Malathion-increased Hepatotoxicity in Diabetic Rats

Authors

  • Ahmad Ahmadipour Pharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
  • Ali Mandegary Pharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.; Department of Pharmacology & Toxicology, School of Pharmacy, Kerman University of Medical Sciences, Kerman, Iran.
  • Mohammad Mehdipour Pharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
  • Motahareh Soltani Pharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
  • Seyedeh Azam Hosseini Pharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
  • Somayyeh Karami-Mohajeri Pharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.; Department of Pharmacology & Toxicology, School of Pharmacy, Kerman University of Medical Sciences, Kerman, Iran.
Abstract:

Background: Malathion (MT), an organophosphorus pesticide, induces hepatotoxicity and is associated with hyperglycemia and the development of diabetes mellitus.  Objectives: This study was aimed to evaluate the effects of sub-acute exposure to sub-lethal dose of MT in the liver of diabetic rats.  Methods: Non-diabetic and streptozotocin-induced diabetic rats received MT at a dose of 150 mg/kg/day orally. After 28 days, fasting blood glucose, Glucose Tolerance Test (GTT), serum aminotransferases, and liver histopathology and antioxidant status were examined.  Results: MT impaired GTT, caused alteration in histopathology of histopathology and antioxidant status of liver in non-diabetic rats. Impairment in GTT did not observe in diabetic rats exposed to MT, but histopathology changes and antioxidant status alteration was more severe. Conclusion: Repeated sub-lethal dose of MT exacerbated hepatotoxicity in diabetes condition through further impairment in the antioxidant defense system. 

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Journal title

volume 6  issue 1

pages  53- 60

publication date 2020-12

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