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Nutrition and Cancer

ß-Carotene and ß-Apo-14'-Carotenoic Acid Prevent the Reduction of Retinoic Acid Receptor ß in Benzo[a]pyrene-Treated Normal Human Bronchial Epithelial Cells¹

Nutrition and Cancer Biology Laboratory, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging and ^* Department of Biochemistry, School of Medicine, Tufts University, Boston, MA 02111

²To whom correspondence should be addressed. E-mail: xiang-dong.wang{at}tufts.edu.

Low-dose ß-carotene (BC) supplementation, such as would be provided by daily consumption of 5–9 servings of fruits and vegetables, has no apparent detrimental effects, but rather appears to have a protective effect against cigarette smoke–induced lung lesions in ferrets. In the present study, we investigated the effects of BC, ß-apo-14'-carotenoic acid (14'CA), or benzo[a]pyrene (BP; a primary lung carcinogen from cigarette smoke) treatments, either alone or in combination, on cell growth and expression of the retinoic acid receptor (RAR) of normal human bronchial epithelial (NHBE) cells. We found that both BC and 14'CA inhibited the growth of NHBE cells (P < 0.05) with or without BP. The level of RARß, a tumor suppressor, but not RAR or RAR, was reduced by 50% in the NHBE cells treated with BP. However, treatment with either BC or 14'CA significantly induced the expression of RARß in the NHBE cells, and prevented the reduction of RARß by BP. Furthermore, 14'CA transactivated the RARß promoter primarily via its conversion to retinoic acid (RA). In the presence of 3-mercaptopropionic acid, an inhibitor of fatty acid oxidation, both RA formation and transactivation activity from 14'CA were decreased. These observations indicate that the growth inhibitory effects of BC and ß-apo-carotenoic acid are through their conversion to RA and upregulation of RARß.

KEY WORDS: • ß-carotene • ß-apo-carotenoids • retinoic acid receptor • lung cancer

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