Abstract:

Arsenic (As) is a natural pollutant, which exposure is related to a variety of diseases like hypertension, diabetes, cancer and neurodegenerative or neurodevelopment impairment but, the exact mechanism by which As exposure could be toxic is still unclear. Studies employing different models of Astoxicity suggested that As could cause ROS generation and antioxidant depletion in biological systems, including controversial data related to RNS generation and nitrosative damage. The hypothesis of the present work is that acute As exposure could trigger an imbalance in the production of RNS in brain, leading to nitrosative stress and nitrosative-dependent cellular damage. The effect of in vivo exposure to As was studied by histopathology of the tissue, NO2- plus NO3- content, NO generation rate employing Electron Paramagnetic Resonance (EPR) techniques, and the content of nitrotyrosine (NO2-Tyr) of total proteins in rat brain by western blot techniques. The data presented here suggested that the exposure to As increased the production of NO and lipid radicals in brain, leading to nitrosative damage to proteins and a depletion of the hippocampal pyramidal cell layer, that could affect functionality of the brain.

Keywords: