Background/aims: The aim of this study was to investigate the effect of ascorbic acid (AA) an alterations in hepatic secretory and microsomal functions during hepatic ischemia and reperfusion.
Methods: Rats were subjected to 60 min of hepatic ischemia, and 1 and 5 h of reperfusion. Five minutes prior to ischemia, the animals were administered either vehicle or ascorbic acid (AA) (30, 100, 300, and 1000 mg/kg) intravenously.
Results: The serum aminotransferase level and lipid peroxidation were markedly higher as a result of ischemia/reperfusion. These increases were significantly attenuated by AA doses of 30 and 100 mg/kg but were augmented by dose of 1000 mg/kg. Bile flow and cholate output were markedly decreased by ischemia/reperfusion. AA doses of 30 and 100 mg/kg restored but dose of 1000 mg/kg inhibited their secretion. Both the cytochrome P(450) content and aminopyrine N-demethylase activity were decreased by ischemia/reperfusion, which were prevented by AA doses of 30 and 100 mg/kg but were aggravated by dose of 1000 mg/kg. Aniline p-hydroxylase activity was elevated by ischemia/reperfusion, and this was prevented by AA doses of 100, 300 and 1000 mg/kg.
Conclusions: Ischemia/reperfusion diminishes the hepatic secretory and microsomal functions. AA has both antioxidant and pro-oxidant effects, depending upon the dose.