Vol. 6, Issue 1, Part A (2024)

Arsenic is a naturally occurring element that may be found in both inorganic and organic forms throughout the environment. It is believed that inorganic arsenic are particularly detrimental to human health. Human exposure to inorganic arsenic is mostly caused by polluted drinking water, despite the fact that food and water are the main sources of inorganic arsenic exposure for people. In Bangladesh, West Bengal, China, Taiwan, Thailand, Ghana, Argentina, Chile, Mexico, Hungary, Canada, the United Kingdom, and some parts of the United States, widespread arsenic pollution of groundwater has been documented. However, if arsenic enters the neonate, it may pass the blood-brain barrier (BBB) and have an immediate impact on the central nervous system (CNS). Tight connections between capillary endothelial cells in the brain and epithelial cells in the choroid plexus make up the BBB, a structure designed to keep proteins and other tiny molecules from interacting with the cerebrospinal fluid. Additionally, as succinyl coA is present in complex II of the electron transport chain, arsenic prevents the synthesis of succinyl CoA, hinders the generation of ATP in cells, and completely shuts off the energy supply. Neurotransmitters, which are in charge of facilitating cell-to-cell communication in the brain, are impacted by arsenic-induced neurotoxicity. Arsenic serves to induce dopamine and serotonin levels while inversely regulating norepinephrine levels. The arsenic impact alters the amounts of Ɣ-aminobutyric acid (GABA), glutamate, and other biogenic amines. As a result of the arsenic threat, the levels of various inflammatory indicators, including IL-6, TNF-α, IL-1, and IFN-Ɣ, as well as mitochondrial apoptotic markers like bax, bak, bid, and bim change in neural tissues. The goal of this review paper is to provide an in-depth investigation of the mechanistic approach to arsenic-mediated neurotoxicity.