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Exess Ethanol intake is usually toxic in health. Chronic ethanol consumption causes oxidative damage in liver. Cytochrome P450 2E1 (CYP2E1) participates to the ethanol decomposition. Excess ethanol intake affects more microsomal enzyme CYP2E1 activity than ADH resulting in causing oxidant stress. CYP2E1 has been to be a major contributor to ethanol-induced oxidant stress. CYP2E1 induced ethanol conversion to acetaldehyde. Acetaldehyde is malignant metabolite for vasodilation substance, flushing induction, and respiratory distress induction as well as exhibiting to be intense reactive and toxic. Acetaldehyde combined with phospholipid, amino acid residues, and sulphydryl group may transform cell surface antigen and induce lipid
peroxidation and oxidant stress as well as depleting antioxidant enzyme glutathione (GSH). In this study, we investigated the inhibition of ethanol-induced CYP2E1 by Curcuma longa L. Extract. The cell lines used were HepG2 E47 cells that expressed human CYP2E1 and
HepG2 C34 cells which did not express CYP2E1. CYP2E1 enzymatic activity was determined in E47 and C34 cells by measuring the fluorescence and western blot. In consequence, Curcuma longa L. Extract was recognized to inhibit the ethanol-induced CYP2E1 enzymaticactivity.