© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 1, 60-66,
January 6, 1999
© 1999 Oxford University Press
REPORTS |
Retinoid Signaling and Activator Protein-1 Expression in Ferrets Given ß-Carotene Supplements and Exposed to Tobacco Smoke
Affiliations of authors: X.-D. Wang, N. I. Krinsky, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University and Department of Biochemistry, Tufts University School of Medicine, Boston, MA; C. Liu, R. T. Bronson, D. E. Smith, R. M. Russell, Jean Mayer United States Department of Agriculture Human Nutition Research Center on Aging at Tufts University.
Correspondence to: Xiang-Dong Wang, M.D., Ph.D., Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington St., Boston, MA 02111 (e-mail:Wang_CN{at}HNRC.TUFTS.EDU).
BACKGROUND: Epidemiologic studies have demonstrated that
individuals who eat more fruits and vegetables and/or have high levels
of serum ß-carotene have a lower risk of cancer, especially lung
cancer. However, recent human intervention studies using ß-carotene
supplements have shown an increase in the risk of lung cancer among
smokers and asbestos workers. In this study, we used an animal model
system to evaluate the hazard associated with a combination of
high-dose ß-carotene supplementation and tobacco smoking.
METHODS: Ferrets were given a ß-carotene supplement,
exposed to cigarette smoke, or both for 6 months. Cell proliferation
and squamous metaplasia in lung tissue were assessed by examination of
proliferating-cell nuclear antigen expression and histopathologic
examination, respectively. ß-Carotene and retinoid concentrations
in lung tissue and plasma samples were analyzed by high-performance
liquid chromatography. Expression of genes for retinoic acid receptors
(RARs) and activator protein-1 (encoded by the c-Jun and c-Fos genes)
in lung tissue specimens was examined by western blotting.
RESULTS: A strong proliferative response in lung tissue and
squamous metaplasia was observed in all ß-carotene-supplemented
animals, and this response was enhanced by exposure to tobacco smoke.
When compared with control groups, all three treatment groups had
statistically significantly lower concentrations of retinoic acid in
lung tissue, and they exhibited 18%-73% reductions in RARß
gene expression; however, RAR
and RAR
gene expression was not
reduced. Ferrets given a ß-carotene supplement and exposed to
tobacco smoke had threefold to fourfold elevated expression of the
c-Jun and c-Fos genes. CONCLUSIONS: Diminished retinoid
signaling, resulting from the suppression of RARß gene expression
and overexpression of activator protein-1, could be a mechanism to
enhance lung tumorigenesis after high-dose ß-carotene
supplementation and exposure to tobacco smoke.
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