Carcinogenesis, Vol 18, 1855-1857, Copyright © 1997 by Oxford University Press
B Prokopczyk, S Amin, DH Desai, C Kurtzke, P Upadhyaya and K El-Bayoumy
We reported earlier that continuous feeding of 1,4-
phenylenebis(methylene)selenocyanate (p-XSC) inhibited lung tumor induction
by the tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-
(3-pyridyl)-1-butanone (NNK) in the A/J mouse (El-Bayoumy et al.,
Carcinogenesis, 14, 1111-1113, 1993). The present investigation was
designed to determine whether p-XSC inhibits pulmonary neoplasia induced by
NNK in female A/J mice during the initiation phase of carcinogenesis or
during the post-initiation phase. The naturally occurring selenomethionine
was also included in this study. Doses higher than 4 p.p.m. of
selenomethionine can induce toxic effects, therefore, dietary
supplementation of this compound was selected at a dose level of 3.75
p.p.m. However, we were able to give p-XSC at selenium levels of 7.5 and 15
p.p.m., as mice can tolerate such doses in this form without any adverse
effects. NNK was given by a single i.p. injection at dose of 10 micromol in
0.1 ml of saline. Selenomethionine did not show chemopreventive activity
when administered in either phase of tumorigenesis. In contrast, p-XSC
significantly reduced lung tumor multiplicity regardless of whether it was
given during the initiation phase of tumorigenesis (P = 0.0009 at both
levels of selenium) or post-initiation (P = 0.0009 at 15 p.p.m. and P =
0.036 for 7.5 p.p.m.). This is the first report describing that the
synthetic organoselenium compound, p-XSC, can effectively block and
suppress chemically (NNK)-induced lung tumor development in mice.
ARTICLES
Effects of 1,4-phenylenebis(methylene)selenocyanate and selenomethionine on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone- induced tumorigenesis in A/J mouse lung
American Health Foundation, Valhalla, NY 10595, USA.
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