Mercury

Abstract

New findings on the environmental fate of Hg indicate that lakes can be contaminated by long distance transport on mercury vapor in the atmosphere and that higher levels of Me Hg in fish are associated with acidification of lakes and with the creation of hydroelectric reservoirs. Considerable progress has been made in the understanding of the disposition and metabolism of mercury in the body. Inhaled mercury vapor rapidly enters cells in view of its lipid solubility. Inside the cell, it is oxidized by the enzyme, catalase, to inorganic divalent mercury. The latter may be the proximate toxic species. Me Hg also crosses cell membranes rapidly but, in this case, probably by forming water-soluble complexes whose structures mimic those of endogenous substrates that are transported on specific carriers. The mechanism of damage to the central nervous system by mercury vapor is still unknown. The kidney damage probably arises from the effect of inorganic mercury on immunocompetent cells causing them to produce antibodies that affect the glomerulus. The selective damage by Me Hg to specific anatomical areas of the brain and the long latent period are still unexplained. Most studies have focused on the earliest biochemical lesion, the inhibition of protein synthesis. Prenatal damage occurs in all areas of the developing brain. Cell division and abnormal neuronal migration are the processes primarily affected. The destruction of microtubules in neuronal and astrocystic cells offers a plausible explanation of the deranged cytoarchitecture. Prenatal effects such as delays in the normal development of prenatally exposed infants occur at exposures substantially lower than those associated with the onset of adult poisoning.