Antioxidant activity of dietary canthaxanthin

Abstract

It has been suggested that canthaxanthin (CX), ß‐carotene, and other carotenoids may inhibit carcinogenesis via antioxidant activity. CX has been shown to inhibit lipid peroxidation in liposomes; this experiment was designed to assess the antioxidant activity of CX in biological membranes. Chicks were fed semipurifled diets supplemented with placebo beadlets or CX beadlets (5 g beadlets/kg diet; 0.5 g CX/kg diet) for five weeks. Diets were deficient in vitamin E and selenium to maximize the power of detecting an antioxidant effect of CX and to induce exudative diathesis, which is a vitamin E and selenium deficiency disease of chicks. Dietary CX had no effect on the onset, incidence, or severity of exudative diathesis. Liver homogenates from CX‐fed chicks exhibited significantly (p = 0.02) decreased formation of thiobarbituric acid‐reactive substances over time in ferrous ion‐induced peroxidations.

Because dietary CX increased hepatic α‐tocopherol content, subsequent peroxidations were conducted in membrane fractions prepared from placebo and CX livers matched for α‐tocopherol content. In this system, CX was marginally but inconsistently protective against peroxidation at both 15 torr O2 (p =: 0.12) and 150 ton O2 (p = 0.07). Nanomolar changes in hepatic α‐tocopherol, unlike CX, substantially altered rates of peroxidation. These results suggest that under these conditions, dietary CX increased resistance to lipid peroxidation primarily by enhancing membrane α‐tocopherol levels and secondarily by providing weak direct antioxidant activity.