Administration to rats of 100 mg/kg of 1,3-difluoro-2-propanol (DFP), the major ingredient of the pesticide Gliftor, resulted in citrate accumulation in the kidney after a 3-h lag phase. Inhibition of aconitate hydratase in the kidney and the development of symptoms typical of sodium fluoroacetate (1080) poisoning in DFP-intoxicated rats suggested metabolism of DFP to (-)erythrofluorocitrate.
The conversion of DFP to the toxic metabolite was found to involve defluorination by a microsomal mixed-function oxidase in the liver, induced by phenobarbitone and inhibited by piperonyl butoxide. Administration to rats of pyrazole (90 mg/kg body weight) decreased the activity of the mixed-function oxidase-dependent defluorination of DFP. When administered to rats either 2 h before or 2 h after DFP (100 mg/kg body weight) it eliminated symptoms of poisoning, prevented citrate and fluoride accumulation, and decreased aconitate hydratase inhibition in the kidney. The antidotal properties of pyrazole, the mode of toxic action of (-)erythrofluorocitrate, and the potential for DFP to replace 1080 in fauna management programs in Australia is discussed.
|Author||Mead, R. J., Feldwick, M. G. and Bunn, J. T.|
|Secondary title||Wildlife Research|
|Control method||Poison / Toxin|
|Region||Australia - national|