Life Sciences 78 (2006) 1378 – 1384 www.elsevier.


Effect of bacoside A on brain antioxidant status in cigarette smoke exposed rats
K. Anbarasi a, G. Vani a, K. Balakrishna b, C.SR Shyamala Devi c,*
a c

Department of Biochemistry, University of Madras, Guindy Campus, Chennai-600 025, India b Central Research Institute (Siddha), Chennai-600 106, India Department of Biochemistry, University of Madras, Guindy Campus, Chennai-600 025, India Received 30 March 2005; accepted 11 July 2005

Abstract Free radicals mediated oxidative stress has been implicated in the pathogenesis of smoking-related diseases and antioxidant nutrients are reported to prevent the oxidative damage induced by smoking. Therefore, the present study was conducted to evaluate the antioxidant role of bacoside A (triterpenoid saponin isolated from Bacopa monniera) against chronic cigarette smoking induced oxidative damage in rat brain. Adult male albino rats were exposed to cigarette smoke for a period of 12 weeks and simultaneously administered with bacoside A (10 mg/kg b.w./day, p.o.). Antioxidant status of the brain was assessed from the levels of reduced glutathione, vitamin C, vitamin E, and vitamin A and the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase. The levels of copper, iron, zinc and selenium in brain and serum ceruloplasmin activity were also measured. Oxidative stress was evident from the diminished levels of both enzymatic and non-enzymatic antioxidants. Alterations in the levels of trace elements with accumulation of copper and iron, and depletion of zinc and selenium were also observed. Bacoside A administration improved the antioxidant status and maintained the levels of trace elements. These results suggest that chronic cigarette smoke exposure enhances oxidative stress, thereby disturbing the tissue defense system and bacoside A protects the brain from the oxidative damage through its antioxidant potential. D 2005 Elsevier Inc. All rights reserved.
Keywords: Antioxidants; Bacoside A; Bacopa monniera; Cigarette smoking; Lipid peroxidation; Oxidative stress; Trace elements

Introduction There is a preponderance of evidence showing a strong association between cigarette smoking and alarming increase in the mortality rate from smoking-related diseases such as pulmonary diseases, cardio and cerebrovascular diseases, cancers, and several others (US DHHS, 1989). The role of free radicals in the pathogenesis of these diseases has been well documented (Church and Pryor, 1985). Formation of free radicals and reactive oxygen species (ROS) is a normal consequence of a variety of biochemical reactions. However,

* Corresponding author. Old No. 62, New No. 66, Second main road, Gandhi Nagar, Adyar, Chennai-600 020, India. Tel.: +91 44 2441 2575; fax: +91 44 2235 2494. E-mail addresses: (K. Anbarasi), (C.S.S. Devi). 0024-3205/$ - see front matter D 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.lfs.2005.07.030

these free radicals are capable of independent existence and can cause oxidative damage to the tissues through lipid peroxidation (Cross et al., 1987). The human body has an inherent synergistic and multilevel defense mechanism, which comprise of two major classes of cellular protection against ROS (Muzakova et al., 2001). The enzymatic part is represented by free radical scavenger enzymes namely superoxide dismutase, catalase and glutathione peroxidase. The non-enzymatic part includes a large number of natural and synthetic antioxidant compounds (e.g. vitamins, thiols etc.) that have the ability to inhibit oxidative stress by scavenging the highly destructive free radical species. The deleterious effects of the free radicals are kept under check by a delicate balance between the rate of their production and the rate of their elimination by these defense systems (Halliwell, 1994). When there is an excessive addition of free radicals from exogenous sources added to the endogenous production, the available tissue defense system

Several micronutrients and antioxidants of natural origin have been experimentally proved as effective protective agents against smoking induced oxidative stress (Sohn et al. Anbarasi et al. epilepsy. Scissors Standard (W. This organ is highly susceptible to free radical attack because it generates more of these toxicants per gram of tissue than does any other organ and yet not particularly enriched with protective antioxidants (Arivazhagan et al. Animals Adult male albino rats of Wistar strain (120 – 200 g) procured from Tamilnadu University of Veterinary and Animal Sciences (TANUVAS). the major saponins are responsible for the facilitatory and modulatory effects of B. Cigarette smoke was exposed twice daily. The purity of the isolated bacoside A was identified by thin layer chromatography (TLC) and infrared (IR) spectrum analysis using standard bacoside A (data not shown). A major exogenous source of free radicals is cigarette smoke which is a heterogeneous aerosol consisting of more than 4000 compounds including high concentrations of free radicals. epinephrine. calcium antagonistic (Dar and Channa. monniera (Singh et al.. MO. When the normal level of antioxidant defense system is insufficient for the eradication of excessive free radicals.. 1999) and muscle relaxant (Dar and Channa. The rats were provided with standard pelleted rat feed and water ad libitum. Group III—rats administered with bacoside A (10 mg/ kg b. IAEC 01/037/04). 1996). (1988).. ascorbic acid and a-tocopherol were obtained from Sigma Chemical Company. Helen et al. using 8– 10 . Control animals received a corresponding volume of the vehicle suspended in normal saline.. The brain is exposed throughout the life to oxidative stress and a number of diseases of the brain have been hypothesized to involve free radical induced oxidative damage either as a cause or as consequence of the disease processes. 2001). this deficiency in smokers may be enhanced by their generally lower intake of both supplementary and dietary antioxidants (Zondervan et al.. Dilsiz et al. Materials and methods Chemicals and reagents Reduced glutathione. and obtained from Himedia. The obligatory use of the body’s reserve of antioxidants to detoxify the tremendous level of these free radicals in smokers therefore results in severe antioxidant deficiency status. we have demonstrated the protective effect of bacoside A against smoking induced toxicity in rat brain (Anbarasi et al. Further.. Standard bacoside A was purchased from Natural Remedies Private Limited. In view of the antioxidant property of Bacopa monniera (Tripathi et al. Stough et al. 2003). Preliminary studies indicated that bacosides.. (Nadkarni. the duration of each exposure was 3 h with an interval of 10 min between each cigarette../day for 12 weeks. 1996). P. administration or supplementation of exogenous antioxidants has a protective role to play (Rekha et al./day. Locally available brand of cigarette. NADPH. India. 1999. on the antioxidant defense system in rat brain has been investigated (Anbarasi et al. Aqueous suspension of bacoside A in 1% gum acacia was given orally to the experimental animals at a dosage of 10 mg/kg b. All other chemicals and reagents used were of reagent grade and highest purity. Group II and Group IV rats were exposed to cigarette smoke for a period of 12 weeks as described earlier (Anbarasi et al. Bacopa monniera Linn. which is held in high repute as a potent nerve tonic (Chopra et al. thereby predisposing them to the development of life threatening diseases. monniera improves memory and mental function (Roodenrys et al. 1956). 1988). the effect of bacoside A. and reactive oxygen and nitrogen species (Stedman.. Hence. the present study was undertaken to assess the neuroprotective role of bacoside A against oxidative stress in the brain of rats exposed to cigarette smoke by measuring the enzymatic and non-enzymatic antioxidants. 2005a.. Preclinical and clinical studies have shown that B. Recently. Experimental design The animals were divided into four groups of 6 animals each. 1997) properties. 1993. Group IV—rats exposed to cigarette smoke and simultaneously administered with bacoside A.. Bacoside A The plant Bacopa monniera was collected in and around Chennai. 2001). anxiety. Bangalore. Group I—control. Louis.O. is used in the indigenous systems of medicine for the treatment of various nervous system ailments such as insomnia. Chennai.. India were used for the present study.b). Briefly. USA. Central Research Institute (Siddha)..w. hysteria etc.).w.D & H. Group II—rats exposed to cigarette smoke. The dammarane type triterpenoid saponin-bacoside A was isolated from the plant by the standard procedure followed by Singh et al. 1976). The plant has been shown as a potent free radical scavenger and antioxidant (Tripathi et al. 1996). India and authenticated by Dr. Besides it also exhibits vasodilatory (Channa et al. India.o. Koul et al. The experiments were carried out in accordance with the guidelines provided by the Institutional Animal Ethical Committee (No. / Life Sciences 78 (2006) 1378 – 1384 1379 becomes overwhelmed resulting in oxidative damage to the tissues. 2003). St.. India. They were acclimatized to the laboratory conditions and maintained under 12 h light and dark cycles at 25 T 2 -C.. Brindha.K. Mumbai. 1968). which retains the biological activity of Bacopa monniera. p. 1999. 2005c). Bacoside A is the dammarene type triterpenoid saponin isolated from the plant Bacopa monniera. manufactured by Hyderabad Deccan Cigarette Factory was used in the present study. Wills).. 2002). 2002. 2001).. the rats were exposed to side stream cigarette smoke in whole body smoke exposure chamber. and trace elements.

4NS 263.19 T 0.4 and used for biochemical studies.5 T 2. Biochemical analysis Superoxide dismutase was assayed by the method of Misra and Fridovich (1972). (Values are expressed as mean T SD. E.50 T 0.20# 0.1380 K. . vitamin C.15* 9. NS—non significant.53 T 2.57 T 0. Statistical analysis Results are expressed as mean T SD (n = 6).154 T 0.21 T 0. Glutathione reductase. Statistical comparisons are made between Group I vs.46 T 14. Se: Ag/g wet tissue. glutathione peroxidase.12 T 15. Group II vs.05) in GSH levels with no significant changes in other parameters as compared with Group I rats. The activity of glutathione peroxidase was assayed by measuring the amount of GSH consumed in the reaction mixture by the method of Rotruck et al.2* 15. GR: Amoles of NADPH oxidized/min/mg protein.14# 13.28* 0.10* 3. (1973). Vitamins C.42 T 0. Group IV.70 T 0. Group II and Group III. and A when compared to control rats.3NS 0. which utilizes NADPH to convert oxidized GSH to reduced form. (Values are expressed as mean T SD.2 268. A significant decrease ( P < 0.20* 4. Serum ceruloplasmin activity was assayed by following the procedure as described by Ravin (1961). pH 7. Fe.32* 0.52 T 1.41 T 0. and vitamin A in the brain of control and experimental animals Parameters GSH Vitamin C Vitamin E Vitamin A Group I 6.102 T 0.33 T 12.89 T 0.32 T 0. Statistical comparisons are made between Group I vs.80* 4.35@ 1. / Life Sciences 78 (2006) 1378 – 1384 Table 2 Levels of reduced glutathione (GSH). *—p < 0.1 M Tris – HCl.02NS Group IV 5.157 T 0.50 T 3. Brain tissue was excised carefully and immediately washed in ice-cold saline.001) activities of these enzymes as compared to Group II rats. Table 1 Activities of superoxide dismutase (SOD).001) in the activities of the antioxidant enzymes was observed in Group II rats exposed to cigarette smoke compared to Group I rats.001) in the levels of the nonenzymatic antioxidants was observed in Group IV rats when compared to Group II rats. Group IV. Vitamin C was measured according to the method of Omaye et al. NS—non significant. One unit of the enzyme activity is defined as the amount of enzyme required for the autooxidation of epinephrine by 50% per minute. The same brand of locally available cigarette was used throughout the experiment (Scissors Standard).06 T 0. (1979) using DTC reagent. vitamin C.001. Protein was estimated by the method of Lowry et al.15 5. n = 6). Group IV.2 Group II 17.58 T 0. (1946).02 Group II 3. Statistical comparisons are made between Group I vs.30 0. Bacoside A per se administered Group III rats showed a significant ( P < 0.24 1.13* 4.08NS 5.85 T 0. was assayed by the method of Stall et al. vitamin A in the brain of control and experimental animals. Cu.001) in the levels of glutathione and vitamins C.022 0. A significant increase ( P < 0. NS—non significant.34* 0.01* 5.78 T 1.02* Group III 3. iron (Fe).81 T 0. Statistical comparisons are made between Group I vs.1* 0. *—p < 0. n = 6). and glutathione reductase in brain of control and experimental animals are summarized in Table 1.5* (Values are expressed as mean T SD.8* 358. Group II vs. Vitamin E was measured according to the method of Quaife and Dju (1948) using dipyridyl reagent and vitamin A was measured by the method of Otto et al. Copper.03 Group II 1. Group II vs.9 13. A 10% (w/v) homogenate was prepared in 0. Group IV.2 T 3. Group II and Group III.25* 0.20* 1. glutathione peroxidase (GPx) and glutathione reductase (GR) in the brain of control and experimental animals Parameters SOD CAT GPx GR Group I 2.26NS 0.6 T 3.05# Group IV 2.92 T 0.84 T 0. vitamin E. GPx: Amoles of GSH oxidized/min/mg protein. zinc and iron was estimated using atomic absorption spectrophotometer after digestion with nitric acid and perchloric acid and selenium using coupled atomic emission spectrophotometer and flurometer. Group IV rats showed increased ( P < 0. and selenium (Se) in the brain of control and experimental rats Parameters CP Cu Fe Zn Se Group I 38. E.82 T 0. catalase (CAT).32* 0.56 T 0. *—p < 0.8 T 3.05. Group II and Group III. Group II rats exposed to cigarette smoke showed a significant decrease ( P < 0. the animals were killed by cervical decapitation.17 T 0. n = 6).6 0.0* 2.2NS NS Group IV 35. Reduced glutathione was measured according to the procedure of Moron et al.001.30 T 0. Catalase activity was measured by following decomposition of H2O2 according to the method of Beers and Sizer (1952). catalase.2 4.58 T 15. Unit GSH: Amoles/mg protein.01) increase in their activities as compared to Group I rats which shows the enzymatic activation of antioxidants by bacoside A.20# 5.6 T 2. vitamin E.02* cigarettes per day. Group II vs.12 T 0. Results The activities of superoxide dismutase.92 T 0. Anbarasi et al. Units: SOD: units/mg protein. CAT: Amoles of H2O2 decomposed/min/mg protein.78 T 0. Group II and Group III. Student’s t-test was used for the statistical evaluation of the data obtained.58 T 0.13 10. (1979) using DTNB reagent.8 T 2.04NS 12.50 T 2. Units: CP: units/mg protein. At the end of experimental period (12 weeks).05* 11.0 12.01* Group III 6.0* Group III 39.0* 282.75 T . Group III rats administered with bacoside A alone registered an increase ( P < 0.25 T 3.26 T 2.61 T 0. Table 2 shows the levels of reduced glutathione.0 T 3. #—p < 0.5* 24. Blood was collected and serum separated by centrifugation.87 T 0. (1969). @—p < 0.146 T 0.89 T 0.01.42 T 2. zinc (Zn). Zn.001.2* 0.02 12.14 T 0.25 T 2. and A: mg/g wet tissue.03* Table 3 Serum ceruloplasmin (CP) activity and the levels of copper (Cu). (1951).

showing decreased activities of superoxide dismutase (SOD). / Life Sciences 78 (2006) 1378 – 1384 1381 Serum ceruloplasmin activity and the levels of copper.. 1999). Modulation of antioxidant status by increased lipid peroxidation during exposure to cigarette smoke has been reported in various organs (Baskaran et al. which further makes the cells more vulnerable to peroxidative damage (Nadiger et al. E and A. besides its consumption by the antioxidant enzymes GPx and GST (Baskaran et al. However. selenium and ceruloplasmin activity were significantly increased ( P < 0.. Anbarasi et al. a decrease in SOD activity upon smoke exposure could have resulted from its inactivation by tar phase oxidants. 2005a). Delibas et al. An increase in the activities the antioxidant enzymes has been demonstrated upon exposure to cigarette smoke for 4 weeks (Baskaran et al. after prolonged exposure.001). which is catalytically involved in the production of oxygen free radicals. Our previous finding showed that cigarette smoke exposure increased both basal and induced lipid peroxidation in the rat brain (Anbarasi et al. whereas GPx is sensitive to lower concentration. 1996. in part because it is highly enriched with non-heme iron. in order to cope with the tremendous increase in the production of ROS (Gutteridge and Halliwell.001) and the levels of zinc. Hence it is possible that bacoside A might be involved in the activation of enzymic antioxidants.K. Bacoside A administration increased the activities of SOD. Smoking-induced depletion of GSH in kidney. 1994). Chitra et al. Baskaran et al.001) in cigarette smoke exposed to Group II rats compared to Group I rats. SOD is the first enzyme in antioxidant defense that scavenges superoxide radicals to form H2O2 and hence diminishes the toxic effects of the radical. Gutteridge and Halliwell.. Under an oxidative stress. 2004). 1994).. Rohini et al. 1995). 1993). GR is an important enzyme for the maintenance of intracellular concentration of reduced glutathione (Gutteridge and Halliwell. GSH and these vitamins are tightly linked to each other in a way that it helps to replenish vitamin C which in turn regenerates vitamin E and A (Rani and Panneerselvam. 1994). monniera has been reported under different conditions (Sumathy et al. Our results are in corroboration with the above findings. 2001). Ascorbate is the first strong reductant in the aqueous phase that readily reacts with cigarette . 1998).. However. The activity of ceruloplasmin. namely hydroxyl. zinc. Acute exposure to cigarette smoke enhances the production of these antioxidant enzymes as a result of adaptive response. During acute smoke exposure. an increase in CAT activity was observed by Baskaran et al.. 1997). 1997). and the levels of zinc and selenium were significantly decreased ( P < 0. The presence and production of the free radicals from smoke lower this enzyme. the toxic effects of cigarette smoke appear to override the adaptive mechanism of the body tissues. the brain contains a relatively high degree of polyunsaturated fatty acids that are particularly good substrates for peroxidation reactions (Halliwell and Gutteridge. No significant changes were observed in these parameters in Group III rats compared to Group I rats. and selenium in the brain of control and experimental rats are shown in Table 3. 1997. as indicated by a decrement in the levels of these enzymes (Hulea et al.. Acetaldehyde. 2003). CAT is involved in the detoxification of high concentrations of H2O2. 1987). which consequently mitigate the damage caused by cigarette smoke (Hilbert and Mohsenin. iron. and superoxide radicals (Pryor. Reduced glutathione (GSH) serves as the brain’s primary antioxidant defense against prooxidant stress and the level of brain GSH was significantly lowered after exposure to cigarette smoke. a major aldehyde from the smoke has been shown to deplete the cells of their GSH by conjugating with it. Hence. The quinone – semiquinone radicals from the tar phase of cigarette smoke are capable of reducing molecular oxygen to superoxide radicals whose excessive generation inactivates this enzyme (Duthie and Arthur.... An increase in GPx activity is expected when the activity of CAT is not sufficient to cope with the oxidative stress. Enhancement of these enzymes in liver and kidney by B. a decrease in the activity of CAT in the present study suggests the inability of host antioxidant defense to meet the oxidative stress following chronic exposure to cigarette smoke. peroxyl. while the levels of copper and iron were significantly increased ( P < 0. Inhibition of CAT activity in rat brain and liver by cigarette smoke has been reported (Mendez-Alvarez et al. In addition. 1985).. Absence of an augmentation in GPx activity upon smoke exposure in our study has been hypothesized to arise from a decrease in the levels of GSH that is essential for the conjugation of lipid peroxides. nitric oxide.. The sustained release of reactive free radicals from the tar and gas phases of smoke imposes an oxidant stress. 1999..001) in Group IV rats compared to Group II rats. the antioxidant enzyme levels are increased. Cigarette smoke is a complex milieu possessing an array of free radicals and ROS. the decrease in GSH levels could possibly be related to the inability of host tissue to synthesize GSH that is reflected from decrease in vitamin C. promotes lipid peroxidation and consequently perturbs the antioxidant defense system in the blood and tissues of smokers (Pryor and Stone. The brain contains less CAT levels and hence GPx has a major role in quenching H2O2 and other peroxides which otherwise will lead to the production of hydroxyl and peroxyl radicals in the presence of iron (Bast and Barr. (1999). glutathione peroxidase (GPx) and glutathione reductase (GR) in smoke exposed rat brain. 1996). GPx and GR. 2000. 1994) and reduced availability of GSH could have resulted in the reduction of activity of GR upon smoke exposure. This depletion was directly associated with elevation in brain lipid peroxidation which could be attributed to its protection against ROS generated by smoke. (2000) reported increased antioxidant enzymes in rat frontal cortex. Hence. 1999). catalase (CAT). CAT. The levels of copper and iron were significantly decreased ( P < 0. leading to accumulation of H2O2 and lipid hydroperoxides further worsening the damage (Pryor. 1999). lung and liver has also been reported (Anand et al. striatum and hippocampus upon administration of B. 2001. Bhattacharya et al. Discussion The brain is extremely vulnerable to oxidative stress. monniera.

2003a. 1995). Antioxidant effect of bacoside A in the brain of rats exposed to cigarette smoke. 1997) and vitamin A effectively quenches singlet oxygen (Helen and Vijayammal. and the activity of ceruloplasmin in cigarette smoke exposed rat brain. Bacoside A has been shown to quench superoxide radicals. smokers are constantly overexposed to free radicals through inhalation of long-lived carbon. the heavy metal from tobacco. K.05.. 2005a. 135 – 140. anti-lipid peroxidative and antioxidant activities in the brain tissue. Vani. 2002). However. A. The present study also revealed depletion in the levels of non-enzymatic antioxidants such as vitamin C. K. CSM Medical University. G. 1981). 1999. 1997. inhibit formation of free radicals. 1996). C. However. 1990). gammaglutamyl transpeptidase and lipid peroxidation in kidney of rats exposed to cigarette smoke. the cofactor for the enzyme SOD has been shown to protect the brain during ischemia or hypoglycemia (Choi. R. Chronic cadmium toxicity to sperm of heavy cigarette smokers: immunomodulation by zinc. 2003.. New Delhi is gratefully acknowledged. Dashti.... A decrease in serum ceruloplasmin activity has been reported in smokers (Pacht and Davis. Zinc and selenium therapy has been found to be effective during cigarette smoking (Al-Bader et al. It is quite likely that soluble iron and copper are highly toxic to brain. dt 20. / Life Sciences 78 (2006) 1378 – 1384 smoke oxidants and affords considerable protection to the cells (Kallner et al.M. carotenoids.b). The lipid-soluble.S. Also cigarette smoke exposure resulted in decreased serum ceruloplasmin activity.. monniera has been shown to chelate the transition metals. and terminate lipid peroxidation at the initiation level itself (Tripathi et al.. 2004). decreased the bioavailability of selenium and zinc and hence depletes the antioxidant status (Preston. Vani (Grant No: 9/115(511)/2000. E and A in the brain of rats exposed to cigarette smoke. Anbarasi. 1999). Similarly. an increase in GSH levels against smoking induced depletion in the brain indicates neuroprotective role of bacoside A. 1987). Rohini et al. further studies pertaining to the precise mechanism of action of Bacoside A are warranted. C.S. References Al-Bader. an organ highly prone to oxidative stress against chronic smoking induced toxicity and hence may have useful properties as a natural antioxidant supplement.V.. 1996.. Dilsiz et al. complexed to some components of tar such as odiphenols (Cross et al. Anbarasi et al. EMR-I. The levels of trace elements like zinc and selenium in brain were decreased upon exposure to cigarette smoke. the results of our investigation suggest that bacoside A can be a potent antioxidant in the brain. Anbarasi. 2001.04. monniera following increased GSH levels have been reported (Sumathy et al. Archives of Andrology 43. 1996). dt 06. Zinc.. K. Lucknow.and oxygencentered radicals that subsequently deplete the plasma and tissue stores of these micronutrients (Brown et al.. Selenium functions as an important nutrient of the brain and being a component of GPx..E. Conclusion The above findings show that chronic cigarette smoking induces an oxidative stress on the brain by augmenting lipid peroxidation and diminishing both enzymatic and non-enzymatic antioxidant status. EMR-I. Thus. Administration of bacoside A restored the levels of zinc and selenium. K. and retinol (Handelman et al. Cadmium. alterations in mineral metabolism are secondary to chronic diseases associated with long-term smoking.. peroxyl and nitric oxide radicals (Russo et al. 1999.. Anand. 1988).. U. Anti-oxidant enzymes. capable of preventing brain damage caused by oxidative stress. 2001) and effectively scavenge the hydroxyl. G.. Anbarasi (Grant No: 9/115(593)/2003. Omu. which accelerate the oxidant injury through the formation of hydroxyl radicals via Haber-Weiss/Fenton reaction (Lapenna et al. Pamuk et al. Acknowledgements The financial assistance provided to Ms. Hepatoprotective and nephroprotective effect of B. The question remains whether this might have contributed to the manifestation of brain damage or it was a consequence of brain damage. A. K. However. Anand. Devi. 486 – 488.. In vitro exposure of plasma to cigarette smoke resulted in the destruction of tocopherols. The observed increase in the levels of copper and iron in the brain could be due to the mobilization of iron from ferritin and copper from copperbinding protein induced by cigarette smoke exposure. more effectively than ascorbic acid (Pawar et al... Presented at the International Conference on Role of Free Radicals and Antioxidants in Health and Disease. Transition metal complexes are known to play a major role in free radical biology and cigarette tar contains large amounts of metals..1382 K. Effect of bacoside A on membrane-bound ATPases in the brain of rats exposed to . Balakrishna. H. Thus. probably by preventing cadmium mediated toxicity. (February 10 – 12). bacoside A could have protected the brain from cigarette smoke-induced rise in copper and iron as a metal chelator. 1989).. it plays a major role in preventing free radical mediated cell damage (Bou-Resli et al. C.. 1991). Bacoside A ameliorates cigarette smoking induced peroxidative changes probably through its free radical scavenging. B.. 1994). Devi..2003) and Dr. Damaged brain tissue undergoes rapid lipid peroxidation. membrane bound vitamin E reacts with peroxyl radicals present in the smoke and terminates lipid peroxidation (Brown et al.... Balakrishna. Ceruloplasmin is a copper binding protein which functions as a ferroxidase that oxidizes iron to Fe3+ and thereby prevents accumulation of free iron. This may in part reflect the increased levels of free iron and copper upon cigarette smoke exposure.2000) by the Council of Scientific and Industrial Research (CSIR). India. presumably because metals released by cell disruption are not safely sequestered (Floyd. Administration of bacoside A increased glutathione levels in the brain. This could also be the reason for the maintenance of the antioxidant vitamins which otherwise would be spared in scavenging these radicals from smoke. 1997). Indian Journal of Experimental Biology 34. Agarwal..

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