The Effects of Arsenic Exposure on Neurological and Cognitive Dysfunction in Human and Rodent Studies: A Review

被引：9
作者：
Tyler C.R. [1 ]
Allan A.M. [1 ]
机构：
[1] Department of Neuroscience, University of New Mexico School of Medicine, Albuquerque, NM
来源：
Current Environmental Health Reports | 2014年 / 1卷 / 2期
基金：
美国国家卫生研究院;
关键词：
Adult; Alzheimer’s disease; Anxiety; Arsenate; Arsenic; Arsenite; Children; Cholinergic; Cognition; Cortisol; Depression; Development; DNA methylation; Epigenetics; Exposure; Glucocorticoid receptor; Glutamatergic; Histone modifications; HPA; IQ; Lead; Monoaminergic; Mood disorders; Neurogenesis; Neurological deficits; Neurotoxicity; Teratogen;
D O I：
10.1007/s40572-014-0012-1
中图分类号：
学科分类号：
摘要：
Arsenic toxicity is a worldwide health concern as several millions of people are exposed to this toxicant via drinking water, and exposure affects almost every organ system in the body including the brain. Recent studies have shown that even low concentrations of arsenic impair neurological function, particularly in children. This review will focus on the current epidemiological evidence of arsenic neurotoxicity in children and adults, with emphasis on cognitive dysfunction, including learning and memory deficits and mood disorders. We provide a cohesive synthesis of the animal studies that have focused on neural mechanisms of dysfunction after arsenic exposure including altered epigenetics; hippocampal function; glucocorticoid and hypothalamus-pituitary-adrenal axis (HPA) pathway signaling; glutamatergic, cholinergic and monoaminergic signaling; adult neurogenesis; and increased Alzheimer’s-associated pathologies. Finally, we briefly discuss new studies focusing on therapeutic strategies to combat arsenic toxicity including the use of selenium and zinc. © 2014, The Author(s).
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页码：132 / 147
页数：15
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共 119 条
  • [71] Luo J.H., Et al., Effects of arsenic exposure from drinking water on spatial memory, ultra-structures and NMDAR gene expression of hippocampus in rats, Toxicol Lett, 184, 2, pp. 121-125, (2009)
  • [72] Tyler C.R., Allan A.M., Adult hippocampal neurogenesis and mRNA expression are altered by perinatal arsenic exposure in mice and restored by brief exposure to enrichment, PLoS One, 8, 9, (2013)
  • [73] Luo J.H., Et al., Arsenite exposure altered the expression of NMDA receptor and postsynaptic signaling proteins in rat hippocampus, Toxicol Lett, 211, 1, pp. 39-44, (2012)
  • [74] Martinez E.J., Et al., Moderate perinatal arsenic exposure alters neuroendocrine markers associated with depression and increases depressive-like behaviors in adult mouse offspring, Neurotoxicology, 29, 4, pp. 647-655, (2008)
  • [75] Klein C., Et al., Zinc induces ERK-dependent cell death through a specific Ras isoform, Apoptosis, 11, 11, pp. 1933-1944, (2006)
  • [76] Martinez-Finley E.J., Et al., Reduced expression of MAPK/ERK genes in perinatal arsenic-exposed offspring induced by glucocorticoid receptor deficits, Neurotoxicol Teratol, 33, 5, pp. 530-537, (2011)
  • [77] Bodwell J.E., Kingsley L.A., Hamilton J.W., Arsenic at very low concentrations alters glucocorticoid receptor (GR)-mediated gene activation but not GR-mediated gene repression: complex dose-response effects are closely correlated with levels of activated GR and require a functional GR DNA binding domain, Chem Res Toxicol, 17, 8, pp. 1064-1076, (2004)
  • [78] Bodwell J.E., Et al., Arsenic disruption of steroid receptor gene activation: complex dose-response effects are shared by several steroid receptors, Chem Res Toxicol, 19, 12, pp. 1619-1629, (2006)
  • [79] Davey J.C., Et al., Arsenic as an endocrine disruptor: effects of arsenic on estrogen receptor-mediated gene expression in vivo and in cell culture, Toxicol Sci, 98, 1, pp. 75-86, (2007)
  • [80] Ahir B.K., Et al., Systems biology and birth defects prevention: blockade of the glucocorticoid receptor prevents arsenic-induced birth defects, Environ Health Perspect, 121, 3, pp. 332-338, (2013)
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