Journal Article

Inhibitory effects of 6-phenylhexyl isothiocyanate on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone metabolic activation and lung tumorigenesis in rats

Stephen S. Hecht, Neil Trushin, Jeffrey Rigotty, Steven G. Carmella, Anna Borukhova, Shobha Akerkar, Dhimant Desai, Shantu Amin and Abraham Rivenson

in Carcinogenesis

Volume 17, issue 9, pages 2061-2067
Published in print September 1996 | ISSN: 0143-3334
Published online September 1996 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/17.9.2061
Inhibitory effects of 6-phenylhexyl isothiocyanate on
                    4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone metabolic activation and lung
                    tumorigenesis in rats

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This study examined the effects of 6-phenylhexyl isothio-cyanate (PHITC) on lung tumorigenesis in F344 rats induced by the tobacco-specific nitrosamine 4-(methylnitros-amino)-1-(3-pyridyl)-1-butanone (NNK). Two biomarkers of NNK metabolism, 4-hydroxy-1-(3-pyridyl)-1-butanone (HPB)-releasing hemoglobin adducts and 4-(methylnitros-amino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronide (NNAL-Glue) in urine, were also quantified during the course of the tumor induction experiment. Rats were divided into groups as follows: (1) NNK, 2 p.p.m. in drinking water, 60 rats; (2) NNK, 2 p.p.m. in drinking water and PHITC, 1 μmol/g NIH-07 diet, 60 rats; (3) PHITC, 1 μmol/g NIH-07 diet, 20 rats; (4) control, 20 rats. PHITC was added to the diet for 1 week prior to and during 111 weeks of NNK treatment. There were no effects of PHITC on body weight, mortality, blood chemistry or hematology. Seventy percent of the rats treated with NNK had adenoma or adenocarcinoma of the lung. In the rats treated with NNK plus PHITC, the total percent incidence of lung tumors was 26% (P < 0.01 compared with NNK). PHITC had no effect on the total incidence of exocrine pancreatic tumors induced by NNK. The rats treated with PHITC and NNK had significantly lower levels of HPB-releasing hemoglobin adducts throughout the course of the bioassay than did those treated with NNK alone and significantly higher levels of NNAL plus NNAL-Glue excreted in urine at two time points during the bioassay. These results demonstrate that near lifetime administration of PHITC to rats strongly inhibits the metabolic activation and lung tumorigenicity of NNK.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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