Selenium in the liver facilitates the biodilution of mercury in the muscle of Planiliza haematocheilus in the Jiaozhou Bay, China

Abstract

There are increasing evidences that the biodilution effect can significantly reduce the biomagnification of mercury (Hg) in fish. The significant antagonism of selenium (Se) -Hg may have a potential diluting effect on Hg in fish; however, there is still lack of knowledge on such effect. To reveal the Se-Hg interaction and its role in controlling the biodilution effect of Hg, we investigated levels of Hg and Se in the muscle and liver of redlip mullet from Jiaozhou Bay, China, an urbanized semi-enclosed bay highly impacted by human activities. In general, Hg levels in fish muscle were significantly negatively correlated to the levels of Se in the liver and fish size for fish with a size of < 200 mm, indicating that the antagonistic effect of Se on Hg increased with fish growth. This relationship was not significant for fish with a size of > 200 mm, possibly because the normal metabolism of Hg in muscle was hindered by homeostatic regulation or physiological activities such as gonadal development in vivo. Furthermore, the molar ratio of Se in the liver/Hg in the muscle was significantly increasing with Se/Hg in the liver, suggesting that the liver may be the key organ involved in Se-Hg antagonism. Moreover, both ratios continued to decrease with increasing fish size, implying that the antagonistic effect weakens with fish growth. These results indicate that Hg sequestration by liver may be a key mechanism of Se-Hg antagonism in fish and function as a driver for the biodilution effect of Hg, especially at a size of < 200 mm. These findings are further supported by the established linear model of Se-Hg antagonism at different developmental stages.