A STUDY OF THE MECHANISM OF ACUTE TOXIC EFFECTS OF HYDRAZINE, UDMH, MMH, AND SDMH.
Technical documentary rept., Sep 62-Sep 63,
HINE LABS INC SAN FRANCISCO CALIF
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The mechanism and site of toxic activity of hydrazine, UDMH 1,1-dimethylhydrazine, MMH methylhydrazine, and SDMH 1,2-dimethylhydrazine were investigated by acute toxicity studies in mice, by studying cardiovascular and autonomic effects in dogs, by noting the effect on convulsions of transection of the central nervous system at several levels in dogs, and by evaluating selected protective agents in mice. Four separate mechanisms of action are suggested by differences in pharmacologic activity. SDMH has a markedly delayed toxicity, in mice, as compared to the other hydrazines. MMH manifests its MAO inhibitory activity by intensifying the response to tyramine. Hydrazine convulsions are cortical in origin, while UDMH, SDMH and MMH convulsions originate in a pre-pontine area. Protection from convulsions and death due to hydrazine is afforded, in mice, by arginine or ornithine. Protection is provided from the effects of both UDMH and MMH, in mice, by pyridoxine and amino-oxyacetic acid. p-chlorobenzaldehyde and p-nitrobenzaldehyde protect against the effects of UDMH, but not MMH p-dimethylaminobenzaldehyde protects against the effects of MMH but not UDMH. Author