期刊
CARCINOGENESIS
卷 22, 期 8, 页码 1173-1178出版社
OXFORD UNIV PRESS
DOI: 10.1093/carcin/22.8.1173
关键词
-
类别
资金
- NCI NIH HHS [CA56875] Funding Source: Medline
- NIEHS NIH HHS [ES06694] Funding Source: Medline
Results from recent intervention trials indicated that supplemental beta -carotene enhances lung cancer incidence and mortality among smokers. It was hypothesized that beta -carotene was exerting its deleterious effects through a prooxidant effect in the smoke-exposed lung. To test this hypothesis we examined the interactions of beta -carotene and cigarette smoke in transformed human bronchial epithelial cells. We studied the effects of beta -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 beta -carotene levels to decrease over time. The oxidation of beta -carotene by smoke generated various oxidation products, including 4-nitro-beta -carotene, beta -apo-carotenals and beta -carotene epoxides. Peroxidation of membrane lipids by gas phase smoke progressed at a slower rate than did oxidation of beta -carotene and incorporation of beta -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 beta -carotene in cells. beta -Carotene incorporation in cells was not found to accelerate the rates of alpha -tocopherol and glutathione depletion by cigarette smoke. Our results indicate that beta -carotene is more sensitive than lipids to cigarette smoke oxidation, but that this preferential oxidation of beta -carotene does not lead to a prooxidant effect in human bronchial epithelial cells.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据