Yoshida M, Satoh H, Sumi Y
Department of Chemistry, St. Marianna University School of Medicine, Miyamae-ku, Kawasaki, Japan.
Toxicology. 1997 May 16;119(3):193-201. doi: 10.1016/s0300-483x(96)03611-6.
Ethanol (Et-OH), which is an inhibitor of catalase, reduces oxidation of mercury vapor (Hg0) into ionic mercury (Hg2+). Consequently, exposure of pregnant animals to Hg0 with pretreatment of Et-OH causes penetration of larger amount of Hg0 to the fetus. The fate of Hg0 in the fetus of pregnant guinea pigs, thus penetrated, was investigated. Et-OH pretreatment of the dams resulted in the transfer of more mercury to the fetuses and led to a marked increase in mercury in the fetal liver. Furthermore, according to the mercury distribution in the fetal organs, the animals in the Et-OH-pretreated group fell into two subgroups: a group of fetuses (subgroup 1) had higher mercury concentrations in the brain, heart and kidney compared with the group which was exposed to Hg0 without Et-OH-pretreatment (Hg0 group) and another group (subgroup 2) with similar organ mercury concentrations to that of the Hg0 group. Determination of metallothionein (MT) concentrations showed that MT concentration in the fetal liver of subgroup 2 was significantly higher than that of subgroup 1 and the Hg0 group. Further, the Sephadex G-75 chromatography of the cytosol of the fetal liver in subgroup 2 revealed that most of mercury, about 66%, was bound to metallothionein-like protein. On the other hand, in the cytosol of fetal liver of subgroup 1, a small amount, about 10% appeared in fractions corresponding to MT. These findings suggest that fetal hepatic MT plays a significant defense role against mercury crossing the placenta and is involved in regulating for the mercury distribution in the fetus.
