Chronic Arsenic Exposure

Arsenic is a group-I toxicant and a co-carcinogen which has been shown to increase the cognitive dysfunction even at a lower concentration [1]. It has been shown to have more intense effect in children [2]. Chronic arsenic exposure induces a significant deficits in the long term memory in children [3]. Inorganic arsenic modulates locomotor activity and behavioral task suggesting the impairment of sensory and motor nerves [4]. Epidemiological studies reveal that chronic arsenic exposure through drinking water causes cerebral infarction, microvascular diseases and impairment in neural conduction [5]. A significant elevation of malondialdehyde level in response to arsenic exposure is noticed with a decrease in mitochondrial- and cytosolic- superoxide
Subchronic level of arsenic exposure can affect the level of monoamine neurotransmitters in mice brains. Arsenic can downregulate the concentrations of norepinephrine (NE), dopamine (DA), monoamine oxidase (MAO) and 5-OH tryptamine (5-HT) in the cerebrum or cerebellum of mice. Arsenic increases acetylcholinesterase in brain tissue [7, 8]. The oxidative damage results in structural deformities in the myelin sheath of nerve fibers and degradation in the terminals of the mossy-fibers impairing synaptic function and spatial memory [9]. Mechanistically, an elevated export of GSH and accelerated consumption of cellular glucose resulted in lactate production [10]. In addition, arsenic-treated astrocytes revealed a higher toxic potential of arsenite compared to arsenate, accompanied with a loss of total cellular glutathione with an increase in the cellular glutathione disulfide content
Arsenic exposure renders the brain tissue vulnerable to the free-radical attack resulting in apoptosis in the neural cells. Report suggests that arsenic exposure to mouse litters increased neuronal necrosis and mitotic impairment resulting in cerebellar immaturity [12]. However, arsenic induced neurotoxicity is not fully elucidated and its therapeutic outcome is out of