Acute ethanol administration caused prominent hepatic microvesicular steatosis with mild necrosis and an elevation of serum ALT activity, induced a significant decrease in hepatic glutathione in conjunction with enhanced lipid peroxidation (oxidative stress) and increased hepatic TNF (necrosis factor-alpha) production. Supplementation with a standardized silymarin with its both antioxidant and antiinflammation properties decreases TNF production and attenuated these adverse changes induced by acute ethanol administration. In view of its nontoxic nature, it may be developed as an effective therapeutic agent for alcoholinduced liver disease by its antioxidative stress and antiinflammatory features [56] .