Carcinogenesis, Vol 19, 2139-2143, Copyright © 1998 by Oxford University Press
GD Stoner, C Adams, LA Kresty, SG Amin, D Desai, SS Hecht, SE Murphy and MA Morse
The ability of dietary isothiocyanates to inhibit the esophageal metabolism
of N'-nitrosonornicotine (NNN) was examined in F344 rats. Following feeding
of benzyl isothiocyanate (BITC), phenethyl isothiocyanate (PEITC),
3-phenylpropyl isothiocyanate (PPITC), 4- phenylbutyl isothiocyanate
(PBITC) or 6-phenylhexyl isothiocyanate for 2 weeks, rats were killed and
the esophagi were incubated in vitro with [5-3H]NNN. While dietary BITC,
PEITC and PBITC all decreased NNN metabolism, dietary PPITC had the
greatest effect, yielding inhibition ranging from 55 to 91% of the control
production of various NNN metabolites. To determine the chemopreventive
efficacy of PPITC on NNN- induced esophageal tumorigenesis, rats were fed
AIN-76A diets containing 0, 1.0 or 2.5 micromol/g PPITC and were given
untreated drinking water or drinking water containing 5 p.p.m. NNN. After
87 weeks, the experiment was terminated and the esophageal tumors were
counted. Rats that were given untreated drinking water developed no tumors.
Rats that were given 5 p.p.m. NNN and unadulterated AIN-76A diet had an
esophageal tumor incidence of 71% and a multiplicity of 1.57 tumors/animal.
The two dietary concentrations of PPITC reduced the incidence and
multiplicity of NNN-induced esophageal tumors by >95%. These results
demonstrate the remarkable chemopreventive efficacy of PPITC in the
NNN-induced esophageal tumor model.
ARTICLES
Inhibition of N'-nitrosonornicotine-induced esophageal tumorigenesis by 3-phenylpropyl isothiocyanate
Division of Environmental Health Sciences, The Ohio State University School of Public Health and The Ohio State University Comprehensive Cancer Center, Ohio State University, CHRI, Columbus 43210, USA. stoner.21@osu.edu
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