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.
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.
Authors: N B V Barbosa; J B T Rocha; D C Wondracek; J Perottoni; G Zeni; C W Nogueira Journal: Chem Biol Interact Date: 2006-08-17 Impact factor: 5.192
Authors: David L Eaton; Robert B Daroff; Herman Autrup; James Bridges; Patricia Buffler; Lucio G Costa; Joseph Coyle; Guy McKhann; William C Mobley; Lynn Nadel; Diether Neubert; Rolf Schulte-Hermann; Peter S Spencer Journal: Crit Rev Toxicol Date: 2008 Impact factor: 5.635