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MERCURY 184
2. HEALTH EFFECTS
production (Suda and Hirayama 1992). The promotion and inhibition of the hydroxyl radical formation and
the hydroxyl radical scavenger, affected inorganic mercury production. These results suggest that hydroxyl
radicals produced from microsomes may play a predominant role in alkyl mercury degradation.
NADPH-cytochrome P-450 reductase is known to be responsible for hydroxyl radical production in liver
microsomes. Alkyl mercury degradation varied in proportion to the enzyme activities and hydroxyl radical
production. These results suggest that hydroxyl radicals produced by cytochrome P-450 reductase might be
the primary reactive species that induces alkyl mercury degradation. In vitro studies using a peroxidasehydrogen
peroxide-halide system indicated that besides the hydroxyl radical, hypochlorous acid (HOCl)
scavengers are also capable of degrading methylmercury (Suda and Takahashi 1992). Also, metallic
mercury exhaled in mice dosed with methylmercury was dependent on the level of inorganic mercury
present in the tissue (Dunn and Clarkson 1980). The cation then enters the oxidation-reduction cycle, and
metabolism occurs as discussed previously under Inorganic Mercury.
A small amount of an oral dose of methylmercuric chloride can also be converted into inorganic mercury in
the intestinal flora (Nakamura et al. 1977; Rowland et al. 1980). However, inorganic mercury is poorly
absorbed across the intestinal wall and, therefore, most of it is excreted.
Phenylmercury also rapidly metabolizes to inorganic mercury (Nordberg 1976). The metabolism of phenyl­
mercury involves hydroxylation of the benzene ring to an unstable metabolite that spontaneously releases
inorganic mercury. Consequently, its tissue disposition following initial metabolism resembles that seen
after the administration of inorganic salts (Gage 1973).
Studies in mice indicate that toxicity from exposure to dimethylmercury is the result of metabolic
conversion of dimethylmercury to methylmercury, and that dimethylmercury does not enter the brain until
it has been metabolized to methylmercury, which occurs over the first several days following absorption
(Ostland 1969). Nierenberg et al. (1998) report the results of an analyses of mercury content in the hair of a
48-year-old female who died subsequent to an acute exposure to dimethylmercury. The results are
consistent with the kinetic profiles for methylmercury, and support the hypothesis of a rapid conversion of
dimethylmercury to a methylmercury metabolite.