Efficacy of vitamin C against oxidative damages and apoptosis in hepatocytes of mice treated with phenylhydrazine

Phenylhydrazine (PHZ) as a well-known hemolytic agent can induce a variety of adverse effects including hepatotoxicity. The main goal of the present study was to examine the possible efficacy of vitamin C against PHZ-induced oxidative damages and apoptosis in mouse liver. In this randomized controlled experimental study, adult male mice were assigned to four groups of eight mice each. Two groups of mice received PHZ at a dose of 60 mg/kg per 48 hours intraperitoneally for 35 days. Vitamin C was administered to one of these groups at a dose of 250 mg/kg per day intraperitoneally four hours before PHZ injection. A vehicle-treated control group and a vitamin C-only treated group were also included. Serum and hepatic samples were collected 24 hours after the last treatment and subjected to biochemical and histomorphometric and histochemical examinations, respectively. The data were analyzed by one-way analysis of variance followed by Duncan test for post hoc comparisons. PHZ treatment caused a significant elevation (P < 0.05) in serum concentrations of aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase and malondealdehyde and decreased serum level of total antioxidant capacity, superoxide dismutase and albumin. Moreover, PHZ significantly increased apoptosis and diameters of hepatocytes and their nuclei as well as number of Kupffer cells. Remarkably, vitamin C pretreatment improved all changes in the above-mentioned parameters. Vitamin C can modulate PHZ-induced oxidative injuries and apoptosis in mouse liver due to its antioxidant activities.