Selenium induces mercury isotope fractionation and detoxification in marine fish.

Prey fish are vital in transferring nutrients and contaminants from lower to higher trophic levels. Although the role of selenium (Se) on mercury (Hg) detoxification has been identified in marine mammals and seabirds, the metabolic pathways of Hg-Se interaction in fish remain unknown. We used Hg stable isotopes (δ202Hg, Δ199Hg) to characterize the internal dynamics of methylmercury (MeHg) and inorganic Hg (IHg) in the presence and absence of Se in juvenile olive flounders (Paralichthys olivaceus). The fish were exposed to MeHg- (1,223 ng/g, n = 31) and IHg-amended (1,515 ng/g, n = 31) food pellets for 4 weeks (bioaccumulation phase) and switched to control or Se-amended food pellets for 10 weeks (excretion phase). During the bioaccumulation phase, the Hg isotopic composition of all fish tissues shifted toward their respective food pellets. During the excretion phase, significant negative δ202Hg shifts (0.27-0.59 ‰) were recorded in the liver of fish initially fed MeHg food pellets and then switched to Se food pellets, which is indicative of Se-induced hepatic MeHg demethylation. Fish fed IHg food pellets and then switched to control or Se food pellets exhibited similar isotopic behavior, suggesting that Se plays a minor role in IHg excretion. Both δ202Hg and Δ199Hg of the liver shifted toward IHg food pellets even during the excretion phase, which we attribute to slow intestinal IHg mobilization and redistribution to the liver. We found that the liver is the major site for MeHg demethylation in the presence of Se and that Se plays a relatively minor role in IHg excretion. Tissue-specific Hg isotope dynamics and interaction with Se should be considered in future Hg ecotoxicological assessments in fish.
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