Effects of methylmercury on the microvasculature of the developing brain.
ABSTRACT The study, undertaken with the aim of further investigating the effects of methylmercury (MeHg) exposure on the developing brain, was performed in the cerebellum of chick embryos, chronically treated with a MeHgCl solution dropped onto the chorioallantoic membrane, and in control embryo cerebella. Quantitative evaluations, performed by cold vapour atomic absorption spectrophotometry, demonstrated a high mercury content in the chorioallantoic membrane, encephalon, liver and kidney of the treated embryos. The morphological observations showed severe neuronal damage consisting of degenerative changes of the granules and Purkinje neurons. The effects on astrocytes were even more severe, since they were extremely rare both in the neuropil and around the vessel wall. Compared with the controls, the cerebellar vessels of MeHg-treated embryos showed immature morphology, poor differentiation of endothelial barrier devices, and high permeability to the exogenous protein horseradish peroxidase. These findings support the hypothesis that MeHg-related neuronal sufferance may be secondary to astrocytic damage and suggest that the developmental neurotoxicity of this compound could also be related to astrocyte loss-dependent impairment of blood-brain barrier (BBB) differentiation.
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ABSTRACT: Abstract To evaluate the protector effect of ascorbic acid (AA) against anxiogenic-like effect induced by methylmercury (MeHg) exposure, adult zebrafish were treated with AA (2 mg g(-1), intraperitoneal [i.p.]) before MeHg administration (1.0 μg g(-1), i.p.). Groups were tested for the light/dark preference as a behavioral model of anxiety, and the content of serotonin and its oxidized metabolite tryptamine-4,5-dione (T-4,5-D) in the brain was determined by high-performance liquid chromatography. MeHg has produced a marked anxiogenic profile in both tests, and this effect was accompanied by a decrease in the extracellular levels of serotonin, and an increase in the extracellular levels of T-4,5-D. Added to this, a marked increase in the formation of a marker of oxidative stress accompanied these parameters. Interestingly, the anxiogenic-like effect and biochemical alterations induced by MeHg were blocked by pretreatment with AA. These results for the first time demonstrated the potential protector action of AA in neurobehavioral and neurochemical alterations induced by methylmecury exposure demonstrating that zebrafish model could be used as an important tool for testing substances with neuroprotector actions.Zebrafish 06/2014; · 2.88 Impact Factor
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ABSTRACT: There are scarce data on the neurotoxicity in mammalian induced by tannery wastewaters. Previously, the anxiogenic effect of tannery wastewater was demonstrated in mice, while wastewater submitted to photoelectrooxidation process (PEO) treatment did not affect the anxiety state. Considering that species may response differently to xenobiotics, the aim of the present work was to study the effects of exposure to tannery wastewaters (non-PEO or PEO-treated) on behavioural and neurochemical markers in another species of laboratory animals, specifically Wistar rats. Male Wistar rats were given free access to water bottles containing non-PEO or PEO-treated tannery wastewaters (0.1, 1 and 5% in drinking water). During the exposure, behavioural tests of anxiety (elevated plus-maze, neophobia, open field and light-dark box), depression (forced swimming) and memory (inhibitory avoidance, novel object and discriminative avoidance) were performed. On the 30th day, brain structures were dissected out to evaluate cellular oxidative state (hippocampus, cerebellum and striatum) and acetylcholinesterase activity (hippocampus and striatum). Exposure to tannery effluent with or without photoelectrochemical treatment did not alter any behavioural and neurochemical parameters evaluated. Our data indicate that Wistar rats may not be an adequate species for ecotoxicological studies involving tannery effluents and that POE treatment did not generate other toxic compounds.Physiology & Behavior 04/2014; · 3.16 Impact Factor