ORIGINAL CONTRIBUTIONS |
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| Year : 2001 | Volume
: 55
| Issue : 6 | Page : 309--312 |
Plasma lipid peroxidation and vitamin E levels in smokers
S Kharb, V Singh, PS Ghalaut, A Sharma, GP Singh
Department of Medicine and Biochemistry, Pt. B. D. Sharma PGIMS, Rohtak,
Correspondence Address:
S Kharb
Department of Medicine and Biochemistry, Pt. B. D. Sharma PGIMS, Rohtak
How to cite this article:
Kharb S, Singh V, Ghalaut P S, Sharma A, Singh G P. Plasma lipid peroxidation and vitamin E levels in smokers.Indian J Med Sci 2001;55:309-312
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How to cite this URL:
Kharb S, Singh V, Ghalaut P S, Sharma A, Singh G P. Plasma lipid peroxidation and vitamin E levels in smokers. Indian J Med Sci [serial online] 2001 [cited 2013 May 21 ];55:309-312
Available from: http://www.indianjmedsci.org/text.asp?2001/55/6/309/12059 |
Full Text
Chronic cigarette smoking represents a major risk factor for the development of atherosclerosis associated with coronary and peripheral vascular disease[1]. Cigarette smoking increases the concentration of triglycerides and lowers the concentration of high density lipoprotein cholesterol (HDL-C)[1]. Cigarette smoke contains abundant amount of oxidants which may promote oxidative modification of low density lipoprotein (LDL) and contribute to the pathogenesis of atherosclerosis. There is strong evidence that lipid peroxidation - and further oxidative modification of LDL increases its atherogenecity[2]. Alpha tocopherol is lipid soluble antioxidant carried in LDL. It inhibits lipid peroxidation and may play an important role in preventing atherogenic modification of LDL[3]. The present study is aimed at evaluating lipid peroxidation, vitamin E status and lipid profile in healthy smokers.
We studied thirty healthy smokers and 25 non smoking healthy adults in the age group 30 - 50 years ( employees and medical students of Pt. B. D. Sharma PGIMS, Rohtak ). Subjects were excluded from the screening if they had known endocrinologic disorders, diabetes mellitus, renal insufficiency, hepatic disease, illnesses characterized by an acute phase response or history of taking lipid owering drugs or vitamin E supplements. Entrance criteria for smoker group included subjects who smoked atleast 8 cigarettes per day for 8-15 years. After overnight fasting peripheral venous blood was drawn. Serum was seperated by centrifugation and biochemical studies were performed. The lipid profile was estimated enzymatically and serum malonaldehyde ( MDA ) was estimated by thiobarbituric reaction[4]. Serum vitamin E was assayed spectrofluorometricaily[5].
RESULTS
Smokers had higher values of MDA as compared to nonsmokers (p -2) anion from cigarette smoke may reach the vascular endothelium and can then react with nitric oxide (NO -) to form peroxynitnte anion, a highly reactive intermediate with strong cytotoxic potency[6]. Thus, the damaging free radicals in cigarette smoke may cause either direct arterial wall injury or may initiate and/or accelerate secondary processes including depletion of antioxidants ( such as vitamin E), protein peroxidation and activation of phagocyte - platelet-endothelial cell interaction[7],[8]. In the present study, low levels of vitamin E were observed amongst the smokers as compared to non-smokers. Also, an inverse relationship between MDA and vitamin E was observed. An imbalance between proxidant and antioxidants within the vasculature may also be operative in smokers since plasma levels of vitamin E are in general lower in smokers as compared to non smoker control subjects, a phenomenon that appears to reflect increased metabolism as the result of oxidant load rather than decreased intake. Frei[9] reported that invitro exposure of blood plasma to gas phase of cigarette smoke did not influence lipid peroxidation until the endogenous ascorbic acid had been completely oxidized, in contrast, alpha - tocopherol was not consumed at a significant rate in those studies. This suggests that cigarette smoking might deplete hydrophilic antioxidants much earlier than lipophilic ones. Demonstration of low level of antioxidant vitamin E in chronic smokers suggests that antioxidant therapy with vitamin E may limit the cardiovascular consequences of chronic smokers.
References
| 1 | Sackett DL, Gibson RW, Brass IDJ, Pickren JW. Relation between aortic atherosclerosis and the use of cigarettes and alcohol an autopsy study. N Engl J Med 1968; 279; 1413-20. |
| 2 | Steinberg D, Parthasarathy S, Carew TL, Rhoo JC, Whitztum JL. Beyond cholesterol modification of low density lipoprotein that increase its atherogenecity. N Engl J Med 1989; 320; 915-24. |
| 3 | Miwa K, Mlyagi Y, lgawa A, Nakagawa K, inoue H. Vitamin E deficiency in variant angina, Circulation 1996, 94;14-8. |
| 4 | Placer ZA, Cushmann LL, Johnson BG. Estimation of products of lipid peroxidation in biological systems. Anal -Biochem 1960; 16; 359-64.. |
| 5 | Costagliola C, Julian G, Menzione M. Effect of vitamin E on glutathione content in red blood cells, aqueous humour and lens of human and other species. Exp Eye Res 1986;43;905-16. |
| 6 | White CR, Brock TA, Chong LY, Crapo J. Briscoe P, Ku D et al. Superoxide and perioxynitrite in atherosclerosis. Proc Nati Aced Sci USA 1994; 91; 1044-8. |
| 7 | Recnick AZ, Cross CE, Hu ML, Suzuki YZ, Khwaja S, Safadl A, et al, Modification of plasma proteins by cigarette smoke as as measured by protein carbonyl formation. Biochem J 1992; 286; 607-11. |
| 8 | Blache D. Involvement of hydrogen and lipid peroxides in acute tobacco smoking induced platelet hyperactivity. Am J Physiol 1995; 268; H67985. |
| 9 | Frei B. Ascorbic acid protects lipids in human plasma. low density lipoprotein against oxidative damage. Am J Clin Nutr 1991; 54; 1113S-8S. |
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