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Mitochondrial oxidative stress and dysfunction in arsenic
neurotoxicity: A review.; PY2016;Maharshi Dayanand University, India (印度);_WJD_2019-0902_V001R01_IR92_RvD20190902_
Source (資訊來源):
Info cited on 2019-09-02-WD1 (資訊引用於 中華民國108年9月2日) by 湯偉晉
(WeiJin Tang)
#
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J Appl Toxicol. 2016 Feb;36(2):179-88. doi:
10.1002/jat.3256. Epub 2015 Oct 29.
Mitochondrial oxidative stress and dysfunction in arsenic
neurotoxicity: A review.
Mitochondrial
oxidative stress and dysfunction in arsenic neurotoxicity: A review.
Mitochondrial oxidative stress and dysfunction in arsenic
neurotoxicity: A review.
Mitochondrial
oxidative stress and dysfunction in arsenic neurotoxicity: A review.
Mitochondrial oxidative stress and dysfunction in arsenic
neurotoxicity: A review.
Prakash C1, Soni M1, Kumar V1.
Author information
1
Department of Biochemistry, Maharshi Dayanand University,
Rohtak, 124001, Haryana, India.
Abstract
Arsenic is a toxic metalloid
present ubiquitously on earth. Since the last decade, it has gained considerable attention due
to its severe neurotoxic effects. Arsenic can cross the blood-brain barrier and accumulate in different regions of the brain
suggesting its role in neurological diseases. Arsenic
exposure has been associated with reactive oxygen species generation, which is supposed to be one of the mechanisms of arsenic-induced oxidative stress. Mitochondria, being the major source of reactive oxygen species
generation may present an important target of arsenic toxicity. It is
speculated that the proper functioning of the brain depends largely on
efficient mitochondrial functions. Multiple
studies have reported evidence of brain mitochondrial impairment after arsenic
exposure. In
this review, we have evaluated the proposed mechanisms of arsenic-induced
mitochondrial oxidative stress and dysfunction. The understanding of molecular
mechanism of mitochondrial dysfunction may be helpful to develop therapeutic
strategies against arsenic-induced neurotoxicity. The ameliorative measures
undertaken in arsenic-induced mitochondrial dysfunction have also been
highlighted.
Copyright © 2015 John Wiley & Sons, Ltd.
KEYWORDS:
arsenic; membrane potential; mitochondrial dysfunction;
neurotoxicity; oxidative stress
PMID: 26510484 DOI: 10.1002/jat.3256
[Indexed for MEDLINE]
KEYWORDS added by WeiJin Tang:
Glutathione,
cysteine
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