Molecular Mechanism of Arsenic-Induced Neurotoxicity including Neuronal Dysfunctions

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.

Alzheimer’s Disease Association with Metals and Metalloids Concentration in Blood and Urine

“…Exposure to arsenic causes brain damages such as neuronal necrosis and apoptosis [ 51 ], oxidative stress [ 52 ], Tau hyperphosphorylation [ 28 ], and transcriptional activation of Aβ precursor protein gene [ 53 ]. The main pathways contributing to arsenic-induced neurotoxicity are oxidative stress, increased apoptosis in cerebral neurons, and increased axonal degeneration [ 54 ].…”

Arsenic: A Review on a Great Health Issue Worldwide

“…Arsenic exists in three allotropes: gray, yellow, and black arsenic; the gray form is the most common and important to industry. Gray arsenic is brittle and has a relatively low Mohs hardness of 3.5; its density is 5.73 g/cm 3 (Table 1). The most volatile, least dense, and the most toxic form is represented by yellow arsenic, which is soft and waxy, with a density of 1.97 g/cm 3 ; it is rapidly transformed into gray arsenic by light.…”

“…Gray arsenic is brittle and has a relatively low Mohs hardness of 3.5; its density is 5.73 g/cm 3 (Table 1). The most volatile, least dense, and the most toxic form is represented by yellow arsenic, which is soft and waxy, with a density of 1.97 g/cm 3 ; it is rapidly transformed into gray arsenic by light. Black arsenic, glassy and brittle, can be formed by cooling vapor at about 150-220 • C and by crystallizing arsenic in the presence of mercury vapors.…”

“…Most problems related to arsenic are the result of its mobilization under natural conditions. However, an important additional impact was due to anthropogenic sources, such as mining activity, combustion of fossil fuels, use of arsenical pesticides, herbicides and crop desiccants, and the use of arsenic as an additive to livestock feed, specifically for poultry [2,3]. Although the use of arsenical pesticides and herbicides has decreased significantly in the past decades, its use as wood preservative is still common.…”

Biotechnological Innovations from Ocean: Transpiring Role of Marine Drugs in Management of Chronic Disorders

“…With increasing age, the incidence of neurodegenerative diseases also increases, and they are more common in the elderly age group of patients. The main factor that is associated with the process of neurodegeneration is aging [ 65 , 66 ]. These diseases are mainly characterized by loss in the functioning of neurons and the formation of misfolded proteins, accompanied by their aggregation, extracellular intracellular deposits, and neuronal cell death.…”