An in vivo experiment was conducted to assess selenium bioaccumulation and bioaccessibility through the food chain and its effect on Hg toxicity. For this purpose 72 chickens were fed under different controlled conditions. Chickens were exposed to a common basal diet or a diet supplemented with Hg(II), MeHg, and Se(IV). Enzymatic digestion (feed, chicken muscle, liver, and kidney) as well as simulated human gastric and intestinal digestion (chicken muscle) led to the identification of selenomethionine (SeMet) in all the samples analyzed. Therefore, although chickens have no efficient mechanism for SeMet synthesis they can be considered as a source of SeMet due to its diet and the plant-animal food chain. The kidneys were the target organ for both total Se and SeMet in chickens (1604 +/- 136 and 128 +/- 6 microg kg(-1), respectively), but the greatest body store, among the tissues studied, was the muscle in both cases (84-96% of total Se). Long-term administration of inorganic and organic mercury did not alter SeMet distribution significantly. The antagonistic effect of Se on Hg toxicity by favoring MeHg demethylation is discussed.