Apoptosis and necrosis in developing brain cells due to arsenic toxicity and protection with antioxidants

Chattopadhyay, Santanu; Bhaumik, Sraboni; Purkayastha, Madhumita; Basu, Saurav; Chaudhuri, Aditi Nag; Gupta, Sumanta

doi:10.1016/s0378-4274(02)00282-5

Cited by 144 publications

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“…Furthermore, there was a close relationship between the level of As exposure and the proportion of apoptotic cells. Chattopadhyay et al (2002) showed that human fetal brain explants exposed to As in tissue culture showed apoptosis 19) . These studies indicated that As exposure induces death of neuronal cells in the brain tissue by apoptotic processes in vivo and in vitro.…”

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confidence: 99%

“…Yen et al (2011) found that the TUNEL-positive neuronal cells were significantly increased in the cerebral cortex of mice exposed to 0.5 and 5 ppm As for 6 consecutive weeks 16) . Chattopadhyay et al (2002) showed that human fetal brain explants exposed to As in tissue culture exhibited apoptosis 19) . However, there have been few studies reporting that As exposure induced hippocampal neural apoptosis in vivo.…”

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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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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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“…The recovery of the depleted GSH was significantly greater in presence of vitamins such as -carotene, ascorbic acid, -tocopherol (Rabbani et al, 2002). Rats exposed to arsenic showed increased generation of nitric oxide and reactive oxygen species (ROS), loss of glutathione content, increase in lipid peroxidation and decrease superoxide dismutase (Chattopadhyay et al, 2002;Shi et al, 2004). The administration of ascorbic acid or atocopherol showed partial reversal of the effects indication possible protection from arsenic toxicity.…”

Section: Discussionmentioning

confidence: 99%

“…Availability of appropriate levels of anti-oxidants may help in the overall balance of the degenerative effects and the survival mechanism (Chattopadhyay et al, 2002). Arsenic administration significantly increased the serum TBARs, nitric oxide and decreased the whole blood GSH levels in rabbits indicating oxidative stress in vivo.…”

Section: Introductionmentioning

confidence: 99%

Effect of ascorbic acid on reduced glutathione level in arsenic-loaded isolated liver tissues of rat

Saha

2008

Bangladesh J Pharmacol

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Isolated liver tissues of rat were loaded with trivalent arsenic and were exposed in presence and absence of ascorbic acid. The amount of reduced glutathione (GSH) in normal liver tissue was 52.0 ± 0.2 mg/g protein.Addition of arsenic to the tissues reduced the amount of GSH to 11.5 ± 0.3 mg/g protein. But when the arsenic loaded liver tissues were incubated with ascorbic acid at the concentration of 20 mg/mL, the amount of GSH was 14.2 ± 0.1 mg/g protein. There was 22.6% increase of GSH level which was statistically significant (p<0.001) when compared with arsenic alone. This study suggests that ascorbic acid increased the GSH level in arsenic-treated rat's liver. Article InfoReceived:18

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“…besides technological solutions like removal of as from drinking water, it has been also described repeatedly that various phytochemicals -plantderived substances with a biological effect [34] -can be protective against as-caused damages. ascorbic acid and alpha-tocopherol diminished mitochondrial damage and lipid peroxidation in as-exposed rats [3]; the same two antioxidants also reduced oxidative damage and cell death in vitro in rat and human fetal brain tissue [5]. Rutin, the phytochemical used in the present work, is found in a number of edible plants like buckwheat [18] or citrus fruits and rhubarb [9].…”

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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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Apoptosis and necrosis in developing brain cells due to arsenic toxicity and protection with antioxidants

Cited by 144 publications

References 22 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

Effect of ascorbic acid on reduced glutathione level in arsenic-loaded isolated liver tissues of rat

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

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