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Hepatic Oxidative Damages and Glucose Tolerance in Diabetic Rats Exposed to Repeated Oral Doses of Diazinon

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Background: Environmental pollutants including organophosphate insecticides impair glucose metabolism by altering hepatic oxidation and play an important role in the development of diabetes and its complications. The aim of this study was to assess the impacts of repeated oral doses of Diazinon, an organophosphate insecticide, which is known to impair the glucose metabolism and its tolerance through oxidative stress in the rat liver. Methods: Diabetes was induced in rats by a single dose of freshly prepared Streptozotocin at 60 mg/kg. Both normal and diabetic rats were exposed to daily oral Diazinon at 20 mg/kg for 21 days. Subsequently, the effects on the rats’ liver were assessed by glucose tolerance test, histopathology examinations and antioxidant capacity measurement. Results: The glucose tolerance tests showed impairment in the non-diabetic rats exposed to Diazinon, while the difference in glucose tolerance between the diabetic rats treated with or without Diazinon was not significant. Diazinon in diabetic rats caused greater histopathological changes along with significant elevations in the lipid peroxidation and antioxidant enzymes, including superoxide dismutase and catalase in the liver tissue. Conclusion: Subacute exposure to Diazinon exacerbated hepatotoxicity by inducing oxidative stress in diabetic rats. The superoxide dismutase and catalase activities increased due to the oxidative damages in rats’ liver caused by Diazinon.
Title: Hepatic Oxidative Damages and Glucose Tolerance in Diabetic Rats Exposed to Repeated Oral Doses of Diazinon
Description:
Background: Environmental pollutants including organophosphate insecticides impair glucose metabolism by altering hepatic oxidation and play an important role in the development of diabetes and its complications.
The aim of this study was to assess the impacts of repeated oral doses of Diazinon, an organophosphate insecticide, which is known to impair the glucose metabolism and its tolerance through oxidative stress in the rat liver.
Methods: Diabetes was induced in rats by a single dose of freshly prepared Streptozotocin at 60 mg/kg.
Both normal and diabetic rats were exposed to daily oral Diazinon at 20 mg/kg for 21 days.
Subsequently, the effects on the rats’ liver were assessed by glucose tolerance test, histopathology examinations and antioxidant capacity measurement.
Results: The glucose tolerance tests showed impairment in the non-diabetic rats exposed to Diazinon, while the difference in glucose tolerance between the diabetic rats treated with or without Diazinon was not significant.
Diazinon in diabetic rats caused greater histopathological changes along with significant elevations in the lipid peroxidation and antioxidant enzymes, including superoxide dismutase and catalase in the liver tissue.
Conclusion: Subacute exposure to Diazinon exacerbated hepatotoxicity by inducing oxidative stress in diabetic rats.
The superoxide dismutase and catalase activities increased due to the oxidative damages in rats’ liver caused by Diazinon.

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