Abstract
Arsenic poisoning is a global health problem. Chronic exposure to arsenic has been associated with the development of a wide range of diseases and health problems in humans. Arsenic exposure induces the generation of intracellular reactive oxygen species (ROS), which mediate multiple changes to cell behavior by altering signaling pathways and epigenetic modifications, or cause direct oxidative damage to molecules. Antioxidants with the potential to reduce ROS levels have been shown to ameliorate arsenic-induced lesions. However, emerging evidence suggests that constructive activation of antioxidative pathways and decreased ROS levels contribute to chronic arsenic toxicity in some cases. This review details the pathways involved in arsenic-induced redox imbalance, as well as current studies on prophylaxis and treatment strategies using antioxidants.
Highlights
Arsenic is the 33rd element in the periodic table of elements
Oxidative stress mediated by reactive oxygen species (ROS) is a common denominator in arsenic toxicity. here, we summarized ROS-related pathways in arsenic toxicity, as well as prophylaxis and therapeutic potential of antioxidants to combat arsenic toxicity
Our previous study found that stable knockdown (KD) of NRF2 in human keratinocytes (HaCaT) significantly increased the sensitivity to acute cytotoxicity of inorganic arsenite, whereas KEAP1-KD cells showed a significant resistance to arsenite toxicity [94]
Summary
Arsenic is the 33rd element in the periodic table of elements. It displays features of both a metal and a non-metal, and called metalloid. it is referred as a heavy metal from a toxicological point of view [1]. The major route of exposure is via drinking water due to natural contamination of groundwater by inorganic arsenic in the earth’s crust, which threatens the health of more than 140 million people worldwide [5,6]. MMA III and DMA III are more potent inhibitors of glucose-stimulated insulin secretion (GSIS) in isolated islets than iAs III [20]. These studies obscure the role of arsenic methylation in its toxicity, and again suggest that variance in arsenic methylation contributes to inter-individual susceptibility to arsenic-induced adverse health effects [21,22,23]. Oxidative stress mediated by reactive oxygen species (ROS) is a common denominator in arsenic toxicity. here, we summarized ROS-related pathways in arsenic toxicity, as well as prophylaxis and therapeutic potential of antioxidants to combat arsenic toxicity
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