Further Study of the Mechanism of Acute Toxic Effects of 1,1-Dimethylhydrazine, Methylhydrazine, and 1,2-Dimethylhydrazine

Investigations were designed to explore mechanisms of toxic action of SDMH, UDMH, and MMH. SDMH is more toxic when administered in strongly acid (less than pH 1.0) or alkaline (pH 11.0) solutions than when administered in buffered solutions. The acute toxicity to mice of unbuffered SDMH- dihydrochloride is not different from hydrochloric acid. The tenfold difference between the acute toxicity of SDMH at 24 and 168 hours for mice is not seen in rats or dogs. The degree and time course of liver damage in mice is such that it is probably responsible for the delayed deaths seen in this species. The previously reported selective protective action of various substituted benzaldehydes against UDMH and MMH in mice was not observed in rats. Prophylactic treatment with amino-oxyacetic acid provided protection to rats against the lethal effects of UDMH, but not against the effects of MMH. The mechanism and site of action of UDMH (1,1-dimethylhydrazine), MMH (methylhydrazine), and SDMH (1,2-dimethylhydrazine) were investigated. Discrete localized lesions produced in specific areas of the otherwise intact brain stem by suction or electrolytic destruction modify or abolish UDMH-induced convulsions in dogs. The area from which these convulsions arise has been localized to a ventral mid-collicular site.