Arsenic induced changes in growth development and apoptosis in neonatal and adult brain cells in vivo and in tissue culture

Chattopadhyay, Santanu; Bhaumik, Sraboni; Chaudhury, Aditi Nag; Gupta, Sumanta

doi:10.1016/s0378-4274(01)00535-5

Cited by 129 publications

(68 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been demonstrated previously that arsenic treatment to animals increased the levels of LPO [34], even at low doses leading to apoptosis and necrosis of brain cells [35,36], suggesting cellular injury by action of free radicals. Therefore, increase in LPO observed in the present study following arsenic treatment to rats, could be a consequence of increased free radical production and/or consequent suppression in the activity of antioxidant defense enzymes and glutathione levels.…”

Section: Resultsmentioning

confidence: 99%

Neuroprotective Role of Quercetin against Arsenic Induced Oxidative Stress in Rat Brain

Nirankari¹,

Kamal

Dhawan

2016

J Environ Anal Toxicol

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 99%

Neuroprotective Role of Quercetin against Arsenic Induced Oxidative Stress in Rat Brain

Nirankari¹,

Kamal

Dhawan

2016

J Environ Anal Toxicol

View full text Add to dashboard Cite

“…al. (50) found that arsenic exposure altered neural networking and led to an increase in reactive oxygen intermediates. The same research team demonstrated that among As exposed rats during pregnancy, fetal brain neurons underwent apoptotic changes and neuronal necrosis (48).…”

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

View full text Add to dashboard Cite

“…Rodriguez et al reported that As exposure decreased locomotor activity and induced behavioral disorders in the rats 9) . Chattopadhyay et al observed that As resulted in abnormal changes in brain cell membrane, lost ground matrix, inhibited neural networking and apoptotic in natal mice 10) . In previous study, we also found that environmentally relevant levels of As exposure induced learning and memory impairment and pathological changes in the brain tissues in vivo 11,12) .…”

Section: Discussionmentioning

confidence: 99%

Abnormal Expression of 8-Nitroguanine in the Brain of Mice Exposed to Arsenic Subchronically

Piao

et al. 2011

INDUSTRIAL HEALTH

View full text Add to dashboard Cite

Arsenic (As) is a well-known carcinogen and a notorious health killer on the earth. The regional As toxicosis is becoming a global problem of public health. An anthropogenic source of arsenic exposure stems from the widespread use of arsenical drugs in food-animal production in the United States and China. This use results in residual contamination of food products from animals raised with the drugs, as well as environmental contamination associated with disposal of wastes from these animals 1) . Chronic exposure to As resulting in neurotoxicity to nervous system has been receiving more and more attention. The intelligence quotient (IQ) of children in As-rich region was found to be lower than that of children in low As area, and the difference was remarkable 2) . It was shown in animal experiments that As could pass through blood-brain barrier and invade the brain parenchyma, and there was a noticeable correlation between the extent of As exposure and the concentration of As in the brain of guinea pigs and rats 3) . Chaudhuri et al. discovered that even if the As concentration fell into the provisional guideline issued by World Health Organization's (WHO), As could impair the oxidation-reduction equilibrium, enhance the peroxidation level of cephalopin, decrease the glutathione concentration and render the brain tissue vulnerable Abstract: To provide molecular toxicological evidences for exploring the mechanism of arsenicinduced neurotoxicity the accumulation of arsenic (As), the formation of 8-nitroguanine (8-NO 2 -G) were examined in brain tissue of mice exposed to arsenic. And the gene expressions of inducible NOS (iNOS), superoxide dismutase 1 (SOD1) and peroxiredoxin 2 (Prdx2) were also analyzed by GeneChip. In the result, the concentration of As in the brain tissue of mice was 4.00, 13.70, 21.48 and 29.88 ng/g in the controls and experimental groups exposed to 1, 2 and 4 mg/l As 2 O 3 , respectively and increased in dose-response manner. Nervous cells in the brain of mice exposed to As showed disappearances of axons, vacuolar degeneration in cytoplasm and karyolysis, whereas no such pathological changes were observed in the control group. Weak immunoreactivity against 8-NO 2 -G was observed in the brain tissue of mice given 1 or 2 ppm arsenic trioxide. More intensive immunoreactivity was found in cells at 4 ppm and it was mainly distributed in cytoplasm. The expressions of SOD1 and Prdx2 were down-regulated in the brain of mice exposed to As, but iNOS expression was not disturbed by As exposure. No the 8-NO 2 -G immunoreactivity or abnormal expressions of these genes in brain tissue were observed in controls. These results indicate that As induces high expression of 8-NO 2 -G in brain tissues of mice and that RNA in the cells may be modified by overproduced reactive nitrogen species.

show abstract

Arsenic induced changes in growth development and apoptosis in neonatal and adult brain cells in vivo and in tissue culture

Cited by 129 publications

References 22 publications

Neuroprotective Role of Quercetin against Arsenic Induced Oxidative Stress in Rat Brain

Neuroprotective Role of Quercetin against Arsenic Induced Oxidative Stress in Rat Brain

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

Abnormal Expression of 8-Nitroguanine in the Brain of Mice Exposed to Arsenic Subchronically

Contact Info

Product

Resources

About