Protective effects of vitamins C and E against hepatotoxicity induced by methyl parathion in rats

UZUNHİSARCIKLI M., KALENDER Y.

ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY, vol.74, no.7, pp.2112-2118, 2011 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 74 Issue: 7
  • Publication Date: 2011
  • Doi Number: 10.1016/j.ecoenv.2011.07.001
  • Journal Name: ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.2112-2118
  • Keywords: Organophosphate insecticide, Methyl parathion, Hepatotoxicity, Electron microscopy, Vitamin C, Vitamin E, FREE-RADICAL METABOLISM, INDUCED CARDIOTOXICITY, BIOCHEMICAL INDEXES, ORGANOPHOSPHORUS, TOXICITY, DIAZINON, LIVER, INSECTICIDE, EXPOSURE, HEALTH
  • Gazi University Affiliated: Yes

Abstract

Male rats were given vitamins C+E, methyl parathion, or both daily via gavage for seven weeks. Body weight was decreased while liver weight increased significantly at the end of fourth and seventh weeks in the methyl parathion- and methyl parathion plus vitamin-treated groups. Serum total protein, albumin, triglyceride, low density lipoprotein-cholesterol (VLDL-cholesterol) levels decreased, and serum alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl-transferase (GGT), lactate dehydrogenase (LDH), and total cholesterol levels increased significantly in the methyl parathion- and the methyl parathion plus vitamin-treated rats. There was a statistically significant difference for all biochemical parameters when the methyl parathion plus vitamin-treated group was compared with methyl parathion-treated group. In electron microscopic investigation, cytopathological alterations were observed in hepatocytes of the methyl parathion- and the methyl parathion plus vitamin-treated rats. As a result, methyl parathion-induced hepatotoxicity is reduced by vitamins C+E, but vitamins C+E did not provide complete protection. (C) 2011 Elsevier Inc. All rights reserved.