MECHANISMS OF KIDNEY-CELL INJURY FROM METALS

The most environmentally abundant toxic metals/metalloids (arsenic, ca dmium, lead, and mercury) are each known to produce cell injury in the kidney but the molecular mechanisms underlying these events are now b eing elucidated. It is clear that the nephrotoxicity of these agents i s due, in part, to the fact th at 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 receptorli ke proteins that appear to influence renal tubule cell expression, hav e attracted increased interest as determinants that modulate cell popu lations as special risk for toxicity and renal cancer. The future of m echanistic toxicology studies with regard to how and why only certain renal cell populations become targets for toxicity from these metals/m etalloids and other less common inorganic nephrotoxicants must focus o n the molecular handling of these agents by target cell populations.