Black Homer S
Department of Dermatology, Baylor College of Medicine, Houston, Texas, 77030, USA.
Photochem Photobiol Sci. 2004 Aug;3(8):753-8. doi: 10.1039/b316438a. Epub 2004 Mar 19.
Beta-carotene is a strong singlet oxygen quencher and antioxidant. Epidemiologic studies have implied that an above average intake of the carotenoid might reduce cancer risks. Earlier studies found that the carotenoid, when added to commercial closed-formula rodent diets, provided significant photoprotection against UV-carcinogenesis in mice. Clinical intervention trials found that beta-carotene supplementation evoked no change in incidence of nonmelanoma skin cancer. However, when smokers were supplemented with the carotenoid a significant increase in lung cancer resulted. Recently, employing a beta-carotene supplemented semi-defined diet, not only was no photoprotective effect found, but significant exacerbation of UV-carcinogenesis occurred. Earlier, a mechanism, based upon redox potential of interacting antioxidants, was proposed in which beta-carotene participated with vitamins E and C to efficiently repair oxy radicals and, thus, thought to provide photoprotection. In this schema, alpha-tocopherol would first intercept an oxy radical. In terminating the radical-propagating reaction, the tocopherol radical cation is formed which, in turn, is repaired by beta-carotene to form the carotenoid radical cation. This radical is repaired by ascorbic acid (vitamin C). As the carotenoid radical cation is a strongly oxidizing radical, unrepaired it could contribute to the exacerbating effect on UV-carcinogenesis. Thus, vitamin C levels could influence the levels of the pro-oxidant carotenoid radical cation. However, when hairless mice were fed beta-carotene supplemented semi-defined diet with varying levels of vitamin C (0-5590 mg kg(-1) diet) no effect on UV-carcinogenesis was observed. Lowering alpha-tocopherol levels did result in further increase of beta-carotene exacerbation, suggesting beta-carotene and alpha-tocopherol interaction. It was concluded that the non-injurious or protective effect of beta-carotene found in the closed-formula rations might depend on interaction with other dietary factors that are absent in the semi-defined diet. At present, beta-carotene use as a dietary supplement for photoprotection should be approached cautiously.
β-胡萝卜素是一种强大的单线态氧猝灭剂和抗氧化剂。流行病学研究表明,摄入高于平均水平的类胡萝卜素可能会降低患癌风险。早期研究发现,将这种类胡萝卜素添加到商业封闭式啮齿动物饮食中,能为小鼠提供显著的抗紫外线致癌光保护作用。临床干预试验发现,补充β-胡萝卜素并未改变非黑色素瘤皮肤癌的发病率。然而,给吸烟者补充这种类胡萝卜素会导致肺癌显著增加。最近,采用补充了β-胡萝卜素的半合成饮食,不仅未发现光保护作用,反而出现了紫外线致癌作用的显著加剧。此前,基于相互作用的抗氧化剂的氧化还原电位提出了一种机制,其中β-胡萝卜素与维生素E和C共同作用以有效修复氧自由基,因此被认为能提供光保护。在这个模式中,α-生育酚会首先拦截一个氧自由基。在终止自由基传播反应时,会形成生育酚自由基阳离子,而它又会被β-胡萝卜素修复形成类胡萝卜素自由基阳离子。这个自由基会被抗坏血酸(维生素C)修复。由于类胡萝卜素自由基阳离子是一种强氧化性自由基,如果未被修复,它可能会对紫外线致癌作用产生加剧影响。因此,维生素C水平可能会影响促氧化类胡萝卜素自由基阳离子的水平。然而,当给无毛小鼠喂食补充了β-胡萝卜素且维生素C水平不同(0 - 5590毫克/千克饮食)的半合成饮食时,未观察到对紫外线致癌作用有任何影响。降低α-生育酚水平确实导致β-胡萝卜素加剧作用进一步增强,这表明β-胡萝卜素和α-生育酚之间存在相互作用。得出的结论是,在封闭式日粮中发现的β-胡萝卜素的无伤害或保护作用可能取决于与半合成饮食中不存在的其他饮食因素的相互作用。目前,应谨慎对待将β-胡萝卜素用作光保护膳食补充剂的做法。