Program in Toxicology, University of Maryland, Baltimore 21201.
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.
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