Carcinogenesis, Vol. 22, No. 8, 1173-1178,
August 2001
© 2001 Oxford University Press
MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION |
Interactions of ß-carotene and cigarette smoke in human bronchial epithelial cells
Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ 85721-0207, USA
Results from recent intervention trials indicated that supplemental ß-carotene enhances lung cancer incidence and mortality among smokers. It was hypothesized that ß-carotene was exerting its deleterious effects through a prooxidant effect in the smoke-exposed lung. To test this hypothesis we examined the interactions of ß-carotene and cigarette smoke in transformed human bronchial epithelial cells. We studied the effects of ß-carotene supplementation on rates of gas phase smoke-induced lipid peroxidation, membrane damage and depletion of endogenous antioxidants in BEAS-2B cells. Gas phase cigarette smoke caused cellular ß-carotene levels to decrease over time. The oxidation of ß-carotene by smoke generated various oxidation products, including 4-nitro-ß-carotene, ß-apo-carotenals and ß-carotene epoxides. Peroxidation of membrane lipids by gas phase smoke progressed at a slower rate than did oxidation of ß-carotene and incorporation of ß-carotene into the cells did not enhance the overall rate of lipid peroxidation. Additionally, lactate dehydrogenase release during smoke exposure was also unaffected by the presence or absence of ß-carotene in cells. ß-Carotene incorporation in cells was not found to accelerate the rates of 
-tocopherol and glutathione depletion by cigarette smoke. Our results indicate that ß-carotene is more sensitive than lipids to cigarette smoke oxidation, but that this preferential oxidation of ß-carotene does not lead to a prooxidant effect in human bronchial epithelial cells.
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