Arsenic (As) is
found commonly in nature and exposure to arsenic is unavoidable for human. Not
only the consumption of drinking water and foods contaminated with arsenic but
also occupational exposure to arsenic can cause toxicity. This toxicity can
lead to various diseases. In addition, arsenic-induced formation of ROS and
subsequent depletion of antioxidant cell defences result in disruption of the
antioxidant/prooxidant equilibrium in mammalian tissues. According to its
sulfydryl group binding capacity, arsenic also inhibit the activities of many
enzymes, especially those involved in the uptake of glucose in cells, fatty
acid oxidation and production of glutathione. The induction of oxidative stress
by arsenic may influence gene expression. Genes involved in endogenous defenses
against ROS thus may modify arsenic’s effect. For example, MnSOD, a
metalloenzyme which contains manganese cofactor, is the enzyme placed in the
mitochondria to convert superoxide to hydrogen peroxide and thus has a key role
in quenching free radicals generated by the electron transport chain, and
overexpression of MnSOD can lead to an accumulation of reactive oxygen species
(ROS), which contributors to certain diseases and tumor progression. Second
important enzyme associated with oxidative stress is p22 phox, a critical
enzyme for superoxide production and an essential component of nicotinamide
adenine dinucleotide phosphate (NADPH) and oxidase (NOX). The effect of arsenic
on polymorphism in genes associated with oxidative stress (Mn-SOD and p22phox)
has been discussed in present updated overview.
Journal Section | Articles |
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Authors | |
Publication Date | February 16, 2017 |
Published in Issue | Year 2017 Volume: Volume 2 Issue: İssue 1 (1) - 2.İnternational Congress Of Forensic Toxicology |