Record Display for the EPA National Library Catalog

RECORD NUMBER: 29 OF 31

OLS Field Name OLS Field Data
Main Title Toxicity, interactions, and metabolism of formamidine pesticides in mammals /
Author Hollingworth, R. M., ; Yim, G. K. W.
Other Authors
Author Title of a Work
Yim, G. K. W.
CORP Author Purdue Univ., Lafayette, IN. Dept. of Entomology.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher National Environmental Research Center, Health Effects Research Laboratory,
Year Published 1980
Report Number EPA/600/1-80/028; PB80-205867; EPA-R-803965
Stock Number PB80-205867
Subjects ENVIRONMENTAL POLLUTION and CONTROL. ; Pesticides--metabolism. ; ENVIRONMENTAL POLLUTION & CONTROL ; Pesticides--toxicology
Additional Subjects Toxicology ; Pesticides ; Chlorine organic compounds ; Mammals ; Metabolism ; Interactions ; In vivo analysis ; Insecticides ; Mice ; Distribution ; Laboratory animals ; Bioassay ; Chlordime form ; Formamidines ; Metabolites ; Formamidine/N-(chloro-tolyl)-N-N-dimethyl
Holdings
Library Call Number Additional Info Location Last
Modified
Checkout
Status
NTIS  PB80-205867 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 01/01/1988
Collation 116 pages ; 28 cm.
Abstract
The overall goal of this research project was to investigate the mechanism(s) of acute toxicity of formamidine pesticides in mammals using chlordimeform (N'-(4-chloro-o-tolyl)-N,N-dimethylformamidine) and its metabolites as the primary model compounds. The role of biotransformations, particularly N-demethylation reactions, in generating potentially toxic metabolites was also studied. By comparing the effects of hepatic microsomal mixed function oxidase inducers and inhibitors administered in vivo on the toxicity, metabolism, and distribution of metabolites in mouse tissues, it was concluded that although N-demethylation products are innately more toxic than chlordimeform, they are also less stable, and the best correlation of toxicity was obtained with the total level of formamidines in the brain, rather than with the level of any individual metabolite. In a series of studies with dogs, rabbits, and cats, the cause of death was found to be cardiovascular collapse accompanied by respiratory arrest. Cardiovascular collapse resulted primarily from a peripheral local anesthetic-like effect of chlordimeform. Monoamine oxidase inhibition was not a major factor in lethality. Respiratory arrest was central in origin. Several other central effects of the formamidines were described, some of which may be local anesthetic actions, and a behavioral profile for chlordimeform poisoning in the rat was developed. The effectiveness of various drug treatments as potential therapeutic aids for formamidine intoxication were studied. Formamidines also have aspirin-like actions due to an inability to inhibit prostaglandin synthesis.
Notes
"Performing Agency: Purdue University, Department of Entomology"--Technical rept. data. "Grant Number R-803965. "May 1980"--Technical rept. data. Includes bibliographical references (93-101). Microfiche.