Comparative effects of dietary methylmercury on gene expression in liver, skeletal muscle, and brain of the zebrafish (Danio rerio)

Université Bordeaux 1, Talence, Aquitaine, France
Environmental Science and Technology (Impact Factor: 5.48). 07/2005; 39(11):3972-80. DOI: 10.1021/es0483490
Source: PubMed

ABSTRACT Effects of dietary methylmercury (MeHg) on gene expression were examined in three organs (liver, skeletal muscle, and brain) of the zebrafish (Danio rerio). Adult male fish were fed over 7, 21, and 63 days on three different diets: one control diet (C0: 0.08 microg of Hg g(-1), dry wt) and two diets (C1 and C2) contaminated by MeHg at 5 and 13.5 microg of Hg g(-1), dry wt. Total Hg and MeHg concentrations were determined in the three organs after each exposure duration, and a demethylation process was evidenced only in the liver. Thirteen genes known to be involved in antioxidant defenses, metal chelation, active efflux of organic compounds, mitochondrial metabolism, DNA repair, and apoptosis were investigated by quantitative real-time RT-PCR and normalized according to actin gene expression. Surprisingly, no change in the expression levels of these genes was observed in contaminated brain samples, although this organ accumulated the highest mercury concentration (63.5 +/- 4.4 microg g(-1), dry wt after 63 days). This lack of genetic response could explain the high neurotoxicity of MeHg. coxI and cytoplasmic and mitochondrial sod gene expressions were induced early in skeletal muscle and later in liver, indicating an impact on the mitochondrial metabolism and production of reactive oxygen species. Results demonstrated that skeletal muscle was not only an important storage reservoir but was also affected by MeHg contamination. The expression of the metallothionein mt2 and the DNA repair rad51 genes was up-regulated in liver between 21 and 63 days, whereas in skeletal muscle, mt2 remained uninduced, and gadd and rad51 were found to be repressed.

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    ABSTRACT: Methylmercury (MeHg) is a toxicant of concern for aquatic food chains. In the present study the assimilation and depuration of dietary MeHg and the influence of dietary selenium on MeHg toxicokinetics was characterised in zebrafish (Danio rerio).In a triplicate tank experimental design (n = 3 tanks per treatment group) adult zebrafish were exposed to dietary MeHg (as methylmercury-cysteine) at 5 and 10 μg/g and with or without selenium (as selenomethionine) supplemented to the diets at a concentration of 5 μg/g for eight weeks followed by a four week depuration period.Methylmercury accumulated in muscle, liver and brain of zebrafish; with higher mercury concentrations in liver and brain than in muscle following eight weeks of exposure. In muscle, the mercury concentrations were 3.4 ± 0.2 and 6.4 ± 0.1 μg/g ww (n = 3) in zebrafish fed the 5 and 10 μg Hg/g diets, respectively. During the depuration period, mercury concentrations were significantly reduced in muscle in both the 5 and 10 μg Hg/g diet groups with a greater reduction in the high dose group. After depuration the mercury concentrations were 2.4 ± 0.1 and 4.0 ± 0.3 μg/g ww (n = 3) for zebrafish fed the 5 and 10 μg Hg/g diets, respectively.Data also indicated that supplemented dietary selenium reduced accumulation of MeHg and enhanced the elimination of MeHg. Lower levels of mercury were found in muscle of zebrafish fed MeHg and SeMet compared with fish fed only MeHg after eight weeks exposure; the mercury concentration in muscle were 5.8 ± 0.2 and 6.4 ± 0.1 μg/g ww (n = 3) for zebrafish fed the 10 μg Hg/g + 5 μg Se/g diet and the 10 μg Hg/g diet, respectively. Furthermore, the elimination of MeHg from muscle during the four week depuration period was significantly greater in the fish fed the diet containing SeMet compared to a control diet; the mercury concentrations were 3.3 ± 0.1 and 4.0 ± 0.3 μg/g ww (n = 3) for zebrafish fed the 5 μg Se/g and the control diets, respectively. In summary, dietary SeMet reduces the accumulation and enhances the elimination of dietary MeHg in muscle of zebrafish.
    Aquatic Toxicology 11/2014; DOI:10.1016/j.aquatox.2014.11.010 · 3.51 Impact Factor
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    ABSTRACT: The effect of methylmercury (MeHg) on glass eels' propensity to migrate, mitochondrial activity and antioxidative defence systems were investigated. Marine glass eels were first sorted in an experimental flume according to their response to dusk. Fish responding to the decrease in light intensity by ascending in the water column and moving with or against the flow were considered as having a high propensity to migrate (migrant). Glass eels still sheltering at the end of the 24 hr catching period were considered as having a low propensity to migrate and were called non-migrant. Migrant and non-migrant glass eels were then individually tagged and exposed to isotopically enriched (201)MeHg (50 ng L(-1)) for 11 days. The effect of contamination was studied on muscle fibre structure, and the expression level of genes involved in mitochondrial activity and antioxidative defence systems. To investigate the effect of MeHg on glass eel behaviour, migrant and non-migrant glass eels were sorted again and the bioaccumulation of (201)MeHg and its demethylation product ((201)Hg(II)) were determined for each individual. MeHg exposure increased activity in non-migrant glass eels but not migratory behaviour. Contamination affected mitochondrial structure and metabolism and suggests a higher oxidative stress and activation of antioxidative defence systems in non-migrant glass eels. Overall, our results suggest that exposure to MeHg might induce an increase in energy expenditure and a higher vulnerability to predation in non-migrant glass eels in the wild. Copyright © 2015 Elsevier Inc. All rights reserved.
    Comparative Biochemistry and Physiology Part C Toxicology & Pharmacology 03/2015; DOI:10.1016/j.cbpc.2015.03.003 · 2.83 Impact Factor


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