Abstract

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[sup 0]), inorganic mercurous (Hg[sup +]) and mercuric (Hg[sup 2+]) compounds, and organic mercuric (R-Hg[sup +] 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 modifymore » or alter renal injury induced by mercury. 170 refs., 7 figs.« less

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