):247-260.
4 Toh T, Morton J, Coxon J, Elder MJ. Medical treatment of cataract. Clin Experiment
Ophthalmol. Sep-Oct 2007;35(7):664-671.
5 Taylor A, Jacques P, Chylack L, et al. Long-term intake of vitamins and carotenoids
and odds of early age-related cortical and posterior subcapsular lens opacities. Am J
Clin Nutr. 2002;75(3):540-549.
6 Christen W, Liu S, Glynn R, Gaziano M, Buring J. Dietary Carotenoids, Vitamins C
and E, and Risk of Cataract in Women: A Prospective Study. Arch Ophthalmol.
2008;126(1):102-109.
7 Hipkiss AR. Chapter 3 Carnosine and Its Possible Roles in Nutrition and Health. In:
Steve LT, ed. Advances in Food and Nutrition Research. Vol Volume 57: Academic
Press; 2009:87-154.
8 Quinn PJ, Boldyrev AA, Formazuyk VE. Carnosine: Its properties, functions and
potential therapeutic applications. Molecular Aspects of Medicine. 1992;13(5):379-444.
9 Babizhayev MA. Failure to withstand oxidative stress induced by phospholipid
hydroperoxides as a possible cause of the lens opacities in systemic diseases and
ageing. Biochim Biophys Acta. Mar 1 1996;1315(2):87-99.
10 Boldyrev AA, Dupin AM, Bunin A, Babizhaev MA, Severin SE. The antioxidative
properties of carnosine, a natural histidine containing dipeptide. Biochem Int. Dec
1987;15(6):1105-1113.
11 Bhuyan KC, Bhuyan DK. Molecular mechanism of cataractogenesis: III. Toxic
metabolites of oxygen as initiators of lipid peroxidation and cataract. Curr Eye Res. Jan
1984;3(1):67-81.
12 Chasovnikova LV, Formazyuk VE, Sergienko VI, Boldyrev AA, Severin SE. The
antioxidative properties of carnosine and other drugs. Biochem Int. 1990;20(6):1097-
1103.
13 Babizhayev MA. Antioxidant activity of L-carnosine, a natural histidine-containing
dipeptide in crystalline lens. Biochim Biophys Acta. Aug 22 1989;1004(3):363-371.
14 Bhuyan KC, Bhuyan DK. Molecular mechanism of cataractogenesis: III. Toxic
metabolites of oxygen as initiators of lipid peroxidation and cataract. Curr Eye Res. Jan
1984;3(1):67-81.
15 Özmen B, Özmen D, Erkin E, Güner I, Habif S, BayIndIr O. Lens superoxide
dismutase and catalase activities in diabetic cataract. Clinical Biochemistry.
2002;35(1):69-72.
16 Sweeney MHJ, Truscott RJW. An Impediment to Glutathione Diffusion in Older
Normal Human Lenses: a Possible Precondition for Nuclear Cataract. Experimental Eye
Research. 1998;67(5):587-595.
17 Babizhayev M, Deyev A, Yermakova V, Remenshchikov V, Bours J. Revival of the
Lens Transparency with N-Acetylcarnosine. Current Drug Therapy. 2006:91-116.
18 Babizhayev MA, Costa EB. Lipid peroxide and reactive oxygen species generating
systems of the crystalline lens. Biochim Biophys Acta. Feb 22 1994;1225(3):326-337.
19 Hipkiss A. Carnosine, a protective, anti-ageing peptide? The International Journal of
Biochemistry & Cell Biology. 1998;30(8):863-868.
20 Hipkiss AR, Brownson C. A possible new role for the anti-ageing peptide carnosine.
Cellular and molecular life sciences : CMLS. 2000;57(5):747-753.
21 Seidler NW, Yeargans GS, Morgan TG. Carnosine disaggregates glycated [alpha]-
crystallin: an in vitro study. Archives of Biochemistry and Biophysics. 2004;427(1):110-
115.
22 Attanasio F, Cataldo S, Fisichella S, et al. Protective effects of L- and D-carnosine
on alpha-crystallin amyloid fibril formation: implications for cataract disease.
Biochemistry. Jul 14 2009;48(27):6522-6531.
23 Lerner BC, Varma SD, Richards RD. Polyol pathway metabolites in human
cataracts. Correlation of circulating glycosylated hemoglobin content and fasting blood
glucose levels. Archives of ophthalmology. 1984;102(6):917-920.
24 Azuma M, Inoue E, Oka T, Shearer TR. Proteolysis by calpain is an underlying
mechanism for formation of sugar cataract in rat lens. Current eye research.
1995;14(1):27-34.
25 Tat’yanenko L, Bogdanov G, Varfolomeev V, Kotel’nikova R, Smirnov L.
Bioantioxidants as inhibitors of aldehyde reductase. Pharmaceutical Chemistry Journal.
1996;30(6):361-362.
26 Yan H, Harding JJ. Carnosine protects against the inactivation of esterase induced
by glycation and a steroid. Biochim Biophys Acta. Jun 30 2005;1741(1-2):120-126.
27 Yan H, Guo Y, Zhang J, Ding Z, Ha W, Harding JJ. Effect of carnosine,
aminoguanidine, and aspirin drops on the prevention of cataracts in diabetic rats. Mol
Vis. 2008;14:2282-2291.
28 Soustov LV, Chelnokov EV, Sapogova NV, et al. [Like anticataract agents, the
antiaggregants of lens crystallin. Communication 2. Study of the impact of chaperon-like
(protective) activity of short-chain peptides on the rate of UV-induced aggregation of
betaL-crystallins by eximer laser]. Vestn Oftalmol. Mar-Apr 2008;124(2):6-8.
29 Shi Q, Yan H, Li MY, Harding JJ. Effect of a combination of carnosine and aspirin
eye drops on streptozotocin -- induced diabetic cataract in rats. Mol Vis. 2009;15:2129-
2138.
30 Williams DL, Munday P. The effect of a topical antioxidant formulation including N-
acetyl carnosine on canine cataract: a preliminary study. Vet Ophthalmol. Sep-Oct
2006;9(5):311-316.
31 Sweeney MHJ, Truscott RJW. An Impediment to Glutathione Diffusion in Older
Normal Human Lenses: a Possible Precondition for Nuclear Cataract. Experimental Eye
Research. 1998;67(5):587-595.
32 Babizhayev MA, Deyev AI, Yermakova VN, et al. Efficacy of N-acetylcarnosine in the
treatment of cataracts. Drugs R D. 2002;3(2):87-103.
33 Babizhayev MA, Deyev AI, Yermakova VN, et al. N-Acetylcarnosine, a natural
histidine-containing dipeptide, as a potent ophthalmic drug in treatment of human
cataracts. Peptides. 2001;22(6):979-994.
34 Babizhayev MA. Rejuvenation of visual functions in older adult drivers and drivers
with cataract during a short-term administration of N-acetylcarnosine lubricant eye
drops. Rejuvenation Res. Fall 2004;7(3):186-198.
35 Babizhayev MA, Burke L, Micans P, Richer SP. N-Acetylcarnosine sustained drug
delivery eye drops to control the signs of ageless vision: glare sensitivity, cataract
amelioration and quality of vision currently available treatment for the challenging
50,000-patient population. Clin Interv Aging. 2009;4:31-50.
36 Hipkiss AR. Chapter 3 Carnosine and Its Possible Roles in Nutrition and Health. In:
Steve LT, ed. Advances in Food and Nutrition Research. Vol Volume 57: Academic
Press; 2009:87-154.
37 Ibid.
38 Ibid.
39 Babizhayev MA, Yermakova VN, Sakina NL, Evstigneeva RP, Rozhkova EA,
Zheltukhina GA. N alpha-acetylcarnosine is a prodrug of L-carnosine in ophthalmic
application as antioxidant. Clin Chim Acta. Oct 15 1996;254(1):1-21.
40 Babizhayev MA, Burke L, Micans P, Richer SP. N-Acetylcarnosine sustained drug
delivery eye drops to control the signs of ageless vision: glare sensitivity, cataract
amelioration and quality of vision currently available treatment for the challenging
50,000-patient population. Clin Interv Aging. 2009;4:31-50.
41 Babizhayev MA. Analysis of lipid peroxidation and electron microscopic survey of
maturation stages during human cataractogenesis: pharmacokinetic assay of Can-C N-
acetylcarnosine prodrug lubricant eye drops for cataract prevention. Drugs R D.
2005;6(6):345-369.
42 Babizhayev MA. Ocular drug metabolism of the bioactivating antioxidant N-
acetylcarnosine for vision in ophthalmic prodrug and codrug design and delivery. Drug
Dev Ind Pharm. Oct 2008;34(10):1071-1089.
43 Babizhayev MA. Analysis of lipid peroxidation and electron microscopic survey of
maturation stages during human cataractogenesis: pharmacokinetic assay of Can-C N-
acetylcarnosine prodrug lubricant eye drops for cataract prevention. Drugs R D.
2005;6(6):345-369.
44 Tianyang Z, Ling Z, Liya W, Junjie Z. Ocular Pharmacokinetics of Carnosine 5% Eye
Drops Following Topical Application in Rabbit. Journal of Ocular Pharmacology and
Therapeutics. 2010:100119131610026.
45 Yan H, Guo Y, Zhang J, Ding Z, Ha W, Harding JJ. Effect of carnosine,
aminoguanidine, and aspirin drops on the prevention of cataracts in diabetic rats. Mol
Vis. 2008;14:2282-2291.
46 Hipkiss AR. Chapter 3 Carnosine and Its Possible Roles in Nutrition and Health. In:
Steve LT, ed. Advances in Food and Nutrition Research. Vol Volume 57: Academic
Press; 2009:87-154.
47 Hipkiss A. Would carnosine or a carnivorous diet help suppress aging and
associated pathologies? Annals of the New York Academy of Sciences. 2006;1067:369-
374.
NMJ_APR10_NP

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