The interaction of ethanol and aflatoxin B
1 (AFB
1)-induced hepatotoxicity was studied in male Wistar rats using the activity of plasma GOT and GPT, liver triglyceride and histopathologic changes of liver necrosis as indices. Pretreatment of four oral doses of ethanol (4.0 g/kg BW each) at 48, 45, 24 and 21 hrs prior to AFB
1 (0.5 to 2.0 mg/kg BW) single i.p. administration caused a significant increase in the activity of PGOT (6 folds) and PGPT (5 folds), liver triglycerides (2 folds) and severity of liver necrosis at 48 hrs after AFB
1 administration. Ethanol pretreatment potentiated AFB
1-induced hepatotoxicity by increasing MFO enzymes, aniline hydroxylase and P-nitroanisole-O-demethylase activity and lipid peroxidation, and decreasing in cytochrome b
5, epoxide hydrolase activity and hepatic glutathione content. However, it did not cause any significant change in the activity of NADPH-cytochrome c reductase and glutathione-S-transferase and cytochrome P-450. These results suggest that potentiation of ethanol pretreatment on AFB
1-induced hepatotoxicity may due to an increase in the metabolic formation of AFB
1-2, 3-oxide and subsequent binding to DNA.
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