Selenium safeguards the liver against 5flurouracil-induced toxicity

Hepatotoxic effect of 5-Fluourouracil (5-FU) can deprive cancer patients of maximum therapeutic benefits. Aim: This study assessed the ability of selenium (Se) to protect against hepatotoxicity induced by 5-FU in rats. Forty adult albino rats were groups and used. Rats in group A (control) were treated intraperitoneally (ip) with 0.2ml of normal saline daily for 5 days. Rats in groups B1-B3 were treated with 0.125 mg/kg, 0.25 mg/kg and 0.50 mg/kg of Se ip daily for 5 days respectively. Rats in group C were treated with 20 mg/kg of 5-FU ip daily for 5 days. Rats in groups D1-D3 were treated with 0.125 mg/kg, 0.25 mg/kg and 0.50 mg/kg of Se prior to treatment with 20mg/kg of 5-FU ip daily for 5 days respectively. After treatment, rats were euthanized; blood samples were collected and evaluated for serum liver function parameters. Liver was evaluated for biochemical parameters and histology. Results: Significant (p<0.001) increases in liver and serum aminotransferases, gamma glutamyl transferase, lactate dehydrogenase, alkaline phosphatase, total and conjugated bilirubin levels were observed in 5-FU-treated rats when compared to control. Furthermore, liver glutathione peroxidase, superoxide dismutase, catalase and glutathione levels were significantly (p<0.001) decreased whereas malondialdehyde levels were significantly (p<0.001) increased in 5-FU-treated rats when compared to control.  Hepatocyte necrosis was observed in 5-FU-treated rats. Nonetheless, 5FU-induced hepatotoxicity was significantly abrogated in rats supplemented with 0.125 mg/kg (p<0.05), 0.25 mg/kg (p<0.01) and 0.5 mg/kg (p<0.001) of Se in a dose-dependent fashion when compared to 5-FU-treated rats. Se may have clinical benefit in hepatotoxicity caused by 5-FU. Keywords: 5-fluorouracil, hepatocyte, toxicity, selenium, abrogation, rats