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: 5.33). 07/2005; 39(11):3972-80. DOI: 10.1021/es0483490
Source: PubMed


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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Available from: Jean-Charles Massabuau, Nov 28, 2014
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    • "In Hg contaminated areas, studies with fish have demonstrated high Hg burdens in the liver (Navarro et al., 2009; Mieiro et al., 2012), 70% of which was accumulated in the inorganic form (I-Hg) (Mieiro et al., 2009). Liver has been acknowledged to be the primary target organ for Hg (Wang et al., 2013) as well as the main detoxifying organ, being able to demethylate organic mercury (O-Hg) into I-Hg forms (Gonzalez et al., 2005). Yasutake and Hirayama (2001) found that Hg demethylation occurs mainly in mitochondria, which is in agreement with findings by Wang et al. (2013) that HgCl 2 affects several proteins related with mitochondrial function. "
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    • "Fish studies suggest that MeHg may disturb reproductive hormones, mediating smaller gonad development or atrophy, delays in spawning and effects on fecundity (Klaper et al., 2006, 2008), and act gender-specifically (Liu et al., 2013). Oxidative stress and apoptosis have been suggested to be two of the main effects of MeHg exposure in fish (Gonzalez et al., 2005; Klaper et al., 2008; Berg et al., 2010; Cambier et al., 2010; Richter et al., 2011). Conducting studies with Atlantic salmon (Salmo salar), it has recently been shown that oxidative stress is one of the major effects of MeHg exposure (Olsvik et al., 2011a; Nøstbakken et al., 2012a,b). "
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    • "They were however, down-regulated following MeHgCl exposure. Previous publications in a variety of species report inconsistent induction of metallothioneins in response to MeHgCl exposure [41-44]. The present study is the first to report a down-regulation of metallothionein gene expression in response to MeHgCl exposure. "
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