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Physiological implications of mercury's effects on selenium availability.

Mercury (Hg) is a global pollutant that humans are exposed to in the form of methylmercury (MeHg) present in fish. The toxic effects of MeHg make it a potential health problem, and it is listed by the International Program of Chemical Safety as one of the most dangerous chemicals in the environment. Although adults can experience neurological effects when exposed to high concentrations of MeHg, advisories have mainly arisen because of the increasing concerns regarding MeHg's effects in the developing nervous systems of unborn and growing children. While the placental barrier can stop many toxic elements, MeHg crosses the placenta and accumulates at higher concentrations on the fetal side than on the maternal. Worsening the situation for the developing fetus, MeHg also crosses the blood-brain barrier where it exhibits long-term retention. These factors exacerbate Hg's neurotoxicity and conspire to intensify its pathologic effects in brain and endocrine tissues. Although Hg toxicity is well described, its molecular mechanism is poorly understood and the effects of chronic low-dose exposures remain undetermined

It is well recognized that Hg and sulphur (S) bind together to form complexes. This binding property is the basis of chelating therapy used as a treatment in cases of acute mercury poisoning. The complexes between Hg and selenium (Se) are less generally known but of much higher affinity. Physiologically, S is far more abundant than Se, yet because of Se's higher affinity, Hg selectively binds with Se to form insoluble HgSe. This interaction has been assumed to be a protective effect, whereby supplemental Se complexes the Hg and prevents negative effects in animals fed otherwise toxic amounts of Hg. Numerous studies have shown Se supplementation counteracts the negative impacts of exposure to Hg, particularly in regard to neurotoxicity, fetotoxicity, and developmental toxicity. The ability of Se compounds to decrease the toxic action of Hg has been established in all investigated species of mammals, birds, and fish. However, similar to Hg toxicity itself, the molecular mechanism of Se's protective effect against Hg toxicity is well described, but poorly understood.

Dietary Se is essential in supporting functions of enzymes with important metabolic roles, and beneficial in augmenting immunocompetence and cancer chemoprevention. Present in tissue-specific distributions in all cells of all creatures, approximately 25 Se-containing proteins have been recognized. Se-enzymes possess Se in the form of selenocysteine located at their active sites, employing Se's broad catalytic redox potential. Selenoprotein activities appear to be especially important in brain, pituitary, and thyroid, since even after feeding selenium-deficient diets for many generations, it is virtually impossible to deplete the selenium in these tissues,. Consequently, any substance that can enter the brain and disrupt selenoprotein synthesis in these tissues will accomplish what multigenerational selenium deficiency cannot.

MeHg not only has the ability to cross the blood-brain barrier, but its exceptionally high affinity for Se may enable it to specifically sequester Se and diminish selenoprotein synthesis. The Hg-binding affinity constant of the free selenides that form during each cycle of selenocysteine synthesis have an exceptionally high affinity constant for Hg: [10.sup.45]. HgSe precipitates have extremely low solubility, ranging from [10.sup.-58] 58 to [10.sup.-65], thus they are thought to be metabolically inert. Therefore, it is reasonable to assume that not only does Se have an effect on Hg's bioavailability, but Hg may also have an effect on Se bioavailability. Therefore, the understanding of the protective effect of Se against Hg exposure may actually be backwards. Mercury's propensity for Se sequestration in brain and endocrine tissues may inhibit formation of essential Se-dependent proteins. Hence, Se's protective effect against Hg toxicity may simply reflect the importance of maintaining sufficient Se to support normal synthesis of Se-dependent enzymes and the sensitivity to Hg-induced neurotoxicity may be due to the balance of rig and Se. In this regard, the health risks of MeHg exposure may vary in response to individual and regional differences in selenium intake.

We conducted a series of rat studies to investigate the influence of Se status on sensitivity to Hg toxicity. Our studies confirm selenium's protective effect against mercury toxicity. Se-deficient rats were sensitive to Hg exposure, while rats fed diets containing adequate amounts of Se were far more resistant and rats fed Se-rich diets showed no signs of mercury toxicity. Tissue samples are in the process of being analyzed for mercury, selenium, and selenoenzyme activity. Likewise, the stoichiometry of Hg with the Se present in the tissues is currently being investigated. Further research in these areas will provide valuable information that is needed to understand the true impact of rig exposure as well as identify populations which may be protected or at greater risk to Hg's toxic effects.

L.J. Raymond * and N.V.C. Ralston

University of North Dakota, Energy & Environmental Research Center, Grand Forks, ND 58202
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Title Annotation:Professional Communications
Author:Raymond, L.J.; Ralston, N.V.C.
Publication:Proceedings of the North Dakota Academy of Science
Date:Apr 1, 2005
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