ADVANCES IN UNDERSTANDING THE RENAL TRANSPORT AND TOXICITY OF MERCURY

As a result of industrialization and changes in the environment during the twentieth century, humans and animals are exposed to numerous chemical forms of mercury Including elemental mercury vapor (Hg°), inorganic mercurous (Hg+) and mercuric (Hg2+) compounds, and organic mercuric (R- Hg+or R-Hg-R; where R represents any organic ligand) compounds. The risk of exposure and subsequent intoxication is of increasing concern because of the steadily increasing deposition of mercury in the environment (Fitzgerald & Clarkson, 1991). All forms of mercury have nephrotoxic effects, although disposition and toxicity of mercury in tissues can vary depending on the chemical form of mercury. For example, the initial toxic effects of both elemental mercury and organic forms of mercury are observed in the nervous system. This is due to their lipophilicity, which allows them to cross the blood-brain barrier. At later times, hepatotoxicity and nephrotoxicity can develop. With inorganic mercurous or mercuric salts, the most prominent effect is nephrotoxicity. Until recently, little was known about the mechanisms involved in the nephropathy induced by mercury. The purpose of this article is to review recent data on the intrarenal accumulation and disposition, nephrotoxicity, and target site specificity of mercury, and factors that modify or alter renal injury induced by mercury.Elemental mercury is oxidized in erythrocytes or in tissues to inorganic mercury (Hg2+), 1 so that consideration of the fate of elemental mercury vapor is similar to that of inorganic mercury (Magos & Clarkson, 1977; Magos et al., 1978). Oxidation of elemental mercury must take place for chemical interaction with cellular molecules to occur. Since the general patterns of tis-. © 1988 by Hemisphere Publishing Corporation.