Liver disease / lecithin / oxidative stressModulation of lecithin activity by vitamin-B complex to treat long term
consumption of ethanol induced oxidative stress in liver.
Das SK, Vasudevan DM
Indian J Exp Biol. 2006 Oct ; 44(10): 791-801
Alcoholic liver disease (ALD) develops as a consequence of priming and
sensitizing mechanisms rendered by cross-interactions of primary
mechanistic factors and secondary risk factors. Chronic alcohol abuse
and its progression to ALD are associated with abnormal metabolism and
low tissue or plasma levels, or both, of many micronutrients.
Glutathione depletion is considered the most important sensitizing
mechanism. In the present study efficacy of lecithin with vitamin-B
complex to treat ethanol induced oxidative stress was compared with the
effect of lecithin alone, tocopheryl acetate (vitamin E), as well as
capacity of hepatic regeneration during abstention. Ethanol (1.6g / kg
body weight/ day for 4 weeks) affects body weight in 16-18 week old
male albino rats of Wistar strain weighing 200-220 g. Thiobarbituric
acid reactive substance level, nitrite content, protein carbonyl group
level, redox ratio (oxidized to reduced glutathione ratio), superoxide
dismutase activity, and glutathione s-transferase activity
significantly increased on ethanol exposure. Whereas reduced
glutathione content, and activities of catalase, glutathione reductase
and glutathione peroxidase significantly reduced due to ethanol
exposure. These changes were reversed by different treatment. The
results suggest that tocopheryl acetate (vitamin E) could partially
reverse these changes and act as a potential therapeutic agent.
However, lecithin with vitamin-B complex treatment is a promising
therapeutic approach. Furthermore, preventive measures were more
effective than curative treatment. Prevention of oxidative and
nitrosative stress along with correction of nutritional deficiency is
one of the proposed mechanisms for the therapeutic approach.
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