revised final - Agency for Toxic Substances and Disease Registry ...

MERCURY 324
2. HEALTH EFFECTS
selenium available for the selenium-dependent glutathione peroxidase (Cuvin-Aralar and Furness 1991;
Imura and Naganuma 1991; Nylander and Weiner 1991). Selenium-treated animals can remain
unaffected despite an accumulation of mercury in tissues to levels that are otherwise associated with toxic
effects (Skerfving 1978). Support for the proposal that an inert complex is formed comes from the 1:1
ratio of selenium and mercury found in the livers of marine mammals and in the bodies of experimental
animals administered compounds of mercury and compounds of selenium, regardless of the ratio of the
injected doses (Hansen 1988). Mercuric mercury has been shown to form a complex with selenium and a
high-molecular weight protein (Naganuma and Imura 1981). Methylmercury forms a bismethyl-mercury
selenide complex.
Although the fetotoxicity of methylmercuric chloride has been shown to be enhanced by the feeding of a
selenium-deficient diet in mice (Nishikido et al. 1987), additional selenium administration does not
appear to protect against teratogenic effects (i.e., cleft palate) of methylmercuric chloride in mice (Lee et
al. 1979). High doses of selenium administered as selenite for 30 days prior to gestation and through
Gd 18 to mice fed a diet containing high doses of methylmercuric chloride increased the incidence of cleft
palate (Nobunaga et al. 1979). It is possible that cleft palate induction by methylmercury is the result of a
suppression of growth rather than a tissue-specific teratogenic action (Lee et al. 1979). If this were the
case, high doses of selenium that inhibit growth could potentiate the induction of cleft palate by methylmercury
administration. Further discussion of selenium-mercury interactions can be found in Section
2.3.1.2.
Ethanol promotes an increase in the respiratory excretion of metallic mercury by inhibiting the enzyme
catalase, which is responsible for oxidizing metallic mercury to mercuric mercury. This process was
shown in workers who ingested a moderate dose of alcohol and experienced a 50% decrease in mercury
retention upon inhalation exposure to metallic mercury vapor (Nielsen-Kudsk 1973). Also, ethanol
increased the amount of mercury exhaled by people who inhaled metallic mercury vapor or received trace
doses of mercuric chloride (Nielsen-Kudsk 1965). Therefore, less mercury should reach the kidneys and
less renal toxicity should be observed (Nielsen-Kudsk 1965). However, ethanol also allows elemental
mercury to persist longer in the plasma, resulting in prolonged diffusion of elemental mercury throughout
the body (Nielsen-Kudsk 1965). Therefore, ethanol can cause mercury to distribute more easily across
the blood-brain barrier and the placenta, thereby increasing the risk of mercury toxicity to the brain and
the developing fetus. In addition, the oxidation of ethanol with concurrent NADPH generation enhances