MeHg is also readily transferred to the fetus and the fetal brain. Evidence from rat experiments suggests that MeHg transport across the blood-brain barrier occurs via a MeHg-L-cysteine complex, which is transported by the L-system (leucine preferring) amino acid carrier (Kerper et al. 1992). MeHg-cysteine is released in vitro from a MeHg-glutathione complex by the action of γ-glutamyltransferase and dipeptidases (Naganuma et al. 1988). That action suggests that glutathione might play an indirect role in the transport of MeHg into endothelial cells. The MeHg-cysteine or MeHg-glutathione complex would be expected to be water soluble. That would not support the hypothesisthat the rapid uptake of MeHg by the brain is due to lipid solubility in body tissues and fluids. Recently, Fujiyama et al. (1994) proposed that the MeHg-glutathione complex is the mechanism by which MeHg can efflux rat astroglia. Aschner et al. (1991), however, proposed that the MeHg-cysteine complex is the mechanism by which MeHg is exported from astroglia.
A case study of family members that developed classic signs of MeHg poisoning due to the consumption of contaminated pork indicates that the cerebrum and the cerebellum are particularly sensitive to MeHg (Davis et al. 1994). Analyses of various regions of the brain of one female member upon autopsy, several years later, revealed that the extent of brain damage correlated with regional-brain Hg concentrations. Inorganic Hg comprised 82-100% of the total Hg, suggesting that most of the MeHg had been converted to inorganic Hg during the period. The highest levels of Hg were found in the cerebrum and cerebellum. Magnetic Resonance Imaging (MRI) studies showed brain damage in the calcarine cortices, parietal cortices, and cerebellum of other family members. The damage in those areas is believed to underlie many of their persistent clinical signs, because those areas of the brain are responsible for coordination, balance, and sensations