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© 1984 Oxford University Press

research-article

Carbofuran Metabolism and Toxicity in the Rat1

PAUL W. FERGUSON*, MICHAEL S. DEY*, SARAH A. JEWELL* and ROBERT I. KRIEGER{dagger},3

*Department of Environmental Toxicology, University of California Davis, California 95616 {dagger}Department of Veterinary Science, Washington-Oregon-Idaho Regional Program in Veterinary Medicine, University of Idaho Moscow, Idaho 83843

Carbofuran Metabolism and Toxicity in the Rat. FERGUSON, P. W., DEY, M. S., JEWELL, S. A., AND KRIEGER, R. I. (1984). Fundam. Appl. Toxicol. 4, 14–21. The influence of carbofuran metabolism on acetylcholinesterase inhibition has been defined after low dose (50 µg/kg, iv and oral) [carbonyl-14C]carbofuran exposures to male Sprague–Dawley Rats. Red blood cell acetylcholinesterase (RBC AchE) inhibition (83% at 2 min, 37% at 15 min for iv and oral, respectively, with recovery by 3 hr), was correlated with carbofuran plasma concentrations (r = 0.97). Eight-hour sample collection indicated that ultimate carbofuran fate (41–47% l4CO2, 14–15% urine, <1% feces, and 30–31% carcass) was independent of exposure route. Carbofuran absorption (peak plasma levels < 7 min), distribution, and elimination (t½ = 29 ± 5 min) occurred rapidly. 3-Hydroxycarbofuran, a significant oxidative metabolite of carbofuran with anticholinesterase activity, was rapidly formed and subject to enterohepatic circulation (plasma t½ = 64 ± 5 min). Results indicated that rapid RBC AchE recovery closely paralleled carbofuran metabolism and the primary in vivo disposition of 3-hydroxycarbofuran was metabolic conjugation.


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