4.7 Article

Chlorpyrifos induced hepatotoxic and hematologic changes in rats: The role of quercetin and catechin

Journal

FOOD AND CHEMICAL TOXICOLOGY
Volume 55, Issue -, Pages 549-556

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2013.01.056

Keywords

Chlorpyrifos; Catechin; Quercetin; Hepatotoxicity; Histopathology; Oxidative stress

Funding

  1. Gazi University
  2. Gazi University [05/2009-05]

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Chlorpyrifos is an organophosphorus insecticide which is widely used throughout in the world and it caused toxic effects on nontarget organisms especially mammalian. In the present study, catechin, quercetin, chlorpyrifos, catechin + chlorpyrifos, quercetin + chlorpyrifos were given to male rats through gavage for 4 weeks. Serum total protein, albumin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, trigliceride, total cholesterol levels, hematological changes, superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase activities and malondialdehyde content in liver tissues and also histopathological changes of liver were investigated in the rats compared to control group. No significant differences in all investigated parameters were observed between control, catechin and quercetin groups. There were statistically significantly changes in liver function tests, some hematological parameters, antioxidant enzyme activities and malondialdehyde levels in chlorpyrifos treated group compared to control group. In catechin + chlorpyrifos treated group and quercetin + chlorpyrifos treated group we observed the protective effects of catechin and quercetin on examining parameters but not completely. While some histopathological changes detected in liver tissues in chlorpyrifos treated group, less histopathological changes were observed in catechin + chlorpyrifos and quercetin + chlorpyrifos treated groups at the end of the 4th week. As a result, catechin and quercetin significantly reduce chlorpyrifos induced hepatotoxicity in rats. (C) 2013 Elsevier Ltd. All rights reserved.

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