The interaction between mercury (Hg) and selenium (Se) is one of the best known examples of biological antagonism, yet the underlying mechanism remains unclear. This review focuses on the possible pathways leading to the Hg-Se antagonism, with an emphasis on the potential Hg-Se compounds that are responsible for the antagonism at the molecular level (i.e., bis[methylmercuric]selenide, methylmercury selenocysteinate, selenoprotein P-bound HgSe clusters, and the biominerals HgSexS1−x). The presence of these compounds in biological systems has been suggested by direct or indirect evidence, and their chemical properties support their potentially key roles in alleviating the toxicity of Hg and Se (at high Hg and Se exposures, respectively) and deficiency of Se (at low Se exposures). Direct analytical evidences are needed, however, to confirm their in vivo presence and metabolic pathways, as well as to identify the roles of other potential Hg-Se compounds. Further studies are also warranted for the determination of thermodynamic properties of these compounds under physiological conditions toward a better understanding of the Hg-Se antagonism in biota, particularly under real world exposure scenarios.

Mercury-selenium compounds and their toxicological significance: toward a molecular understanding of the mercury-selenium antagonism.

Selenium (Se) supplementation in the nutritionally relevant range counteracts methylmercury (MeHg) toxicity. Since Se tends to be abundant in fish, MeHg exposures alone may not provide an accurate index of risk from fish consumption. Molar ratios of MeHg:Se in the diets and Hg:Se in tissues of exposed individuals may provide a more accurate index. This experiment compared MeHg toxicity in relation to MeHg exposure vs. Hg:Se molar ratios in diets and tissues. Diets were prepared using low-Se torula yeast basal diets supplemented with Na 2 SeO 4 to contain 0.1, 1.0, or 10.0 μmol Se/kg (∼0.01, 0.08, or 0.8 ppm Se), reflecting low-, adequate-, or rich-Se intakes, respectively. Diets contained either low or high (0.5 μmol or 50 μmol MeHg/kg) (∼0.10 or 10 ppm Hg). Sixty weanling male Long Evans rats were distributed into six weight-matched groups (three Se levels × two MeHg levels) that were supplied with water and their respective diets ab libitum for 18 weeks. No Se-dependent differences in growth were noted among rats fed low-MeHg diets, but growth impairments among rats fed high-MeHg were inversely related to dietary Se. After 3 weeks on the diet, growth impairments were evident among rats fed high-MeHg with low- or adequate-Se and after 10 weeks, rats fed low-Se, high-MeHg diets started to lose weight and displayed hind limb crossing. No weight loss or hind limb crossing was noted among animals fed high-MeHg, rich-Se diets. Methylmercury toxicity was not predictable by tissue Hg, but was inversely related to tissue Se ( P P

http://www.soest.hawaii.edu/oceanography/courses_html/OCN331/Mercury3.pdf

Dietary and tissue selenium in relation to methylmercury toxicity.

Selenium Toxicity to Aquatic Organisms

Environmental mercury (Hg) contamination is an urgent global health threat. The complexity of Hg in the environment can hinder accurate determination of ecological and human health risks, particularly within the context of the rapid global changes that are altering many ecological processes, socioeconomic patterns, and other factors like infectious disease incidence, which can affect Hg exposures and health outcomes. However, the success of global Hg-reduction efforts depends on accurate assessments of their effectiveness in reducing health risks. In this paper, we examine the role that key extrinsic and intrinsic drivers play on several aspects of Hg risk to humans and organisms in the environment. We do so within three key domains of ecological and human health risk. First, we examine how extrinsic global change drivers influence pathways of Hg bioaccumulation and biomagnification through food webs. Next, we describe how extrinsic socioeconomic drivers at a global scale, and intrinsic individual-level drivers, influence human Hg exposure. Finally, we address how the adverse health effects of Hg in humans and wildlife are modulated by a range of extrinsic and intrinsic drivers within the context of rapid global change. Incorporating components of these three domains into research and monitoring will facilitate a more holistic understanding of how ecological and societal drivers interact to influence Hg health risks.

/pdf/modulators-of-mercury-risk-to-wildlife-and-humans-in-the-30ob3eigq1.pdf

Modulators of mercury risk to wildlife and humans in the context of rapid global change

The US Environmental Protection Agency (EPA) is revising its strategy to obtain the information needed to answer questions pertinent to water-quality management efficiently and rigorously at national scales. One tool of this revised strategy is use of statistically based surveys of aquatic resources such as lakes, wetlands, rivers, and streams. Implementing large-extent surveys involves decisions that reflect compromises between scientific rigor, consistent and practical implementation over large areas and many participants, and the realities of time and money. Primary constraints result from interactions among management objectives, time lines, funding, and institutional constraints of participants. Secondary constraints arise from the interaction between the survey design (geographic extent, sample size, use of existing data), logistics (sampling period, sample shipping, information management, crew expertise, field training), and the suite of ecological indicators selected (site-scale sampling ...

https://www.jstor.org/stable/10.1899/08-028.1

Acquiring data for large aquatic resource surveys: the art of compromise among science, logistics, and reality

This paper reviews the growing literature dealing with the antagonistic effect of selenium (Se) compounds on the toxicity of mercury (Hg) compounds in higher animals and organisms present in the aq...

Yu-Wei ChenY.-W. Chen

Papers

Selenium and mercury in organisms: Interactions and mechanisms