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Mechanisms of methylmercury-induced neurotoxicity: evidence from experimental studies.
Experimental studies provide the biochemical bases to the understanding of MeHg neurotoxicity, contributing to the discovery of endogenous and exogenous molecules that counteract such toxicity and provide efficacious means for ablating this vicious cycle. Expand
Metals, oxidative stress and neurodegeneration: A focus on iron, manganese and mercury
This review focuses on the neurodegenerative mechanisms and effects of Fe, Mn and Hg, addressing the main sources of exposure to these metals, their transport mechanisms into the brain, and therapeutic modalities to mitigate their neurotoxic effects. Expand
Importance of the lipid peroxidation biomarkers and methodological aspects FOR malondialdehyde quantification
Free radicals induce lipid peroxidation, playing an important role in pathological processes. The injury mediated by free radicals can be measured by conjugated dienes, malondialdehyde,Expand
Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity.
This review addresses the mechanisms of methylmercury (MeHg)-induced neurotoxicity by examining the role of oxidative stress in mediating neuronal damage and provides a mechanistic overview on oxidative stress induced by MeHg that is triggered by a series of molecular events such as activation of various kinases, stress proteins and other immediate early genes culminating in cell damage. Expand
Oxidative stress in MeHg-induced neurotoxicity.
This review discusses potential therapeutic strategies to counteract MeHg-induced toxicity and oxidative stress, emphasizing the use of organic selenocompounds, which generally present higher affinity for MeHG when compared to the classically studied agents. Expand
Ascorbic acid treatment, similarly to fluoxetine, reverses depressive-like behavior and brain oxidative damage induced by chronic unpredictable stress.
A rapid and robust effect of ascorbic acid is indicated in reversing behavioral and biochemical alterations induced by CUS in mice, suggesting that this vitamin may be an alternative approach for the management of depressive symptoms. Expand
Prenatal methylmercury exposure hampers glutathione antioxidant system ontogenesis and causes long-lasting oxidative stress in the mouse brain.
This study is the first to show that prenatal exposure to MeHG disrupts the postnatal development of the glutathione antioxidant system in the mouse brain, pointing to an additional molecular mechanism by which MeHg induces pro-oxidative damage in the developing CNS. Expand
Anticonvulsant effect of GMP depends on its conversion to guanosine
The previously reported effect of GMP as an anticonvulsant seems to be related to its ability to generate guanosine through the action of ecto-5'-nucleotidase, as shown in this study. Expand
Effects of inorganic selenium administration in methylmercury-induced neurotoxicity in mouse cerebral cortex
The data show that inorganic selenium was ineffective in preventing most of the MeHg‐induced brain biochemical alterations, and the most prominent finding was the Selenium‐induced reduction of cells labelled for metal deposition. Expand
Agmatine abolishes restraint stress-induced depressive-like behavior and hippocampal antioxidant imbalance in mice
It is shown that agmatine was able to abrogate the ARS-induced depressive-like behavior and the associated redox hippocampal imbalance observed in stressed restraint mice, suggesting that its antidepressant-like effect may be dependent on its ability to maintain the pro-/anti-oxidative homeostasis in the hippocampus. Expand