Effect of β-Carotene and Canthaxanthin ontert-Butyl Hydroperoxide-Induced Lipid Peroxidation in Murine Normal and Tumor Thymocytes

It has been reported that the anticarcinogenic effect of carotenoids could be related to an antioxidant mechanism. The antioxidant efficiency of β-carotene and canthaxanthin was evaluated in murine normal and tumor thymocytes. Normal and tumor cells were exposed under air totert-butyl hydroperoxide (t-BOOH) and lipid peroxidation was measured in the absence or in the presence of the two carotenoids. Our results show that: (a) Both carotenoids, added at effective and comparable concentrations (from 1 to 50 μM), were able to inhibit t-BOOH-induced malondialdehyde formation in a dose-dependent manner. (b) Canthaxanthin was a more potent antioxidant than β-carotene. (c) The inhibition of lipid peroxidation was greater in tumor thymocytes. (d) Carotenoids were consumed differentially during the incubation with the prooxidant. β-Carotene was consumed faster than canthaxanthin and in a larger amount in tumor than in normal thymocytes. The addition of the iron chelator deferoxamine or the SH group reducing agent dithiothreitol reduced t-BOOH-induced β-carotene consumption in tumor cells but not in normal ones. (e) The loss of endogeneous α-tocopherol induced by t-BOOH was enhanced by the addition of β-carotene, suggesting the possibility of oxidative interactions between the two antioxidants. These results confirmed the antioxidant effectiveness of carotenoids in normal and tumor cells, although differences depending on the kind of cells and carotenoids used were found.