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Abstract
Epidemiologically, a high-carotenoid intake via a fruit- and vegetable-rich diet is associated with a decreased risk of various forms of cancer. The mechanisms by which carotenoids exert this protective effect are controversial. In this study, we examined the potency of a range of carotenoids commonly found in human plasma to induce apoptosis in Jurkat E6.1 malignant T-lymphoblast cells. At a concentration of 20 w M, the order of potency to induce apoptosis after 24 h was: g -carotene > lycopene > lutein> g -cryptoxanthin=zeaxanthin. Canthaxanthin failed to induce apoptosis under these conditions. g -Carotene induced apoptosis in a time- and concentration-dependent manner with a lowest effective concentration of about 3 w M. Pre-conditioning of g -carotene for 72 h destroyed its pro-apoptotic activity almost completely, whereas degradation for 6 h or less did not, indicating that either g -carotene itself and/or an early degradation product of g -carotene are the death-inducing compounds. Apoptosis induced by g -carotene was characterized by chromatin condensation and nuclear fragmentation, DNA degradation, PARP cleavage and caspase-3 activation. The antioxidant BO-653 inhibited the degradation of g -carotene in vitro and significantly increased its cytotoxicity, indicating that a pro-oxidant effect of g -carotene is unlikely to cause its pro-apoptotic activity. The induction of apoptosis in transformed cells by carotenoids may explain their protective effect against cancer formation in humans. Possible pathways for induction of apoptosis by carotenoids are discussed.