Relationship between oxidative metabolites of hydrazine and hydrazine-induced mutagenicity

Toxicol Lett. 1986 May;31(2):131-7. doi: 10.1016/0378-4274(86)90006-8.

Abstract

Hydrazine (Hz) mutagenicity was observed in a test using Escherichia coli B/r strain, WP2 uvrA and was enhanced by the addition of rat liver microsomal fraction containing a generating system, while the enhanced mutagenicity was diminished by the addition of metyrapone to the microsome-free levels. On the other hand, an NADPH-dependent difference spectrum of the metabolic intermediate of Hz-complex, characterized by a maximum level of 448 nm, was also inhibited by metyrapone. The results show that the oxidative intermediates, which are diimide and its precursor, hydrazine free radical [Biochem. Biophys. Res. Commun., 133 (1986) 1086], are responsible not only for hepatotoxicity but also for the enhancement of genotoxicity or mutagenicity.

MeSH terms

  • Animals
  • Escherichia coli
  • Hydrazines / antagonists & inhibitors
  • Hydrazines / metabolism
  • Hydrazines / toxicity*
  • Male
  • Metyrapone / pharmacology
  • Microsomes, Liver / drug effects*
  • Microsomes, Liver / metabolism
  • Mutagenicity Tests
  • Mutagens*
  • Oxidation-Reduction
  • Phenobarbital / pharmacology
  • Rats
  • Rats, Inbred Strains

Substances

  • Hydrazines
  • Mutagens
  • hydrazine
  • Phenobarbital
  • Metyrapone