Evaluation of the ability of d-penicillamine to protect rats against the neurotoxicity induced by zinc pyridinethione, acrylamide, 2,5-hexanedione and p-bromophenylacetylurea.
Dietary exposure of rats to three different concentrations of zinc pyridinethione (ZPT; 166, 332, 498 ppm) caused delayed onset failure in a treadmill test and, at the higher concentrations (332 and 498 ppm), death. Daily treatment with d-penicillamine (d-PEN) increased the latency period for treadmill failure and lethality. Comparable levels of toxicity were achieved only after d-PEN treated rats had consumed 2-3 times more ZPT than rats not treated with d-PEN. In contrast to ZPT, administration of d-PEN did not affect the onset of treadmill failure associated with acrylamide, p-bromophenylacetylurea or 2,5-hexanedione. Thus, d-PEN provided protection which was selective for ZPT.
D020106:Acrylamide; D000178:Acrylamides / Q000037:antagonists & inhibitors; D000818:Animals; D006588:Hexanones / Q000037:antagonists & inhibitors; D008297:Male; D009468:Neuromuscular Diseases / Q000139:chemically induced* / Q000517:prevention & control; D009942:Organometallic Compounds; D010396:Penicillamine / Q000494:pharmacology / Q000627:therapeutic use*; D011725:Pyridines / Q000037:antagonists & inhibitors; D051381:Rats; D011919:Rats, Inbred Strains; D014508:Urea / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors
D000178:Acrylamides; D006588:Hexanones; D009942:Organometallic Compounds; D011725:Pyridines; D020106:Acrylamide; C004506:4-bromophenylacetylurea; D014508:Urea; C011269:2,5-hexanedione; D010396:Penicillamine; C010423:pyrithione zinc