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Biomedical subjects

J E CASIDA

Publications and source records attributed to J E CASIDA.

At least 19 recordsLinked to original sources
PubMed1964

ESTERASE INHIBITORS AS PESTICIDES.

Thirty years of testing has yielded over 120 esterase inhibitors in current use for pest control. Several hundred million pounds of these organophosphates and carbamates are employed each year as insecticides and acaricides and, to a much lesser extent, as anthelmintic agents, nematocides, and herbicides. Systemics or chemotherapeutic agents for control of insect pests of plants and animals first became practical with the organophosphates. Compounds of lower mammalian toxicity and other favorable biological properties continue to appear and displace established compounds and broaden the use areas. Problems of resistance and residues in certain areas of insect control by chlorinated hydrocarbons will result in a further shift to esterase-inhibitors for pest control. Interpretation of the potential hazards of pesticides to man is dependent on the availability of fundamental information on their modes of action combined with use experience; this knowledge is available for the organophosphates and carbamates that act as acetylcholinesterase inhibitors.

Animals↗
PubMed1964

NICOTINIC ACID ANALOGS: EFFECTS ON RESPONSE OF CHICK EMBRYOS AND HENS TO ORGANOPHOSPHATE TOXICANTS.

Embryonic abnormalities are known to be induced in chick embryos when they are injected with certain organophosphate insecticides prior to incubation. The marked teratogenic effects of Bidrin [3-(dimethoxyphosphinyloxy) N, N-dimethyl-cis-crotonamide] can be alleviated by many analogs of nicotinamide and nicotinamide adenine dinucleotide. Successive hydroxylation and N-dealkylation of Bidrin in the egg are not greatly altered by injection of nicotinamide. The delayed neurotoxicity in adult hens after administering tri-o-cresyl phosphate is also partially relieved by administering certain nicotinamide analogs.

Abnormalities, Drug-Induced↗
PubMed1962

Neurotoxic syndrome produced in chickens by a cyclic phosphate metabolite of tri-o-cresyl phosphate--a clinical and pathological study.

A clinical and neuropathological comparison was made between chickens poisoned with tri-o-cresyl phosphate and those treated with the major cyclic phosphate metabolite of tri-o-cresyl phosphate. Ataxia was evident with both materials, and the degree of peripheral neuropathy increased with higher doses of these agents. Morphological changes were evident with the onset of symptoms and increased in number as the neurological signs progressed. Demyelination of the spinal cord following administration of the metabolite occurred at doses considerably below those necessary to effect peripheral nerve degeneration. Axon and myelin damage was prominent with both agents. The relationship between these effects and those produced by certain other organophosphates such as dyflos (diisopropyl fluorophosphonate) is discussed.

Animals↗