Effect of methyl mercury induced free radical stress on nucleic acids and protein: Implications on cognitive and motor functions (original) (raw)
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ECPT, 2019
Citation: Abhishek Jha., et al. "A Study on Prooxidative and Neurotoxic Effects of Mercury Chloride in Rats". EC Pharmacology and Toxicology 7.2 (2019): 112-124. Abstract Mercury is a well-recognized heavy metal neurotoxin but it is believed to cause toxicity by multiple mechanisms. There is a myriad of studies on neurotoxic effects of mercury in animals and oxidative stress has been proposed as major mechanistic pathway. In the present study we examined the prooxidative and neurotoxicological effect of mercury chloride (inorganic mercury-HgCl 2) on the wistar rats. Studies were carried out in two groups: Group 1 (control) and Group 2 (mercury chloride 0.25 mg/kg bwt). Twelve rats with the average weight of (180-200) gm were divided equally in these groups. Oxidative stress markers in mercury administered rats showed a significant (p < 0.001) decrease as reflected by the mean levels of superoxide dismutase and glutathione-s-transferase. There was significant decrease in the enzymatic activity of glutathione peroxidase and catalase (p < 0.0001), and significant (p < 0.001) increase in the glutathione reductase levels in comparison to control. There was significant increase in the lipid peroxida-tion (p < 0.05) and significant decrease in reduced glutathione (p < 0.001) in mercury treated group. Histological observation of the cerebral cortex showed a normal structural architecture in control group while mercury administered group showed degenerative changes, necrosis, perivascular edema and degeneration of neurons. Our studies reinforce the serious consequences of mercury susceptibility in the brain that may lead to impaired functioning of brain in the affected organisms.
Comprehensive Review Regarding Mercury Poisoning and Its Complex Involvement in Alzheimer’s Disease
International Journal of Molecular Sciences
Mercury (Hg) is considered one of the most widespread toxic environmental pollutants, which seems to have multiple effects on organisms even at low concentrations. It has a critical role in many health problems with harmful consequences, with Hg primarily targeting the brain and its components, such as the central nervous system (CNS). Hg exposure was associated with numerous CNS disorders that frequently trigger Alzheimer’s disease (AD). Patients with AD have higher concentrations of Hg in blood and brain tissue. This paper aims to emphasize a correlation between Hg and AD based on the known literature in the occupational field. The outcome shows that all these concerning elements could get attributed to Hg. However, recent studies did not investigate the molecular level of Hg exposure in AD. The present review highlights the interactions between Hg and AD in neuronal degenerations, apoptosis, autophagy, oxidative stress (OS), mitochondrial malfunctions, gastrointestinal (GI) micro...
Oxidative medicine and cellular longevity, 2018
Mercury (Hg) is a highly toxic metal, which can be found in its inorganic form in the environment. This form presents lower liposolubility and lower absorption in the body. In order to elucidate the possible toxicity of inorganic Hg in the hippocampus, we investigated the potential of low doses of mercury chloride (HgCl) to promote hippocampal dysfunction by employing a chronic exposure model. For this, 56 rats were exposed to HgCl (0.375 mg/kg/day) via the oral route for 45 days. After the exposure period, the animals were submitted to the cognitive test of fear memory. The hippocampus was collected for the measurement of total Hg levels, analysis of oxidative stress, and evaluation of cytotoxicity, apoptosis, and tissue injury. It was observed that chronic exposure to inorganic Hg promotes an increase in mercury levels in this region and damage to short- and long-term memory. Furthermore, we found that this exposure model provoked oxidative stress, which led to cytotoxicity and ce...
A Hypothesis and Evidence That Mercury May be an Etiological Factor in Alzheimer’s Disease
International Journal of Environmental Research and Public Health
Mercury is one of the most toxic elements and causes a multitude of health problems. It is ten times more toxic to neurons than lead. This study was created to determine if mercury could be causing Alzheimer’s disease (AD) by cross referencing the effects of mercury with 70 factors associated with AD. The results found that all these factors could be attributed to mercury. The hallmark changes in AD include plaques, beta amyloid protein, neurofibrillary tangles, phosphorylated tau protein, and memory loss—all changes that can be caused by mercury. Neurotransmitters such as acetylcholine, serotonin, dopamine, glutamate, and norepinephrine are inhibited in patients with Alzheimer’s disease, with the same inhibition occurring in mercury toxicity. Enzyme dysfunction in patients with Alzheimer’s disease include BACE 1, gamma secretase, cyclooxygenase-2, cytochrome-c-oxidase, protein kinases, monoamine oxidase, nitric oxide synthetase, acetyl choline transferase, and caspases, all which c...
Frontiers in molecular neuroscience, 2018
Mercury is a toxic metal that can be found in the environment in three different forms - elemental, organic and inorganic. Inorganic mercury has a lower liposolubility, which results in a lower organism absorption and reduced passage through the blood-brain barrier. For this reason, exposure models that use inorganic mercury in rats in order to evaluate its effects on the central nervous system are rare, especially in adult subjects. This study investigated if a chronic exposure to low doses of mercury chloride (HgCl2), an inorganic form of mercury, is capable of promoting motor alterations and neurodegenerative in the motor cortex of adult rats. Forty animals were exposed to a dose of 0.375 mg/kg/day, for 45 days. They were then submitted to motor evaluation and euthanized to collect the motor cortex. Measurement of mercury deposited in the brain parenchyma, evaluation of oxidative balance, quantification of cellular cytotoxicity and apoptosis and density of mature neurons and astr...
Previously it was thought that mercury sulphide in low dose shows good therapeutic effect without producing toxic effects in the human beings. Symptoms like ataxia, speech impairment, visual field constriction, deafness, tremors, mental retardation, coma and even death has been reported due to chronic use of this heavy metal. The aim of our present study is to compare histopathological changes in different parts of brain, so that clinical symptoms following mercury intoxication can be explained. Methods: Freshly prepared sterile solution of mercuric chloride in distilled water (0.33 mg/kg body weight) was orally administered daily to total number of 30 adult albino rats (15 males and 15 females) for a month. 3mm thick sections were taken from cerebrum, cerebellum and hippocampus parts. These sections were processed and then stained by haematoxylin & eosin to be observed in light microscope. Results: Histological pictures of all the three areas were suggestive of multiple foci of necrosis with gliosis. Marked congestion of vessels with perivascular necrosis was also noticed. Increased cellularity of granular layer and molecular layer in cerebellum and hippocampus were seen respectively. Conclusion: The histopathological examination revealed that normal cytoarchitecture of all the three areas of brain were distorted resulting in various neurological disorders.
Journal of Trace Elements in Medicine and Biology, 2019
Despite the vast distribution among tissues, the central nervous system (CNS) represents the main target of methylmercury (MeHg) toxicity. However, few studies have evaluated the effects of MeHg exposure on the CNS at equivalent doses to human environmental exposure. In our study, we evaluated the motor cortex, an important area of motor control, in adult rats chronically exposed to MeHg in a concentration equivalent to those found in fish-eating populations exposed to mercury (Hg). The parameters evaluated were total Hg accumulation, oxidative stress, tissue damage, and behavioral assessment in functional actions that involved this cortical region. Our results show in exposed animals a significantly greater level of Hg in the motor cortex; increase of nitrite levels and lipid peroxidation, associated with decreased antioxidant capacity against peroxyl radicals; reduction of neuronal and astrocyte density; and poor coordination and motor learning impairment. Our data showed that chronic exposure at low doses to MeHg is capable of promoting damages to the motor cortex of adult animals, with changes in oxidative biochemistry misbalance, neurodegeneration, and motor function impairment.
Journal of Trace Elements in Medicine and Biology, 2019
Chronic exposure to mercury chloride (HgCl2) has been shown to promote oxidative stress and cell death in the central nervous system of adult rats displaying motor and cognitive impairments. However, there are no investigations about neurochemical function after this type of exposure in rodents that may be associated with those behavioral changes already reported. Thus, the aim of this study was to analyze glutamatergic and GABAergic dysfunctions in the motor cortex and hippocampus of adult rats, in a model of chronic exposure to HgCl2 in. Twenty rats were exposed to a daily dose of 0.375 mg/kg for 45 days. After this period, they were submitted to motor and cognitive functions tests and euthanized to collect the motor cortex and hippocampus for measurement of mercury (Hg) levels in the parenchyma and neurochemical assays for analysis of glutamatergic and GABAergic functions. It was observed that chronic exposure to HgCl2 promoted increase in total Hg levels in these two brain areas, with changes in glutamatergic transport, but without changes in GABAergic transport. Functionally this model of exposure caused the decrease of the spontaneous motor locomotion and in the process of learning and memory. In this way, our results provide evidences that glutamatergic neurochemical dysfunction can be pointed out as a strong causal factor of motor and cognitive deficits observed in rats exposed to this HgCl2.
ORIGINAL ARTICLES Neurotoxic Effect of Mercury 1
Mercury exposure remain a problem since it is ubiquitous and human exposure is inevitable. Its potent neurotoxic effect is associated with permanent disability and death. Microtubulin and microglia are vulnerable to neurotoxict substance .The alteration of their number in respond to toxic agent will be destructif and deadly to central nervous system.Therefore the present study investigates the dose relationship between mercury exposure and their count in brain. Male rats (Rattus Novergicus) were used to determine the neurotoxic effect of methylmercurychloride on their brain using microglia and microtubulin as parameter. Varying dose of MeHgCl3 from 0,2 mg/BW to 0,8 mg/BW had been administered via nasogastric tube for 21 days, then the brains were removed and microglia & microtubulin count were scored. Microtubulin count were 54.3; 48.1; 39.25; 25.85; 15.65 (CI 95%) respectively. Microglia count were 9,75; 23.95; 32.5;44.4;58.35 (CI 95%) respectively. It could be conclude that methyl...