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Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans
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 o...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845588/ https://www.ncbi.nlm.nih.gov/pubmed/20205737 http://dx.doi.org/10.1186/1743-7075-7-18 |
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author | Park, Jean Soon Chyun, Jong Hee Kim, Yoo Kyung Line, Larry L Chew, Boon P |
author_facet | Park, Jean Soon Chyun, Jong Hee Kim, Yoo Kyung Line, Larry L Chew, Boon P |
author_sort | Park, Jean Soon |
collection | PubMed |
description | 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 T(helper), T(cytotoxic )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-γ 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. |
format | Text |
id | pubmed-2845588 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-28455882010-03-26 Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans Park, Jean Soon Chyun, Jong Hee Kim, Yoo Kyung Line, Larry L Chew, Boon P Nutr Metab (Lond) Research 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 T(helper), T(cytotoxic )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-γ 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. BioMed Central 2010-03-05 /pmc/articles/PMC2845588/ /pubmed/20205737 http://dx.doi.org/10.1186/1743-7075-7-18 Text en Copyright ©2010 Park et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Park, Jean Soon Chyun, Jong Hee Kim, Yoo Kyung Line, Larry L Chew, Boon P Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans |
title | Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans |
title_full | Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans |
title_fullStr | Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans |
title_full_unstemmed | Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans |
title_short | Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans |
title_sort | astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845588/ https://www.ncbi.nlm.nih.gov/pubmed/20205737 http://dx.doi.org/10.1186/1743-7075-7-18 |
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