Selenium concentrations in brain after exposure to methylmercury: relations between the inorganic mercury fraction and selenium

Abstract

Three groups of female monkeys (Macaca fascicularis) were exposed to methylmercury (MeHg, p.o. 50 micrograms Hg/kg body wt per day) for 6, 12, or 18 months. One group was exposed to MeHg for 12 months and kept unexposed for 6 months before sacrifice. Another group of three monkeys was exposed to HgCl2 i.v. for 3 months. Total and inorganic mercury concentrations in occipital pole and thalamus were determined by cold vapor atomic absorption spectroscopy. Selenium concentrations were analyzed by hydride generation atomic absorption spectroscopy. The results indicated an association between concentrations of inorganic mercury and selenium in both occipital pole and thalamus in the MeHg-exposed animals. A linear regression model using concentrations of inorganic mercury (nmol/g wet wt) as independent variable, and selenium concentrations (nmol/g wet wt) as the dependent variable showed significant correlations between the variables in both occipital pole and thalamus (r = 0.85 and r = 0.91, P < 0.0001). The intercept of the regression line was slightly lower (about 2 nmol Se/g wet wt) than the selenium concentrations found in control monkeys (about 3 nmol Se/g wet wt). There was a tendency to a "hockey stick"-shaped relationship between concentrations of selenium and inorganic mercury in the thalamus of monkeys with ongoing exposure to MeHg. An important role for selenium in the retention of mercury in brain is indicated.

Characterization of methylmercury demethylation in the central nervous system.

“…Demethylation has been shown to occur in brain tissue following MeHg exposure (Bjorkman et al, 1995;Charleston et al, 1996;Eto, 2000;Watanabe, 2002). When considering all the above factors, a condition which would result in the greatest toxicity would involve the ingestion of MeHg, distribution to the brain, followed by conversion to iHg.…”

“…Evidence for this phenomenon resulted from the identification of iHg in the brain following exposure to MeHg in humans (Takeuchi & Eto, 1999). This has since 24 been evaluated in vitro in the liver (Suda & Hirayama, 1992;Yasutake & Hirayama, 2001) and brain (Syversen et al, 2006) of rats and in vivo through feeding trials in monkeys (Bjorkman et al, 1995;Charleston et al, 1996;Watanabe, 2002;Vahter et al, 1995).…”

“…Alternative theories for the presence of iHg in the brain involving binding to micronutrients have been proposed (Friberg & Mottet, 1989). The main support for this is the presence of iHg in the brain following inhalation of elemental mercury vapour (Bjorkman et al, 1995;Friberg & Mottet, 1989;Leong et al, 2001). However, accumulation in the brain may be the result of passive diffusion of Hg° across the blood brain barrier (Aschner & Aschner, 1990).…”

Assessing the neurotoxicological risk of methylmercury exposure for beluga whales (delphinapterus leucas) harvested in the Mackenzie Delta Estuary.

“…MeHgcysteine or tiemannite). Methylmercury and iHg are both neurotoxic; however, Se may bind to iHg to form HgSe, a non-toxic Hg complex (Bjorkman et al, 1995). Demethylation of MeHg followed by the formation o f compounds similar to mercury selenide (HgSe) was linked to successful detoxification o f Hg-exposed humans (Korbas et al, 2010).…”

“…More than 95% o f ingested MeHg is absorbed (Aberg et al, 1969) and may cross the blood brain barrier via neutral amino acid transporters (Aschner and Aschner, 1990). Methylmercury may undergo demethylation in the brain (Shapiro and Chan, 2008;Yokel et al, 2006), and co-exposure to selenium (Se) and Hg may increase the rates of MeHg uptake, demethylation, and inorganic Hg (iHg) retention in the brain (Bjorkman et al, 1995;Magos and Webb, 1980;Newland et al, 2006).…”