Effects on Operant Learning and Brain Acetylcholine Esterase Activity in Rats following Chronic Inorganic Arsenic Intake

Tirumuru, Nagaraja; Desiraju, T.

doi:10.1177/096032719401300511

Cited by 103 publications

(37 citation statements)

References 10 publications

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“…al. (45) demonstrated delayed acquisition and extinction of operant behaviors following arsenate exposure in drinking water. Mechanistically, these deficits may be due to increased oxidative toxicity and changes in neurotransmission.…”

Section: Neurotoxicity Of Arsenicmentioning

confidence: 99%

The Challenge Posed to Children's Health by Mixtures of Toxic Waste: The Tar Creek Superfund Site as a Case-Study

Shine²,

Wright

2007

Pediatric Clinics of North America

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Section: Neurotoxicity Of Arsenicmentioning

confidence: 99%

The Challenge Posed to Children's Health by Mixtures of Toxic Waste: The Tar Creek Superfund Site as a Case-Study

Shine²,

Wright

2007

Pediatric Clinics of North America

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“…Arsenic exposure altered locomotor activity in rats [20][21][22][23] and mice [24] and impaired performance in learning tasks [25,26].…”

Section: Introductionmentioning

confidence: 99%

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Shi

Guo

et al. 2010

J Biochem & Molecular Tox

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To better understand the effect of arsenic on central nervous system by prenatal and early life exposure, the oxidative stress and neurotransmitter metabolic enzymes were determined in offspring rats' brain cortex and hippocampus. Forty-eight pregnant rats were randomly divided into four groups, each group was given free access to drinking water that contained 0, 10, 50, and 100 mg/L NaAsO(2) from gestation day 6 (GD 6) until postnatal day 42 (PND 42). Once pups were weaned, they started to drink the same arsenic (As)-containing water as the dams. The level of malondialdehyde in 100 mg/L As-exposed pup's brain on PND 0 and cortex on PND 28 and 42 were significantly higher than in the control group (p < 0.05). Reduced glutathione (GSH) levels showed a clear decreasing trend in pup's cortex and hippocampus on PND 42. Activity of acetylcholinesterase was significantly higher in 100 mg/L As-exposed pup's hippocampus than in control group on PND 28 and 42. mRNA expression of glutamate decarboxylase (GAD(65) and GAD(67)) in 100 mg/L As-exposed pup's cortex or hippocampus on PND 28 and 42 were significantly higher than in control (p < 0.05). These alterations in the neurotransmitters and reduced antioxidant defence may lead to neurobehavioral and learning and memory changes in offspring rats.

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“…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) . The above results indicated that As exposure can induce impairment of learning and memory.…”

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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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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Effects on Operant Learning and Brain Acetylcholine Esterase Activity in Rats following Chronic Inorganic Arsenic Intake

Cited by 103 publications

References 10 publications

The Challenge Posed to Children's Health by Mixtures of Toxic Waste: The Tar Creek Superfund Site as a Case-Study

The Challenge Posed to Children's Health by Mixtures of Toxic Waste: The Tar Creek Superfund Site as a Case-Study

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

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

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