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Considerations on the carcinogenicity of the mushroom poison gyromitrin and its metabolites
Author(s) -
Braun R.,
Dittmar W.,
Greeff U.
Publication year - 1981
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550010502
Subject(s) - chemistry , carcinogen , aqueous solution , dna , thymidine , dna damage , biochemistry , in vivo , uridine , toxicity , mushroom , hydrogen peroxide , rna , organic chemistry , biology , food science , microbiology and biotechnology , gene
Monomethylhydrazine (MMH) and unsymmetrical dimethylhydrazine (UDMH), but not N ‐methyl‐ N ‐formylhydrazine (MFH), a mushroom poison, can be oxidized by the weak oxidant 2,6‐dichlorophenol‐indophenol Hydrogen peroxide is formed by this oxidation, and has been found to cause decay of DNA in aqueous solution as measured by the decreased viscosity of a DNA solution in the presence of the hydrazines. Furthermore, MMH and UDMH but not MFH inhibit the incorporation of [ 3 H]thymidine and [ 3 H]uridine into DNA and RNA of Ehrlich ascites carcinoma (EAC) cells. These experiments show that MFH is an inactive compound in contrast to MMH and UDMH. Since the hydrolysis rate of MFH, to produce MMH, is low, it is concluded that MFH must be activated in vivo into toxic metabolites which are ultimately responsible for the known high carcinogenicity of MFH.

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