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

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.