Endosulfan causes oxidative stress in the liver and brain that involves inhibition of NADH dehydrogenase and altered antioxidant enzyme status in rat

Abstract

Endosulfan, a neurotoxic, highly persistent organochlorine insecticide, is known for its acute and chronic toxicity. We have shown that a single sublethal dose of endosulfan caused high induction of oxidative stress in the liver and brain by altering the antioxidant status, as shown by reduction in the antioxidant enzymes SOD, GPx, GST, GR along with increased ROS and lipid peroxidation. The cerebral region in the brain showed a higher level of oxidative stress than the cerebellum, revealing differential sensitivity of the brain regions to endosulfan. Depletion of natural antioxidants causes the imbalance of redox status in cells, and the role of mitochondrial distress causally related to the cellular oxidative stress in vivo is not well understood. We have shown that reduction in the mitochondrial NADH dehydrogenase activity in the brain is associated with the induction of ROS in endosulfan-treated rats. Although oxidative stress is induced in both the liver and brain, the oxidative damage to the brain has implications for the toxic outcome in view of the brain's lower antioxidant defenses and high oxygen consumption.

Keywords

• Endosulfan
• Oxidative stress
• Lipid peroxidation
• Antioxidant enzymes
• Glutathione
• Mitochondrial NADH dehydrogenase