Antagonism of acute copper(II)-induced renal lesions by sodium 2,3-dimercaptopropanesulfonate.
Acute copper(II) sulfate poisoning in the mouse induces renal tubular degeneration and necrosis. Timely administration of sodium 2,3-dimercaptopropane-sulfonate (DMPS) effectively prevented the development of the morphological renal sequelae of copper intoxication. During the time course of this study (5 days), no copper-induced hepatic lesions were observed. DMPS and its preformed copper complex possess low inherent toxicity with no hepatorenal lesions occurring over a 5-day period. These findings suggest that DMPS may be an effective antidote in acute and chronic copper poisoning in humans.
D058186:Acute Kidney Injury / Q000139:chemically induced*; D000818:Animals; D003300:Copper / Q000037:antagonists & inhibitors* / Q000506:poisoning; D019327:Copper Sulfate; D004112:Dimercaprol / Q000031:analogs & derivatives*; D007668:Kidney / Q000187:drug effects / Q000473:pathology; D007683:Kidney Tubular Necrosis, Acute / Q000139:chemically induced*; D008297:Male; D051379:Mice; D011897:Random Allocation; D014494:Unithiol / Q000494:pharmacology*
D004112:Dimercaprol; D014494:Unithiol; D003300:Copper; D019327:Copper Sulfate