Abstract
The neurotoxicity of methylmercury (MeHg) is well characterised, and the ameliorating effects of selenium have been described. However, little is known about the molecular mechanisms behind this contaminant-nutrient interaction. We investigated the influence of selenium (as selenomethionine, SeMet) and MeHg on mercury accumulation and protein expression in the brain of adult zebrafish (Danio rerio). Fish were fed diets containing elevated levels of MeHg and/or SeMet in a 2 × 2 full factorial design for eight weeks. Mercury concentrations were highest in the brain tissue of MeHg-exposed fish compared to the controls, whereas lower levels of mercury were found in the brain of zebrafish fed both MeHg and SeMet compared with the fish fed MeHg alone. The expression levels of proteins associated with gap junction signalling, oxidative phosphorylation, and mitochondrial dysfunction were significantly (p < 0.05) altered in the brain of zebrafish after exposure to MeHg and SeMet alone or in combination. Analysis of upstream regulators indicated that these changes were linked to the mammalian target of rapamycin (mTOR) pathways, which were activated by MeHg and inhibited by SeMet, possibly through a reactive oxygen species mediated differential activation of RICTOR, the rapamycin-insensitive binding partner of mTOR.
Highlights
Nutrients can modulate the toxic effects of contaminants [1]
Analysis of upstream regulators indicated that these changes were linked to the mammalian target of rapamycin pathways, which were activated by MeHg and inhibited by SeMet, possibly through a reactive oxygen species mediated differential activation of RICTOR, the rapamycin-insensitive binding partner of mTOR
Studies have shown that co-occurring selenium and methylmercury (MeHg) reduce each other's toxic effects [4], and that dietary selenium may be able to explain the apparently contradictory results obtained from epidemiological studies in cohorts chronically exposed to low doses of MeHg [5]
Summary
Nutrients can modulate the toxic effects of contaminants [1]. Studies have shown that co-occurring selenium and methylmercury (MeHg) reduce each other's toxic effects [4], and that dietary selenium may be able to explain the apparently contradictory results obtained from epidemiological studies in cohorts chronically exposed to low doses of MeHg [5]. Mercury is an environmental contaminant that causes toxic effects in humans and wildlife. Methylmercury is readily bioavailable to fish and biomagnifies in the marine food chain, leading to higher levels of mercury in predatory fish [6,7]. Gastrointestinal absorption of MeHg-L-Cys is high, and MeHg is rapidly distributed to all tissues, including the brain [8,9]
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