Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans

Jean Soon Park, Jong Hee Chyun, Yoo Kyung Kim, Larry L Line, Boon P Chew, Jean Soon Park, Jong Hee Chyun, Yoo Kyung Kim, Larry L Line, Boon P Chew

Abstract

Background: Astaxanthin modulates immune response, inhibits cancer cell growth, reduces bacterial load and gastric inflammation, and protects against UVA-induced oxidative stress in in vitro and rodent models. Similar clinical studies in humans are unavailable. Our objective is to study the action of dietary astaxanthin in modulating immune response, oxidative status and inflammation in young healthy adult female human subjects.

Methods: Participants (averaged 21.5 yr) received 0, 2, or 8 mg astaxanthin (n = 14/diet) daily for 8 wk in a randomized double-blind, placebo-controlled study. Immune response was assessed on wk 0, 4 and 8, and tuberculin test performed on wk 8.

Results: Plasma astaxanthin increased (P < 0.01) dose-dependently after 4 or 8 wk of supplementation. Astaxanthin decreased a DNA damage biomarker after 4 wk but did not affect lipid peroxidation. Plasma C-reactive protein concentration was lower (P < 0.05) on wk 8 in subjects given 2 mg astaxanthin. Dietary astaxanthin stimulated mitogen-induced lymphoproliferation, increased natural killer cell cytotoxic activity, and increased total T and B cell subpopulations, but did not influence populations of Thelper, Tcytotoxic or natural killer cells. A higher percentage of leukocytes expressed the LFA-1 marker in subjects given 2 mg astaxanthin on wk 8. Subjects fed 2 mg astaxanthin had a higher tuberculin response than unsupplemented subjects. There was no difference in TNF and IL-2 concentrations, but plasma IFN-gamma and IL-6 increased on wk 8 in subjects given 8 mg astaxanthin.

Conclusion: Therefore, dietary astaxanthin decreases a DNA damage biomarker and acute phase protein, and enhances immune response in young healthy females.

Figures

Figure 1
Figure 1
Concentrations of plasma astaxanthin in human subjects fed 0, 2 or 8 mg astaxanthin daily for 8 wk. a, b Different letters represent significant treatment differences (P < 0.05) as analyzed by protected LSD test. Values are means; variation is expressed as a representative overall standard error.
Figure 2
Figure 2
Lymphocyte proliferation induced with phytohemagglutinin, concanavalin A and pokeweed mitogen in human subjects fed 0, 2 or 8 mg astaxanthin daily for 8 wk. Responses to high concentrations of mitogens (10 mg phytohemmaglutinin/L, 10 mg concanavalin A/L and 5 mg pokeweed mitogen/L final concentration) are shown. a, b Different letters represent significant treatment differences (P < 0.05) as analyzed by protected LSD test. Values are means ± SEM.
Figure 3
Figure 3
Delayed-type hypersensitivity tuberculin test in human subjects fed 0, 2 or 8 mg astaxanthin daily for 8 wk. a, b Different letters represent significant treatment differences (P < 0.05) as analyzed by protected LSD test. Values are means ± overall standard error.
Figure 4
Figure 4
Plasma concentrations of plasma C-reactive protein in human subjects fed 0, 2 or 8 mg astaxanthin daily for 8 wk. a, b Different letters represent significant treatment differences (P < 0.05) as analyzed by protected LSD test. Values are means ± overall standard error.
Figure 5
Figure 5
Concentrations of plasma 8-hydroxy-2'-deoxyguanosine in human subjects fed 0, 2 or 8 mg astaxanthin daily for 8 wk. a, b Different letters represent significant treatment differences (P < 0.05) as analyzed by protected LSD test. Values are means ± overall standard error (OSE = Root MSE÷square root of n+1).

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Source: PubMed

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