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Preventive Role of quercetin against Non-enzymatic Peroxidation and Oxidative stress in Brain Mitochondria induced by Endosulfan in Rat

Author Affiliations

  • 1Laboratory of Cellular and Molecular Biology, University of Jijelijel, ALGERIA
  • 2Department of animal biology, University of Mentouri 1, ALGERIA
  • 3Department of Biology, University of Tebessa, ALGERIA
  • 4Laboratory of Toxicology-Microbiology Environmental and Health, University of Sfax, TUNISIA

Int. Res. J. Earth Sci., Volume 3, Issue (1), Pages 18-23, January,25 (2015)

Abstract

Endosulfan (END) is still in use in north-Africa although it has large environmental ubiquity and toxicity.The non-enzymatic peroxidation and redox status in rat brain mitochondria after END toxicity have not been sufficiently investigated. In the present study, we first investigated the pro-oxidant effect of END on brain mitochondria and its effect upon lipid peroxidation in this organelle. Gavages of END into rats at a dose of 4 mg/kg induced oxidative stress in brain mitochondria, so it provoked a statistically significant reduction of catalase (CAT), superoxide dismutase (SOD), glutathione (GSH) levels and proteins. Significant increase in malonedialdehyde (MDA) levels – an indicator of lipid peroxidation – was observed in neuronal mitochondria. Second, the protective effect of quercetin (QE) (5mg/kg) against endosulfan-induced non-enzymatic peroxidation in the same organelle was also investigated. Indeed, the pretreatment of rats with QE protected brain mitochondria from oxidative stress and membrane modification. This treatment conserves the integrity of mitochondrial membranes following the inhibition of lipid peroxidation. Thus, QE works through the prevention of mitochondrial membrane perforation and the antioxidant defense system of brain mitochondria.

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