Similarly, H. pylori-infected mice responded to astaxanthin treatment with a reduction in gastric inflammation (Bennedsen et al., 1999). Mice given astaxanthin also showed increased cytokine release from splenocytes. Nishino et al. have studied the ability of astaxanthin to inhibit spontaneous liver tumorigenesis in C3H/He mice (Nishino et al., 1999). Fifteen control mice were compared to an equal number of mice treated with astaxanthin (0.2 mg in 0.2 mL of corn oil, intragastric lavage, 3 times per week for 40 weeks). They found that treatment reduced the number of tumors from 0.87 in controls to 0.27 in treated animals (p < 0.05). The percentage of mice with tumors decreased from 53% in controls to 27% in treated animals. Chew has reported that astaxanthin was effective in limiting the growth of mammary tumors in mice (Chew et al., 1999). Tso and Lam treated rats with astaxanthin and found that they were less prone to photic damage than control animals, implying uptake of astaxanthin within the rat retina (Tso and Lam, 1996). Bendich reports that treatment of rats with astaxanthin produced an increase in HDL levels within the blood (Bendich, 1990).
These results are suggestive that the in vivo antioxidant function of astaxanthin may exert a positive influence on health status. Astaxanthin is clearly not an essential dietary component, nor does it have a normal functional role in humans, or for that matter, most animals. It nevertheless may be able to significantly reduce free radical damage in some tissues and its influence and effects should be further investigated. It is important to determine effects of different astaxanthin dosages, to what tissues astaxanthin is transported, and to what levels it accumulates in tissues.
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