Abstract
Arsenic is a key environmental toxicant having significant impacts on human health. Millions of people in developing countries such as Bangladesh, Mexico, Taiwan, and India are affected by arsenic contamination through groundwater. Environmental contamination of arsenic leads to leads to various types of cancers, coronary and neurological ailments in human. There are several sources of arsenic exposure such as drinking water, diet, wood preservatives, smoking, air and cosmetics, while, drinking water is the most explored route. Inorganic arsenic exhibits higher levels of toxicity compared its organic forms. Exposure to inorganic arsenic is known to cause major neurological effects such as cytotoxicity, chromosomal aberration, damage to cellular DNA and genotoxicity. On the other hand, long-term exposure to arsenic may cause neurobehavioral effects in the juvenile stage, which may have detrimental effects in the later stages of life. Thus, it is important to understand the toxicology and underlying molecular mechanism of arsenic which will help to mitigate its detrimental effects. The present review focuses on the epidemiology, and the toxic mechanisms responsible for arsenic induced neurobehavioral diseases, including strategies for its management from water, community and household premises. The review also provides a critical analysis of epigenetic and transgenerational modifications, mitochondrial oxidative stress, molecular mechanisms of arsenic-induced oxidative stress, and neuronal dysfunction.
Highlights
Arsenic is recognized as a primary environmental pollutant that has substantial health impacts on human and other species
Exposure to arsenic disrupts this coupling produces reactive oxygen species (ROS) [97]. (v.) Metabolism of As(III) to As(V) in normal conditions results in the generation of H2O2 [98]. (vi.) ROS are generated during the formation of intermediate arsine species such as dimethylarsenic peroxyl radicals-metabolic by-products of dimethylarsinic acid [99]. (vii.) Methylated 3+ organic arsenicals react with sulfhydryl groups (-SH) in antioxidative proteins and inhibit their activity, which results in a build-up of oxidative stress [100]
Arsenic exposure affects millions of people globally, and epidemiological evidence provides an imperative guide to arsenic risk assessment in food, water and air
Summary
Arsenic is recognized as a primary environmental pollutant that has substantial health impacts on human and other species. Increased arsenic levels in the environment have become a serious human health concern is widely distributed globally [4]. Dissolved arsenic levels in aquatic ecosystems in many developing countries have been reported to be higher than the permissible limit (10 μg/L) set by World Health Organization (WHO). This might be responsible for the disturbed physiological functions such as ion regulation, gene expression, enzyme and immune functions, growth and repair of tissue matrix, reproduction, and development [10]. We discuss recent advances in understanding arsenic neurotoxicity, including the role of epigenetic modulations, mitochondrial oxidative stress, and neuronal dysfunction
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