@article{oai:niigata-u.repo.nii.ac.jp:00023983, author = {木根渕, 英雄}, issue = {8}, journal = {新潟医学会雑誌, 新潟医学会雑誌}, month = {Aug}, note = {Some of the organophosphorus pesticides posess the ability to produce delayed neurotoxicity in exposed animals. The nerve damage begins with ataxia of feet, and the symptoms in severe cases develop to fatal paralysis. The sensitivity to the characteristic neurotoxicity of such organophosphates is remarkably different among species of experimental animals. We used leptophos as a pesticide of this kind. We also used domestic fowls as experimental animals, and found that old hens showed clearly the higher attack rate by the chemical than young chickens did. Strange to say, leptophos remains in the fat tissue of hens for a few weeks. It was supposed that adipose tissue was a sort of storing place of leptophos, but the results of experiments showed the neurotoxicity intensified in the group of thin hens than in the group of obese ones. Recently it was proved that intravenous or dermal administration of leptophos caused similar neurotoxic effect in hens to the case by oral dosing, and pretreatment of hens with phenobarbital, the drug metabolizing enzyme inducer, significantly decreased neurotoxic signs. There is the latest paper that cyanofenphos, an organophosphorus pesticide of the same kind, causes hyperglucosaemia. It was suggested that glucose metabolism related to the specific neurotoxicity.}, pages = {489--493}, title = {有機燐殺虫剤の神経毒性に関する新知見}, volume = {101}, year = {1987} }