The effects of arsenic exposure on the nervous system

Rodrı́guez, V.M.; Jiménez‐Capdeville, María E.; Giordano, Magda

doi:10.1016/s0378-4274(03)00262-5

Cited by 262 publications

(144 citation statements)

References 117 publications

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“…Epidemiological investigations have demonstrated that As causes neurotoxicity including impairments of learning and memory 10,11) . Experimental studies have shown the alteration of locomotor activity and behavioral disorders in experimental animals exposed to As 12−14) .…”

Section: Discussionmentioning

confidence: 99%

“…As is also a potent neurotoxicant, and subchronic or chronic As exposure causes severe nervous system dysfunction 7−9) . Epidemiological studies have demonstrated that exposure to As results in impairments of learning and concentration 10) and deterioration in pattern memory and switching attention in humans 11) . Animals exposed to As showed delay in acquisition and extinction of an operant task 12) , alterations in locomotor behavior and deficits in spatial learning paradigms 13,14) .…”

mentioning

confidence: 99%

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Subchronic exposure to arsenic induces apoptosis in the hippocampus of the mouse brains through the Bcl‐2/Bax pathway

Wang

Bai

Guan

et al. 2015

Journal of Occupational Health

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were found in the hippocampus of As-exposed mice. The expressions of the Bcl-2 gene and its protein in the hippocampus of As-exposed mice were significantly lower than those in the control group (p<0.05). However, the expressions of the Bax gene and its protein, and the expression ratio of Bax/Bcl-2 in the hippocampus were significantly higher in the groups exposed to As than in the control group (p<0.05). Moreover, the activity of caspase-3 in the hippocampus of mice exposed to As was higher than that in the control (p<0.05). Conclusions:These results indicate that subchronic exposure to As induces apoptosis in the hippocampus of mice by disturbing normal Bax/Bcl-2 regulatory pathways. Meanwhile, it is suggested that the induced apoptosis in the hippocampus may be at least partly responsible for As-induced neurotoxicity. (J Occup Health 2015; 57: 212-221) Key words: Apoptosis, Arsenic trioxide, Bax, Bcl-2, Hippocampus, Neurotoxicity Arsenic (As), a naturally occurring toxic metalloid found in both inorganic and organic forms, is ubiquitous in the environment and contaminates water as a result of geological and industrial pollution 1) . Moreover, some kinds of arsenide, such as arsenic trioxide (As 2 O 3 ), are also widely used for the treatment of malignant tumors 2) . In As-contaminated areas, the As concentration in drinking water or groundwater ranges from 0.25 to 2.1 ppm and even reaches >3.0 ppm in some severely contaminated areas 3−5) . Exposure to As has been associated with increasing incidences of various chronic diseases, including peripheral vascular disease, cardiovascular disease, diabetes mellitus, and various cancers 6) . As is also a potent neurotoxicant, and subchronic or chronic As exposure causes severe nervous system Abstract: Subchronic exposure to arsenic induces apoptosis in the hippocampus of the mouse brains through the Bcl-2/Bax pathway: Yachen WANG, et al. Department of Occupational and EnvironmentalHealth, Dalian Medical University, P.R. ChinaObjectives: The aim of this study was to identify whether arsenic (As) exposure could induce hippocampal neural apoptosis in vivo. Methods: Sixty-four mice were randomly divided into 4 groups of 16 each. Group 1 orally received drinking water alone as a control. Groups 2−4 were given arsenic trioxide (As 2 O 3 ) orally at the doses of 1 ppm, 2 ppm and 4 ppm, respectively. All the treatments continued for 60 days. Morphological changes in the hippocampus were observed by HE staining. Apoptosis in the hippocampus was examined by TUNEL assay and transmission electron microscopy. The expression levels of Bcl-2 and Bax genes and their proteins in the hippocampus were determined by realtime PCR and Western blotting. The activity of caspase-3 was determined by spectrophotometry. Results: Abnormal histopathological changes and apoptosis

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Subchronic exposure to arsenic induces apoptosis in the hippocampus of the mouse brains through the Bcl‐2/Bax pathway

Wang

Bai

Guan

et al. 2015

Journal of Occupational Health

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“…36 Many epidemiological studies have demonstrated that chronic exposure to arsenic in drinking water was associated with the increase in rates of various chronic diseases, including cancers, nervous system diseases, peripheral vascular disease (blackfoot disease (BFD), a peripheral artery disease) and endocrine dysfunction in the United States and other countries. [37][38][39][40] Therefore, the United States Environmental Protection Agency (U.S. EPA) recommended a reduction in the maximum contaminant level (MCL) from 50 mg/L to 10 mg/L for arsenic in public drinking water supplies. In Taiwan, the areas along the south-western coast were known to have arsenic contamination in drinking wells or underground water and the hyper-endemic occurrence of a peripheral vascular disease (blackfoot disease) in these area's villages.…”

Section: Arsenicmentioning

confidence: 99%

Heavy metals, islet function and diabetes development

Lin¹,

Yang²,

Huang³

et al. 2009

Islets

204

131

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“…cns damage in as-exposed humans has been described repeatedly (reviewed in [30,36]) but corresponding electrophysiological changes have been mentioned only in a few papers. a single large dose of inorganic as caused complete and partial loss of vis and aud eps, respectively, in a person attempting suicide [8].…”

Section: Electrophysiologymentioning

confidence: 99%

Rutin, a flavonoid phytochemical, ameliorates certain behavioral and electrophysiological alterations and general toxicity of oral arsenic in rats

Sárközi¹,

Papp²,

Máté³

et al. 2015

Acta Biologica Hungarica

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department of public health, university of szeged faculty of medicine, dóm tér 10, h-6720 szeged, hungary (Received: may 5, 2014; accepted: June 23, 2014) arsenic affects large populations and attacks, among others, the nervous system. Waterborne or occupational exposure causes electrophysiological alterations and motor disturbances in humans, and analogous effects were found in animals. certain phytochemicals may be protective against as-caused damages.In the present study it was investigated whether the flavonoid rutin, applied via the drinking water (2 g/L), ameliorates the effects of arsenic given by gavage (10 mg/kg b.w., in form of NaAsO 2 ) on open field motility, evoked cortical and peripheral electrophysiological activity, and body weight gain in adult male Wistar rats. Body weight gain was significantly reduced from the 4 th week of the 6 weeks arsenic treatment and this effect was largely abolished by rutin in the combination treatment group. Rats treated by arsenic alone showed decreased open field motility; latency of the cortical evoked potentials increased and peripheral nerve conduction velocity decreased. these functional alterations were also counteracted by co-administration of rutin, and both the antioxidant and the chelating activity of rutin might have contributed to the ameliorative effect. these results are apparently novel and support the potential role of natural agents in preserving human health in a contaminated environment.

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The effects of arsenic exposure on the nervous system

Cited by 262 publications

References 117 publications

Subchronic exposure to arsenic induces apoptosis in the hippocampus of the mouse brains through the Bcl‐2/Bax pathway

Subchronic exposure to arsenic induces apoptosis in the hippocampus of the mouse brains through the Bcl‐2/Bax pathway

Heavy metals, islet function and diabetes development

Rutin, a flavonoid phytochemical, ameliorates certain behavioral and electrophysiological alterations and general toxicity of oral arsenic in rats

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