Astaxanthin prevents in vitro auto-oxidative injury in human lymphocytes.
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 microM ASTA showed immediate lower rates of O(2)(*-) /H(2)O(2) production whilst NO* and intracellular Ca(2+) levels were concomitantly enhanced (<or=4 h). In long-term treatments (>24 h), the cytotoxicity test for ASTA showed a sigmoidal dose-response curve (LC50 = 11.67 +/- 0.42 microM), whereas higher activities of superoxide dismutase and catalase in 5 microM 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 H(2)O(2). 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.
Cellular Physiology Laboratory, Postgraduate Program-Health Science, CBS, Cruzeiro do Sul University, Tatuapé, São Paulo, Brazil.
Anaysa P
AP
Bolin
Rita C
RC
Macedo
Douglas P
DP
Marin
Marcelo P
MP
Barros
Rosemari
R
Otton
D000328:Adult; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis; D002374:Catalase / Q000378:metabolism; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D005260:Female; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism / Q000494:pharmacology; D007497:Iridoviridae; D008214:Lymphocytes / Q000187:drug effects* / Q000378:metabolism*; D008297:Male; D008934:Mitogens / Q000494:pharmacology; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction; D013482:Superoxide Dismutase / Q000378:metabolism; D024341:Xanthophylls / Q000494:pharmacology
D000975:Antioxidants; D008934:Mitogens; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D024341:Xanthophylls; D009569:Nitric Oxide; C005948:astaxanthine; D006861:Hydrogen Peroxide; D002374:Catalase; D013482:Superoxide Dismutase; D004121:Dimethyl Sulfoxide