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
相关论文
共 52 条
[1]  
AEBI H, 1984, METHOD ENZYMOL, V105, P121
[2]   DNA damage and susceptibility to oxidative damage in lymphocytes:: effects of carotenoids in vitro and in vivo [J].
Astley, SB ;
Hughes, DA ;
Wright, AJA ;
Elliott, RM ;
Southon, S .
BRITISH JOURNAL OF NUTRITION, 2004, 91 (01) :53-61
[3]   β-Carotene inhibits inflammatory gene expression in lipopolysaccharide-stimulated macrophages by suppressing redox-based NF-κB activation [J].
Bai, SK ;
Lee, SJ ;
Na, HJ ;
Ha, KS ;
Han, JA ;
Lee, H ;
Kwon, YG ;
Chung, CK ;
Kim, YM .
EXPERIMENTAL AND MOLECULAR MEDICINE, 2005, 37 (04) :323-334
[4]   Astaxanthin and peridinin inhibit oxidative damage in Fe2+-loaded liposomes:: Scavenging oxyradicals or changing membrane permeability? [J].
Barros, MP ;
Pinto, E ;
Colepicolo, P ;
Pedersén, M .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2001, 288 (01) :225-232
[5]   ATP-dependent reduction of cysteine-sulphinic acid by S-cerevisiae sulphiredoxin [J].
Biteau, B ;
Labarre, J ;
Toledano, MB .
NATURE, 2003, 425 (6961) :980-984
[6]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[7]   Singlet oxygen quenching by dietary carotenoids in a model membrane environment [J].
Cantrell, A ;
McGarvey, DJ ;
Truscott, TG ;
Rancan, F ;
Böhm, F .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 2003, 412 (01) :47-54
[8]  
CARLBERG I, 1985, METHOD ENZYMOL, V113, P484
[9]  
Chew BP, 1996, ANTICANCER RES, V16, P3689
[10]  
Chew BP, 2003, ANTICANCER RES, V23, P3333