Induction of apoptosis by deinoxanthin in human cancer cells.

Background: Deinoxanthin is unique carotenoid isolated from the radioresistant bacterium Deinococcus radiodurans. In the present study, the induction of apoptosis of cancer cells by deinoxanthin was investigated. Materials and Methods: Apoptotic effects were evaluated in HepG2, PC-3, and HT-29 cells, and were measured through cell viability, morphological changes, and a DNA fragmentation assay. Intracellular generation of reactive oxygen species (ROS) was measured using 5-(and 6-)-carboxy-2',7'-dichlorodihydrofluorescein diacetate (carboxy-H2DCF-DA). The expression of apoptotic and anti-apoptotic proteins was assayed by western blotting. Results: The half-maximal inhibitory concentration (IC50) values for deinoxanthin against the HepG2, HT-29, and PC-3 cell lines were 59 mu M, 61 mu M, and 77 mu M, respectively. Deinoxanthin treatment caused an increase in ROS in all tested cells, suggesting possible pro-oxidant activity of deinoxanthin. Pro-caspase-3 was degraded in cancer cells by deinoxanthin treatment. Moreover, BCL2 expression decreased, but that of BAX increased. Conclusion: The present findings demonstrate for the first time the novel functional property of deinoxanthin isolated from radioresistant bacteria as a potent inducer of apoptosis in cancer cells. These data suggest that deinoxanthin could be potentially useful as a chemopreventive agent.