selenium safeguards the liver against 5-fluorouracil induced toxicity

Background: the hepatotoxic effect of 5-fluorouracil (5-fu) can deprive cancer patients of its maximum therapeutic benefits. selenium (se) is a trace element with potential benefits in some animal models of diseases. objectives: this study assessed the ability of se to nullify the hepatotoxic effect of 5-fu in albino rats. methods: in this study, 40 adult male albino rats were grouped into a to d (each 5 rats). rats in group a (control) were treated intraperitoneally (ip) with normal saline (0.2 ml) daily for 5 days. rats in groups b1 to b3 were treated ip with se (0.125, 0.25, and 0.50 mg/kg) daily for 5 days, respectively. rats in group c were treated ip with 5-fu (20 mg/kg) daily for 5 days. rats in groups d1to d3 were treated ip with se with 0.125, 0.25, and 0.50 mg/kg before treatment with 5-fu (20 mg/kg) daily for 5 days, respectively. after treatment, the rats were euthanized, and their blood samples were collected and evaluated for serum liver function. liver samples were evaluated for biochemical and histological parameters. results: liver and serum aminotransferases, gamma-glutamyl transferase, lactate dehydrogenase, alkaline phosphatase, total bilirubin, and conjugated bilirubin levels were significantly (p<0.001) high in 5-fu-treated rats in comparison to the control group. liver glutathione peroxidase, superoxide dismutase (sod), catalase, and glutathione levels were significantly (p<0.001) low whereas the malondialdehyde level was significantly (p<0.001) high in 5-fu-treated rats compared with the control group. moreover, hepatocyte necrosis was observed in 5-fu-treated rats. conclusion: nonetheless, 5-fu-induced hepatotoxicity was significantly nullified in rats supplemented with se (0.125 mg/kg, p<0.05; 0.25 mg/kg, p<0.01, and 0.5 mg/kg, p<0.001) in a dose-dependent fashion in comparison to 5-fu-treated rats. thus, se may have a clinical benefit in 5-fu-induced hepatotoxicity.