Pretreatment with diallylsulphide modulates mercury-induced neurotoxicity in male rats

Ansar, Sabah

doi:10.18388/abp.2015_1064

Cited by 15 publications

(10 citation statements)

References 47 publications

(46 reference statements)

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“…20 Although several in vivo and in vitro studies have suggested that exposure of animals to inorganic or organic forms of mercury is associated with the induction of oxidative stress, human studies are rare in the literature. [21][22][23] In the present study, we found altered oxidative stress status in children exposed to elemental mercury, which was characterized by decreased CAT, GSH-Px activities, and increased MDA level and SOD activity, compared to the controls. GSH-Px is an important selenium (Se) dependent enzyme which can reduce hydroperoxides.…”

Section: Discussionsupporting

confidence: 60%

Evaluation of oxidative stress biomarkers in acute mercury intoxication

Dalkıran¹,

Çarman²,

Ünsal³

et al. 2021

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Objective: Very few studies have evaluated the association between mercury exposure and oxidative stress in humans, particularly in children. This is the first report where we aimed to determine the oxidative stress status of children who were accidently exposed to elemental mercury. Methods: In the present study, the study group was composed of 86 randomly selected children poisoned by mercury; the control group was composed of 78 children who had no history of mercury exposure. At admission, blood samples were collected. Blood superoxide dismutase activity, catalase enzyme activity, and glutathione peroxidase activity were measured by Fridovich, Beutler, and Lawrence Burk methods respectively, and the results were given as U/g Hb . Malondialdehyde level was measured by Ohkawa methods , and the results were given as mmol/ml. Results: Catalase levels were significantly lower in the patient group compared to the control group (1.28±0.62 vs 3.90 ± 0.86 U/g Hb, p<0.01). In exposed children, SOD levels were significantly higher than the controls (5936 ± 810 vs 2226 ± 464 U/g Hb, p<0,05), while the GPx activity was significantly lower (13.01 ± 3.21  vs 34.97 ± 7.32 U/g Hb, p<0.01). The MDA levels of the mercury group were significantly higher than the MDA levels of the control group (2.85±0.84  vs 2.05±0.79 mmol/ml, p<0.05) . Conclusion: The results of the present study showed that acute mercury poisoning causes alteration of oxidative stress status in children exposed to elemental mercury.

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Section: Discussionsupporting

confidence: 60%

Evaluation of oxidative stress biomarkers in acute mercury intoxication

Dalkıran¹,

Çarman²,

Ünsal³

et al. 2021

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“…Endogenous antioxidant molecules (mainly glutathione) and enzymes (such as superoxide dismutase, glutathione peroxidase and catalase) are the main defenses of the cell against free radicals. Although previous studies showed glutathione depletion with IHg intoxication, results of antioxidant enzymes are contradictory with both increase and decrease of enzymatic activities after IHg exposure ( Gutierrez et al, 2006 ; Ansar, 2015 ; Moneim, 2015 ). Therefore, we decided to evaluate the total antioxidant capacity of the cortex as a more reliable marker than each element alone.…”

Section: Discussionmentioning

confidence: 80%

“…Brain tissue is especially sensitive to the deleterious consequences of this imbalance in the redox status. The brain contains large amounts of polyunsaturated fatty acids present in the membranes that are particularly susceptible to free radical attack and thus, to lipid peroxidation ( Lucena et al, 2007 ; Ansar, 2015 ). Considering that lipid peroxidation plays a major role in necrosis and cellular death, the exacerbated lipid peroxidation detected in cortex ( Figures 5 , 6 ) could explain the significant death of both neurons and astrocytes caused by IHg ( Figures 8 , 9 ).…”

Section: Discussionmentioning

confidence: 99%

Exposure to Inorganic Mercury Causes Oxidative Stress, Cell Death, and Functional Deficits in the Motor Cortex

Teixeira

Oliveira

Leão

et al. 2018

Front. Mol. Neurosci.

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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 astrocytes of the motor cortex were performed. It was observed that chronic exposure to inorganic mercury caused a decrease in balance and fine motor coordination, formation of mercury deposits and oxidative stress verified by the increase of lipoperoxidation and nitrite concentration and a decrease of the total antioxidant capacity. In addition, we found that this model of exposure to inorganic mercury caused cell death by cytotoxicity and induction of apoptosis with a decreased number of neurons and astrocytes in the motor cortex. Our results provide evidence that exposure to inorganic mercury in low doses, even in spite of its poor ability to cross biological barriers, is still capable of inducing motor deficits, cell death by cytotoxicity and apoptosis, and oxidative stress in the motor cortex of adult rats.

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“…The main mechanism of Hg toxicity is associated with oxidative stress, as reported by numerous studies (Ansar, ; Ansar and Iqbal, ; Berlin et al, ; Li et al, ). The oxidative action after Hg exposition may be linked to the fact that this metal increases lipid peroxidation (Ansar ), reduces nonenzymatic and enzymatic antioxidants (Agarwal et al, ; Pal and Ghosh, ; Su et al, ) and TSH and NPSH defenses (Farina et al, ; Oliveira V.A. ).…”

Section: Discussionmentioning

confidence: 99%

Acute mercury exposition of virgin, pregnant, and lactating rats: Histopathological kidney and liver evaluations

Oliveira

Favero

Stacchiotti

et al. 2016

Environmental Toxicology

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This work investigated the effects of mercury chloride (HgCl ) acute exposure on virgin, pregnant and lactating rats by determination of renal and hepatic morphological and ultrastructural parameters and the expression of oxidative stress and stress tolerance markers, due to kidney and liver are the organs that more accumulate inorganic mercury. Adult Wistar rats virgin (90 days old), pregnant (18 gestation day) and lactating (7 lactation day) were injected once with HgCl (5 mg/kg) or saline (controls). We observed that HgCl exposure of virgin rats caused significant inflammatory infiltration and severe morphological variations, like glomeruli atrophy, dilatation of Bowman's capsule, tubular degeneration and hepatocytes alteration. Moreover, virgin rats presented mitochondrial modification, important oxidative stress and increase in stress tolerance proteins at both kidney and liver level, compared with virgin controls. In detail, virgin rats exposed to HgCl presented significantly elevated level of inducible nitric oxide synthase, heat shock protein 27 and glucose regulated proteins 75 expressions at both renal tubular and hepatocytes level, respect untreated virgin rats. Interestingly, pregnant and lactating rats exposed to HgCl presented weak renal and liver morphological alterations, showing weak inflammatory infiltration and no significant difference in structural mitochondrial transmembrane protein, oxidative stress markers and stress tolerance proteins expressions respect controls (virgin, pregnant and lactating rats). Although, both control and HgCl -exposed pregnant and lactating rats showed renal glomeruli greater in diameter respect virgin rats. In conclusion, we believe that virgin rats are more sensitive to HgCl toxicity respect pregnant and lactating rats. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1500-1512, 2017.

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Pretreatment with diallylsulphide modulates mercury-induced neurotoxicity in male rats

Cited by 15 publications

References 47 publications

Evaluation of oxidative stress biomarkers in acute mercury intoxication

Evaluation of oxidative stress biomarkers in acute mercury intoxication

Exposure to Inorganic Mercury Causes Oxidative Stress, Cell Death, and Functional Deficits in the Motor Cortex

Acute mercury exposition of virgin, pregnant, and lactating rats: Histopathological kidney and liver evaluations

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