Record Display for the EPA National Library Catalog


OLS Field Name OLS Field Data
Main Title Metabolism and Genotoxicity of 1-Nitropyrene.
Author Ball, L. M. ; Lewtas, J. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC.
Year Published 1984
Report Number EPA-600/D-84-086;
Stock Number PB84-168657
Additional Subjects Aromatic polycyclic hydrocarbons ; Toxicity ; Air pollution ; Metabolism ; Laboratory animals ; Chemical analysis ; Mutagens ; Rats ; Gas chromatography ; Mass spectroscopy ; Bioassay ; Combustion products ; Nitrogen organic compounds ; Pyrene/nitro ; Air pollution effects(Animals) ; High pressure liquid chromatography ; Pyrene/N-acetyl-amino
Library Call Number Additional Info Location Last
NTIS  PB84-168657 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 06/23/1988
Collation 17p
1-Nitropyrene (NP), a nitrated polycyclic aromatic hydrocarbon and a potent bacterial mutagen, has been identified in combustion emissions and may contribute to the burden of genotoxicity associated with air pollution. NP undergoes rapid metabolism by rat hepatic subcellular fractions (S-9, cytosol and microsomes) and isolated cells to both oxidised and reduced products. Metabolism is accompanied by extensive binding to endogenous protein and DNA in isolated hepatocytes, and to calf thymus DNA added to the subcellular fractions. Metabolites of NP have been isolated, identified and characterised by HPLC, HRGC/MS and chemical synthesis. In the intact rat NP is excreted in the urine as phenols of 1-nitropyrene (1-NP-6/8- and -3-OH) and of N-acetyl-1-aminopyrene (NAAP-6- and -8-OH), all extensively conjugated with glucuronic acid. Some of these metabolites are mutagens five-fold more potent in the Ames Salmonella assay than the parent compound. Studies in germ-free rats demonstrated that metabolism by the gut flora and enterohepatic recirculation play a vital role in the production of the highly mutagenic NAAP-6/8-OH. Metabolic species capable of causing genotoxic damage can thus be produced by mammalian mechanisms both alone and in conjunction with bacterial metabolism.