FURTHER TOXICOLOGIC STUDIES OF ACUTE HYDRAZINE TOXICITY IN MICE.
Rept. for 1 Jul 65-31 Mar 66.
CITY OF HOPE MEDICAL CENTER DUARTE CALIF DEPT OF BIOCHEMISTRY
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Toxicologic studies of acute hydrazine toxicity in mice were continued. The results indicate that acute toxicity of hydrazine probably is not mediated through a histamine-release mechanism. Various experiments showed that the type of lethal seizure produced by hydrazine probably has no relationship to the sound-induced seizures in susceptible strains of mice. It was found that sodium phenobarbital had a marked protective effect against hydrazine toxicity when given in subhypnotic amounts. Sodium phenobarbital had an additive protective effect when it was administered together with the previously studied protective mixture AGKO containing arginine, glutamate, alpha-ketoglutarate, and oxalacetate. NaBr also was found to be protective and was found to act additively with either sodium phenobarbital or with the AGKO mixture. It was found in the course of the above experiments that imidazoleacetic acid, a substance not protecting mice against acute hydrazine toxicity, had interesting analgesic and hypnotic effects in mice. The quantitative aspects of these effects were worked out, and it is suggested that this agent should be explored further as a possibility for human use. Author