Astaxanthin prevents in vitro auto-oxidative injury in human lymphocytes

被引:51
作者
Bolin, Anaysa P. [1 ]
Macedo, Rita C. [1 ]
Marin, Douglas P. [1 ]
Barros, Marcelo P. [2 ]
Otton, Rosemari [1 ,2 ]
机构
[1] Univ Cruzeiro Sul, Postgrad Program Hlth Sci, Cellular Physiol Lab, CBS, BR-03342000 Sao Paulo, Brazil
[2] Univ Cruzeiro Sul, Postgrad Program Human Movement Sci, Inst Phys Act & Sport Sci, BR-03342000 Sao Paulo, Brazil
基金
巴西圣保罗研究基金会;
关键词
Antioxidant; Apoptosis; Astaxanthin; Carotenoid; Lymphocyte; Oxidative stress; HYDROGEN-PEROXIDE; GENE-EXPRESSION; STRESS; CAROTENOIDS; MECHANISM; INFLAMMATION; MACROPHAGES; ANTIOXIDANT; SUPEROXIDE; LUTEIN;
D O I
10.1007/s10565-010-9156-4
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Upon mitogen sensitization, lymphocytes undergo proliferation by oxyradical-based mechanisms. Through continuous resting-restimulation cycles, lymphocytes accumulate auto-induced oxidative lesions which lead to cell dysfunction and limit their viability. Astaxanthin (ASTA) is a nutritional carotenoid that shows notable antioxidant properties. This study aims to evaluate whether the in vitro ASTA treatment can limit oxyradical production and auto-oxidative injury in human lymphocytes. Activated lymphocytes treated with 5 A mu M ASTA showed immediate lower rates of O (2) (aEuro cent a') /H2O2 production whilst NOaEuro cent and intracellular Ca2+ levels were concomitantly enhanced (a parts per thousand currency sign4 h). In long-term treatments (> 24 h), the cytotoxicity test for ASTA showed a sigmoidal dose-response curve (LC50 = 11.67 A +/- 0.42 A mu M), whereas higher activities of superoxide dismutase and catalase in 5 A mu M ASTA-treated lymphocytes were associated to significant lower indexes of oxidative injury. On the other hand, lower proliferative scores of ASTA lymphocytes might be a result of diminished intracellular levels of pivotal redox signaling molecules, such as H2O2. Further studies are necessary to establish the ASTA-dose compensation point between minimizing oxidative damages and allowing efficient redox-mediated immune functions, such as proliferation, adhesion, and oxidative burst.
引用
收藏
页码:457 / 467
页数:11
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