
Mechanisms of kidney cell injury from metals.
Author(s) -
Bruce A. Fowler
Publication year - 1993
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.9310057
Subject(s) - nephrotoxicity , metalloid , toxicity , mercury (programming language) , cadmium , chemistry , metal toxicity , cell , kidney , toxicology , biology , biochemistry , metal , endocrinology , organic chemistry , computer science , programming language
The most environmentally abundant toxic metals/metalloids (arsenic, cadmium, lead, and mercury) are each known to produce cell injury in the kidney but the molecular mechanisms underlying these events are now being elucidated. It is clear that the nephrotoxicity of these agents is due, in part, to the fact that urinary elimination is a major route of excretion from the body. The role(s) of molecular factors such as metal-binding proteins, inclusion bodies, and cell-specific receptorlike proteins that appear to influence renal tubule cell expression, have attracted increased interest as determinants that modulate cell populations as special risk for toxicity and renal cancer. The future of mechanistic toxicology studies with regard to how and why only certain renal cell populations become targets for toxicity from these metals/metalloids and other less common inorganic nephrotoxicants must focus on the molecular handling of these agents by target cell populations.