Cerebellar thiol status and motor deficit after lactational exposure to methylmercury

Franco, Jeferson Luís; Teixeira, Adriana; Meotti, Flávia Carla; Ribas, Camila Mafalda; Stringari, James; Garcia, Solange Cristina; Moro, Ângela M.; Bohrer, Denise; Bairros, André Valle de; Dafre, Alcir Luiz; Santos, Adair R.S.; Farina, Marcelo

doi:10.1016/j.envres.2006.02.003

Cited by 91 publications

(56 citation statements)

References 37 publications

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“…Results showed GSH depletion in the rat cerebellum after intracerebroventricular GAL injection, and this data corroborates that GAL injection leads to apoptosis in the cerebellum. Studies showed that low levels of GSH, which may be caused by genetic disorders or increased levels of free radicals, seem to be related to cerebellar lesions that may contribute to motor deficits [16,71,72]. Results also showed that GAL injection provoked protein and Fig.…”

Section: Discussionmentioning

confidence: 82%

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

et al. 2016

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Classical galactosemia is an inborn error of carbohydrate metabolism in which patients accumulate high concentration of galactose in the brain. The most common treatment is a galactose-restricted diet. However, even treated patients develop several complications. One of the most common symptoms is motor coordination impairment, including affected gait, balance, and speech, as well as tremor and ataxia. In the present study, we investigated the effects of intracerebroventricular galactose administration on motor coordination, as well as on histological and biochemical parameters in cerebellum of adult rats. Wistar rats received 5 μL of galactose (4 mM) or saline by intracerebroventricular injection. The animals performed the beam walking test at 1 and 24 h after galactose administration. Histological and biochemical parameters were performed 24 h after the injections. The results showed motor coordination impairment at 24 h after galactose injection. Galactose also decreased the number of cells in the molecular and granular layers of the cerebellum. The immunohistochemistry results suggest that the cell types lost by galactose are neurons and astrocytes in the spinocerebellum and neurons in the cerebrocerebellum. Galactose increased active caspase-3 immunocontent and acetylcholinesterase activity, decreased acetylcholinesterase immunocontent, glutathione, and BDNF levels, as well as caused protein and DNA damage. Our results suggest that galactose induces histological and biochemical changes in cerebellum, which can be associated with motor coordination impairment.

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Section: Discussionmentioning

confidence: 82%

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

et al. 2016

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“…In view of this assumption, it is commonly hypothesized the occurrence of an adaptive response expressed by an activation of the redox-defense system (Franco et al 2006;Stringari et al 2008). However, in the present work a general breakdown of this system was Fig.…”

Section: Oxidative Stress Profilementioning

confidence: 85%

“…A glutathione decrease has been previously found in mouse CNS after mercury exposure (Franco et al 2006); nevertheless, the explanation for this alteration is not completely established. It is known that mercury forms covalent bonds with GSH and a single mercury ion can bind to and cause irreversible excretion of two GSH molecules (Franco et al 2009).…”

Section: Oxidative Stress Profilementioning

confidence: 91%

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Antioxidant system breakdown in brain of feral golden grey mullet (Liza aurata) as an effect of mercury exposure

et al. 2010

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Although brain has been recognized as a primary target for mercury toxicity in mammals, the effects of this metal in fish brain are scarcely described. Thus, the main objective of this study was to assess the mercury threat to feral fish (Liza aurata) by estimating the antioxidant defenses and peroxidative damage in brain, keeping in mind the association with mercury accumulation. Sampling was carried out in an estuarine area historically affected by discharges from a chlor-alkali industry-Laranjo Basin (Ria de Aveiro, Portugal). Total mercury (T-Hg) in brain increased towards the contamination source, clearly indicating mercury exposure. An overall antioxidant depletion was verified in brain of fish collected at the mercury-contaminated stations, since total glutathione content and the studied antioxidant enzymes (catalase-CAT, glutathione peroxidase-GPx, glutathione-S-transferase-GST and glutathione reductase-GR) significantly decreased. In addition, this breakdown of the redox-defense system was significantly correlated with the accumulated T-Hg levels. Unexpectedly, fish exhibited unaltered lipid peroxidation levels, pointing out a higher propensity of mercury to inhibit enzymes than to oxidatively damage lipids in the brain. Nevertheless, an increased susceptibility of the fish's brain was identified, leaving the organ more vulnerable to oxidative stress-related challenges. Overall, the current findings provide information to better understand mechanisms of mercury neurotoxicity in fish.

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“…Mercury levels in the cerebellums of MeHg-exposed dams were about ninefold higher than those found in the cerebellums of control dams (Franco et al 2006). This type of exposure is much more common in humans.…”

Section: Discussionmentioning

confidence: 97%

Protective Effect of Bacopa monniera on Methyl Mercury-Induced Oxidative Stress in Cerebellum of Rats

et al. 2012

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Methyl mercury (MeHg) is a ubiquitous environmental pollutant leading to neurological and developmental deficits in animals and human beings. Bacopa monniera (BM) is a perennial herb and is used as a nerve tonic in Ayurveda, a traditional medicine system in India. The objective of the present study was to investigate whether Bacopa monniera extract (BME) could potentially inhibit MeHg-induced toxicity in the cerebellum of rat brain. Male Wistar rats were administered with MeHg orally at a dose of 5 mg/kg b.w. for 21 days. Experimental rats were given MeHg and also administered with BME (40 mg/kg, orally) for 21 days. After the treatment period, we observed that MeHg exposure significantly inhibited the activities of superoxide dismutase, catalase, glutathione peroxidase, and increased the glutathione reductase activity in cerebellum. It was also found that the level of thiobarbituric acid-reactive substances was increased with the concomitant decrease in the glutathione level in MeHg-induced rats. These alterations were prevented by the administration of BME. Behavioral interference in the MeHg-exposed animals was evident through a marked deficit in the motor performance in the rotarod task, which was completely recovered to control the levels by BME administration. The total mercury content in the cerebellum of MeHg-induced rats was also increased which was measured by atomic absorption spectrometry. The levels of NO(2) (-) and NO(3) (-) in the serum were found to be significantly increased in the MeHg-induced rats, whereas treatment with BME significantly decreased their levels in serum to near normal when compared to MeHg-induced rats. These findings strongly implicate that BM has potential to protect brain from oxidative damage resulting from MeHg-induced neurotoxicity in rat.

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Cerebellar thiol status and motor deficit after lactational exposure to methylmercury

Cited by 91 publications

References 37 publications

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

Antioxidant system breakdown in brain of feral golden grey mullet (Liza aurata) as an effect of mercury exposure

Protective Effect of Bacopa monniera on Methyl Mercury-Induced Oxidative Stress in Cerebellum of Rats

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