Retention and distribution of methylmercury administered in the food in marine invertebrates: Effect of dietary selenium.

Methylmercury is transported along aquatic food chains from the lower trophic levels and selenium modulates the biokinetics of mercury in organisms in complex ways. We investigated the retention of orally administered methylmercury in various marine invertebrates and the effect of selenium hereon. Shrimps (Palaemon adpersus and P. elegans), blue mussels (Mytilus edulis), shore crabs (Carcinus maenas) and sea stars (Asterias rubens) eliminated methylmercury slowly (t½â€¯= ½ to >1 year) and the copepod (Acartia tonsa) faster (t½â€¯âˆ¼â€¯12-24 h). Orally administered selenite augmented elimination of methylmercury in the copepod (in one of two experiments) and blue mussels, but not in shrimps, crabs and sea stars. Selenium generally alters the distribution of the body burden of mercury, leaving more mercury in muscle and less mercury in digestive glands or rest of the body - also in the species where total body retention is not affected.

Selenium reduces the retention of methyl mercury in the brown shrimp Crangon crangon.

Methyl mercury accumulated at the top of aquatic food chains constitutes a toxicological risk to humans and other top predators. Because the methyl mercury enters the aquatic food chains at the lower trophic levels, uptake and elimination processes at these levels affect the methyl mercury content at the higher levels. Selenium modulates the biokinetics of mercury in aquatic organisms in fairly complex ways, increasing mercury retention in some aquatic mammals, but decreasing methyl mercury retention in fish. However, it is not known if selenium modulates methyl mercury accumulation at lower trophic levels in aquatic food chains. Here, we show that selenium administered via the food augments the elimination of methyl mercury from marine shrimp and that the effect is dose-dependent, demonstrable down to natural selenium concentrations in aquatic food items. Selenite, seleno-cystine, and seleno-methionine exert this effect but selenate does not. Our results suggest that the selenium naturally present at the lower trophic levels in marine food chains may play an essential role as a modifier of methyl mercury accumulation at these levels, thereby potentially also affecting biomagnification of methyl mercury toward the higher trophic levels in the aquatic food chains.

Dietary selenium reduces retention of methyl mercury in freshwater fish.

Adverse effects from organic mercury transported along aquatic food chains are health issues in humans and other top predators. Methyl mercury in organisms at the lower food chain levels is eliminated slowly, and laboratory studies have not clarified the role of selenium in the retention of methyl mercury in fish. Here, we investigated the effects of dietary selenium on the retention of organic and inorganic mercury in freshwater fish. Addition of selenite to the food augmented elimination of methyl mercury (but not inorganic mercury) from goldfish Carassius auratus in a dose dependent manner; selenite caused methyl mercury to be lost from the general body rather than from any specific organ. Seleno-cystine and seleno-methionine (but not selenate) likewise promoted elimination of methyl mercury from goldfish. The threshold for the augmenting effect of selenite on the elimination of methyl mercury in the zebra fish Danio rerio was 0.95 µg Se g(-1) food; higher concentrations reduced retention of methyl mercury in a dose dependent manner. Selenium concentrations in the food approaching natural background levels increase the elimination of methyl mercury from fish. Thus, selenium levels in a given aquatic food chain may affect mercury contamination along the food chain.