Abstract

The effect of four carotenoids ( β-carotene, lutein, bixin and canthaxanthin) on the respiratory burst of rat peritoneal macrophages was investigated. The results obtained showed that carotenoids suppressed the luminol-dependent chemiluminescence generated from PMA-stimulated macrophages at the beginning and after 2 min of the stimulation. Canthaxanthin and bixin had higher suppressive activity than β-carotene and lutein. The changes in absorption spectra of carotenoids showed that the absorption by carotenoids was diminished during the stimulation of macrophages by PMA and their absorption peaks were either further diminished or blue-shifted after addition of l-arginine to the system, indicating that the carotenoids were consumed and converted to new compounds during the two processes. By using cell-free systems, it was found that carotenoids could scavenge superoxide anion generated by xanthine/xanthine oxidase system. Their ability to scavenge superoxide anion decreased in the order of canthaxanthin>bixin>lutein> β-carotene. Canthaxanthin also showed the scavenging effect on superoxide anion generated from irradiation of riboflavin. The hydroxyl radical scavenging activity of carotenoids was investigated in the reaction system of Fe 2+ and H 2O 2. There was little difference among their activities. The reaction between carotenoids and nitric oxide led to the decreasing absorption between 400 and 540 nm and the concomitant appearance of the new absorption peaks between 330 and 395 nm. Bleaching of β-carotene, bixin and canthaxanthin by peroxynitrite resulted in the increasing absorption between 290 and 365 nm and the diminishing absorption between 400 and 500 nm. But the increasing absorption between 280 and 490 nm was observed in bleaching of lutein by peroxynitrite. Carotenoids inhibited thiobarbituric acid-reactive substance (TBARS) formation in AAPH-induced lipid peroxidation of PC liposomes in air. The results suggest that the suppressive effect of carotenoids on the respiratory burst of macrophages may be just a way by which carotenoids in vivo protect host cells and tissues from harmful effects of oxygen metabolites overproduced by macrophages and enhance the generation of specific immune responses.

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