The response of rodents to organophosphorus ester induced delayed neurotoxicity (OPIDN) and to an analogous carbamate induced neuropathy was investigated using several dosage regimens in outbred rats and mice. In no case were either rats or mice overtly ataxic 30 days after treatment with any of the compounds tested, even with intramuscular or intraperitoneal administration. Seventeen inbred strains of mice differing in their esterase (Es and Ee) genotypes were treated with organophosphorus esters known to induce paralysis in hens. None of these inbred strains was sensitive to OPIDN. These studies demonstrate that neither altering the route of administration nor variations in the esterase genotype of rodents renders them susceptible to OPIDN. The studies also suggest that the carbamate induced neuropathy is, like OPIDN, difficult to induce in rodents.
|Original language||English (US)|
|Number of pages||7|
|Journal||Archives of Environmental Contamination and Toxicology|
|State||Published - Nov 1983|
ASJC Scopus subject areas
- Health, Toxicology and Mutagenesis