Diphenyl diselenide attenuates hepatic and hematologic toxicity induced by chlorpyrifos acute exposure in rats

Purpose In this study, we investigated the effect of diphenyl diselenide [(PhSe) 2 ] on chlorpyrifos (CPF)-induced hepatic and hematologic toxicity in rats. Methods Rats were pre-treated with (PhSe) 2 (5 mg/kg) via the oral route (oral gavage) once a day for 7 days. On the eighth and ninth days, rats were treated with (PhSe) 2 (5 mg/kg) 30 min prior to CPF (50 mg/kg, by subcutaneous route). The aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase activities were determined in plasma of rats. Lipid peroxidation, protein carbonyl, and non-protein thiol levels as well as catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, and gluthatione S-transferase activities were determined in livers of rats. Hematological parameters were also determined. Results The results showed that CPF caused hepatic oxidative damage, as demonstrated by an increase in lipid peroxidation and protein carbonyl levels which was associated with a decrease in antioxidant defenses. CPF exposure caused a reduction in the leukocyte, indicating hematologic toxicity. (PhSe) 2 was effective in attenuating these toxic effects caused by CPF exposure in rats. Conclusions The results indicated that (PhSe) 2 was effective in protecting the hepatic and hematologic toxicity induced by acute CPF exposure in rats.