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Astaxanthin is a powerful natural biological antioxidant as well as a naturally occurring carotenoid pigment. It is a red pigment occurring naturally in a variety of organisms. Astaxanthin exhibits strong free radical scavenging activity and protects against lipid peroxidation and oxidative damage of LDL-cholesterol, cell membranes, cells and tissues. Studies suggest that it can be 10 times more powerful than other carotenoids and more than 500 times than vitamin E, as a biological antioxidant. There is a growing amount of scientific evidence not only on the safety of astaxanthin for human consumption but on the positive metabolic effect that it may have. Astaxanthin appears to be absorbed in the blood in the same way as other carotenoids which is through the intestinal mucosa.
Several studies have compared astaxanthin's antioxidant activity with that of other carotenoids. As is the case with other carotenoids, astaxanthin is a potent quencher of singlet oxygen. One comprehensive study found astaxanthin to be twice as effective as beta-carotene (and about 80 times more effective than vitamin E) in quenching singlet oxygen in chemical solution (Di Mascio et al . 1991); A second major antioxidant role of carotenoids is in the scavenging of free radicals. A study of carotenoid-radical reactions in chemical solution clearly demonstrated that reactivity rates depend not only on the carotenoid but also on the nature of the radical (Mortensen et al. 1997). In one study, astaxanthin was approximately as effective as canthaxanthin (a xanthophyll structurally similar to astaxanthin), and about 50% more effective than beta-carotene and zeaxanthin, in preventing fatty acid peroxidation in chemical solution (Terao 1989). In a membrane model, astaxanthin was found to be more effective at scavenging peroxyl radicals than was beta-carotene (Palozza and Krinsky 1992). Another study using membrane models found similar results, with astaxanthin better at delaying lipid peroxidation than zeaxanthin, canthaxanthin, or beta-carotene (Lim et al. 1992).
Di Mascio, P., Murphy, M.
E., and Sies, H. (1991) Antioxidant defense systems: the role of carotenoids,
tocopherols, and thiols. Am. J. Clin. Nutr., 53:194S-200S.
Astaxanthin, like vitamin E, is a lipophilic (fat-soluble) antioxidant, and thus might be expected to exert its antioxidant properties in lipid-rich cell membranes and tissues. It was shown in two published studies that, in rats deprived of vitamin E, the resistance of lipids (fats) to oxidation was largely restored by feeding the animals astaxanthin (Kurashige et al. 1990; Miki 1991). In the first study (Kurashige et al. 1990), rats were fed a vitamin E-deficient diet, with or without astaxanthin supplementation at 1 mg per 100 mg feed, for two to four months; control rats received a vitamin E-sufficient diet. Mitochondria were isolated from liver, and erythrocyte ghosts prepared from blood samples. Membrane preparations (intact mitochondria or erythrocyte ghosts) were subjected to oxidation by superoxide generated in situ by an iron-catalyzed xanthine oxidase system. An index of lipid peroxidation, the formation of thiobarbituric acid-reactive (TBA-reactive) substances, was measured colorimetrically. Mitochondria from vitamin E-deficient rats were preincubated with various concentrations of either astaxanthin or vitamin E, and then exposed to superoxide. The percent inhibition of TBA-reactant formation (as compared to controls with no added antioxidant) was measured. At all concentrations tested, astaxanthin inhibited the formation of TBA-reactants more effectively than did vitamin E, and the IC50 concentration was approximately 3 orders of magnitude lower for astaxanthin than for vitamin E. In this system, astaxanthin was a more effective antioxidant than was vitamin E. TBA-reactive metabolite levels were compared between erythrocyte ghost preparations from the three treatment groups. The amount of TBA-reactants was about 15-fold greater in the erythrocyte ghosts from vitamin E-deficient rats than in those from the control group. In erythrocyte ghosts from the astaxanthin-supplemented, vitamin E-deficient rats, the level of TBA-reactants was elevated only about 6-fold over that of the controls, i. e., 2.5-fold less than in the vitamin E-deficient, non-astaxanthin supplemented animals. This indicates that dietary administration of astaxanthin, in the absence of vitamin E, partially restored the in vitro oxidation resistance of erythrocyte membrane ghosts to the levels found in vitamin E-sufficient rats. In the second study (Miki 1991), rats were fed a vitamin E-deficient diet, with or without astaxanthin supplementation at 1 mg per 100 mg feed, for four weeks; control rats received a vitamin E-sufficient diet. The susceptibility to oxidation of erythrocyte ghosts was assayed by a similar xanthine oxidase-generated superoxide system and measurement of TBA-reactants. Lipid peroxidation was high in the vitamin E-deficient rats and negligible in control animals. Rats that received the astaxanthin supplementation had peroxidation levels about half that of the vitamin E-deficient rats, again indicating that dietary astaxanthin restored much though not all of the vitamin E-dependent oxidative resistance of the erythrocyte membranes. Learn about the Health Benefits of Astaxanthin & Canthaxanthin |
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