Chronic exposure to low levels of inorganic arsenic causes alterations in locomotor activity and in the expression of dopaminergic and antioxidant systems in the albino rat (original) (raw)
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Arsenic Toxicity and Neurobehaviors: A Review
Deterioration in public health due to arsenic toxicity is a worldwide concern for clinicians. The subject requires extensive and careful assessment of arsenic toxicity born symptoms, across the geographical boundaries. Arsenic induced deleterious effects have been documented in countries, including India, Bangladesh, Argentina, Australia, China, Hungary, Thailand, Mexico and United States of America, which cover the major part of world population. Arsenic found in soil and drinking water comes from geophysical as well as anthropogenic sources. Humans are exposed to arsenic through food, drinking water and or smelters. Nevertheless, newborns are most sensitive to arsenic insult and if mother is exposed to arsenic at gestational stage, irreversible postnatal cardiac, carcinogenic, behavioral, cognitive and motor disabilities are inevitable. Sufficient data from animal studies on hamsters, mice, rats and rabbits demonstrate arsenic to produce developmental toxicity, which includes malf...
Toxicology and Applied Pharmacology, 2009
Arsenic (As) is a toxic metalloid widely present in the environment. Human exposure to As has been associated with the development of skin and internal organ cancers and cardiovascular disorders, among other diseases. A few studies report decreases in intelligence quotient (IQ), and sensory and motor alterations after chronic As exposure in humans. On the other hand, studies of rodents exposed to high doses of As have found alterations in locomotor activity, brain neurochemistry, behavioral tasks, and oxidative stress. In the present study both male and female C57Bl/6J mice were exposed to environmentally relevant doses of As such as 0.05, 0.5, 5.0, or 50 mg As/L of drinking water for 4 months, and locomotor activity was assessed every month. Male mice presented hyperactivity in the group exposed to 0.5 mg As/L and hypoactivity in the group exposed to 50 mg As/L after 4 months of As exposure, whereas female mice exposed to 0.05, 0.5, and 5.0 mg As/L exhibited hyperactivity in every monthly test during As exposure. Furthermore, striatal and hypothalamic dopamine content was decreased only in female mice. Also decreases in tyrosine hydroxylase (TH) and cytosolic thioredoxin (Trx-1) mRNA expression in striatum and nucleus accumbens were observed in male and female mice, respectively. These results indicate that chronic As exposure leads to gender-dependent alterations in dopaminergic markers and spontaneous locomotor activity, and down-regulation of the antioxidant capacity of the brain.
Biological trace element research, 2018
Chronic exposure to arsenic via drinking water throughout the globe is assumed to cause a developmental neurotoxicity. Here, we investigated the effect of perinatal arsenic exposure on the neurobehavioral and neurochemical changes in the corpus striatum, frontal cortex, and hippocampus that is critically involved in motor and cognition functions. In continuation of previous studies, this study demonstrates that perinatal exposures (GD6-PD21) to arsenic (2 or 4 mg/kg body weight, p.o.) cause hypo-activity in arsenic-exposed rats on PD22. The hypo-activity was found to be linked with a decrease in the mRNA and protein expression of the DA-D2 receptor. Further, a protein expression of tyrosine hydroxylase (TH), levels of dopamine, and its metabolites were also significantly impaired in corpus striatum. The arsenic-exposed groups showed spatial learning and memory significantly below the average in a dose-dependent manner for the controls. Here, we evaluated the declined expression of C...
Decreased nitric oxide markers and morphological changes in the brain of arsenic-exposed rats
Toxicology, 2009
Epidemiological studies demonstrate an association between chronic consumption of arsenic contaminated water and cognitive deficits, especially when the exposure takes place during childhood. This study documents structural changes and nitrergic deficits in the striatum of adult female Wistar rats exposed to arsenic in drinking water (3 ppm, approximately 0.4 mg/kg per day) from gestation, throughout lactation and development until the age of 4 months. Kainic acid injected animals (10mg/kg, i.p.) were also analyzed as positive controls of neural cell damage. Morphological characteristics of cells, fiber tracts and axons were analyzed by means of light microscopy as well as immunoreactivity to neuronal nitric oxide synthase (nNOS). As nitrergic markers, nitrite/nitrate concentrations, nNOS levels and expression of nNOS-mRNA were quantified in striatal tissue. Reactive oxygen species (ROS) and lipid peroxidation (LPx) were determined as oxidative stress markers. Arsenic exposure resul...
The effects of arsenic exposure on the nervous system
Toxicology letters, 2003
Arsenic (As) is a common environmental contaminant widely distributed around the world. Human exposure to this metalloid comes from well water and contaminated soil, from fish and other sea organisms rich in methylated arsenic species, and from occupational exposure.
ABSTRACT: Neurotoxicity by drinking well water contaminated with arsenic (As) or accidentally exposed to As compounds has been described in adults and infants by previous studies. Biomethylation of As generates toxic metabolites that could help explain the adverse effects observed following As exposure in human and in animal models. Here dose related accumulation of methylated As metabolites in mouse brain are studied and show that brain metabolizes arsenite to monomethyl arsonic acid (MMA) and dimethyl arsinic acid (DMA), being DMA the main metabolite in this tissue. Glutathione reductase activity was inhibited at the highest dose tested in liver and brain.
In vivo evaluation of arsenic-associated behavioral and biochemical alterations in F0 and F1 mice
Chemosphere, 2020
h i g h l i g h t s Arsenic induces neurobehavioral and biochemical alterations in both F 0 and F 1 mice. Effects of arsenic are more pronounced in arsenic-exposed F 1 mice than F 0. Accumulation of arsenic is higher in the liver, brain, and kidney of F 1 mice. Arsenic markedly increases arsenic-associated tissue damages in the liver and kidney of F 1 mice. Arsenic-exposed offspring mice are more vulnerable to arsenic exposure.
Journal of Occupational Health, 2005
Oxidative DNA Damage in Relation to Neurotoxicity in the Brain of Mice Exposed to Arsenic at Environmentally Relevant Levels: Fengyuan PIAO, et al. Department of Hygiene, Dalian Medical University, China-To clarify the association between oxidative DNA damage and the neurotoxicity o f a r s e n i c , t h e f o r m a t i o n o f 8-h y d r o x y-2 'deoxyguanosine (8-OHdG) as an index of oxidative DNA damage in the brain was examined in mice fed with drinking water containing 1 or 2 ppm arsenic, using a n H P L C-e l e c t r o c h e m i c a l d e t e c t o r a n d immunohistochemical method. 8-OHdG levels were significantly increased in the brain of mice given arsenic and its immunoreactivity was distributed in the cerebral and cerebellar cortexes. Cerebral cortex neurons and Purkinje cells in the cerebellar cortex showed degenerative changes in accordance with the distribution of 8-OHdG immunoreactivity. The levels of arsenic in this study were lower than those reported in epidemiological studies. Thus, we conclude that environmentally relevant levels of arsenic induce pathological changes through oxidative DNA damage in the brain tissues in vivo and that cerebral and cerebellar cortex neurons seem to be the major targets of arsenic neurotoxicity.
Effect of high arsenic content in drinking water on rat brain
Indian journal of biochemistry & biophysics, 1999
The permissible limit of arsenic content in drinking water is 0.05 ppm, whereas, in many parts of West Bengal the arsenic level in drinking water is 0.1 ppm, frequently 0.3 ppm and even 3.0 ppm, though rarely. In order to assess possible risk to brain function by drinking such water, rats were given arsenic mixed in drinking water at the above four concentrations for 40 days. There was increased lipid peroxidation at all doses of arsenic, including the 'permissible limit', decrease in glutathione level, superoxide dismutase and glutathione reductase activities, indicating the free-radical-mediated degeneration of brain.