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Mutagenic synergy between paraoxon and plant‐activated m ‐phenylenediamine or 2‐acetoxyacetylaminofluorene
Author(s) -
Gichner Tomáš,
Velemínský Jiří,
Wagner Elizabeth D.,
Plewa Michael J.
Publication year - 1996
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/(sici)1098-2280(1996)27:1<59::aid-em8>3.0.co;2-9
Subject(s) - paraoxon , toxicology , biology , genetics , mutagen , chemistry , biochemistry , carcinogen , enzyme , acetylcholinesterase
Paraoxon (diethyl‐ p ‐nitrophenylphosphate) is the toxic, but non‐mutagenic metabolite of the organo‐phosphorus ester insecticide parathion. Although this agent has been used as a deacetylase inhibitor in many studies, we discovered a mutagenic synergy when paraoxon was incubated with plant‐activated m ‐phenylenediamine ( m PDA) or with direct‐acting 2‐acetoxyacetylaminofluorene (2AAAF) and S. typhimurium tester strains. Using non‐toxic concentrations of plant‐activated m PDA and paraoxon a 10‐fold increase in the mutant yield of S. typhimurium was observed. The mutagenicity of the plant‐activated m PDA product required that O ‐acetyltransferase (OAT) be expressed by the S. typhimurium tester strain. However, the paraoxon‐dependent mutagenic synergy was observed using the direct‐acting arylamine metabolite, 2AAAF, with strains YG1024, TA98 and TA98/1,8‐DNP 6 regardless of their OAT activity. This mutagenic synergy is dependent upon the presence of an activated acetylated form of the arylamine. The data presented here demonstrate that this mutagenic synergy is limited to paraoxon and not to the parent compound (parathion) or to a major metabolite of parathion ( p ‐nitrophenol). © 1996 Wiley‐Liss, Inc.