Molecular Basis of Neurodegenerative Changes and Neurotoxicity Linked with Arsenic Exposure: A Review

Abstract

Background

Toxicity with metals like arsenic trioxide is a growing concern as they are responsible to leading neurological diseases. The neurological diseases that are increasing day by day are not specific to any age or gender.

Main Body

In this systematic review, we have collected scientific information related to toxicity of heavy metal which leads to neurological complications. Such an approach incorporates the environmental occurrence of arsenic trioxide, human exposure, clinical significance, impact on the brain, and the mechanisms involved. Mechanistic approach behind arsenic neurotoxicity is oxidative stress, disruption of vital cellular functions such as glutathione depletion and lipid peroxidation and impaired neurotransmitter signaling. Gaining an understanding about these pathways are necessary for creating solutions that effectively lessen the detrimental impacts of (As) exposure on human health. Arsenic exposure exhibits neurodegenerative changes in brain due to oxidative injury, mitochondrial impairments, glutamate excitotoxicity through glutamate transporters, and calcium dysregulation through ryanodine receptors modulation in the brain. Arsenic neurotoxicity has been studied for many years, but in order to comprehend their possible health advantages, their mechanistic significance has recently been investigated. In this review, we have discussed the mechanisms involved in arsenic trioxide mediated neurodegenerations.

Short conclusion

This review provides a summary on current prospective related to neurological consequences of arsenic trioxide. The findings highlights that a multimodal strategy is needed to reduce the health effects of arsenic exposure, including strict industrial process controls, food and water source monitoring, and public awareness programs.