Mechanism behind Arsenic induced Neurotoxicity with emphasis on Neural-protein Expression

Arsenic toxicity is a worldwide health concern as several millions of people are exposed to this toxicant via drinking water, and its exposure affects almost every organ system in the body including the brain. Recent studies showed that even low concentrations of arsenic impair neurological function, particularly children. Studies have shown that even low concentrations of arsenic impair neurological function, mainly in children. Arsenic is known to produce central and peripheral neuropathy, learning and memory impairment, short term memory and lack of concentration and attention, delirium, mood disorders, encephalopathy and decreased psychomotor speed. Features of neurodegeneration such as shrunken, irregular, and darkly stained nuclei and degenerating organelles were observed in cerebral cortex of arsenic treated experimental animals. The exact mechanism involved in the neurotoxic effect of arsenic is unknown. There are studies shows that arsenic induces apoptosis in the hippocampus, mitochondrial oxidative damage, neural protein expression and genetic damage. This review will focus on the mechanism of arsenic neurotoxicity, including oxidative stress, mitochondrial dysfunction, apoptosis in the hippocampus, ultra-structural changes in neuronal cytoskeletal proteins and oxidative DNA damage.