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1.
Eur J Nutr ; 49(8): 447-57, 2010 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-20361333

RESUMO

PURPOSE: The aim of the present study was to evaluate the in vitro effect of carotenoid astaxanthin (ASTA) on the phagocytic and microbicidal capacities, cytokine release, and reactive oxygen species production in human neutrophils. METHODS: The following parameters were evaluated: cytotoxic effect of ASTA on human neutrophils viability, phagocytic and microbicidal capacities of neutrophils by using Candida albicans assay, intracellular calcium mobilization (Fura 2-AM fluorescent probe), superoxide anion (lucigenin and DHE probes), hydrogen peroxide (H2O2, phenol red), and nitric oxide (NO·) (Griess reagent) production, activities of antioxidant enzymes (total/Mn-SOD, CAT, GPx, and GR), oxidative damages in biomolecules (TBARS assay and carbonyl groups), and cytokine (IL-6 and TNF-alpha) release. RESULTS: Astaxanthin significantly improves neutrophil phagocytic and microbicidal capacity, and increases the intracellular calcium concentration and NO· production. Both functional parameters were accompanied by a decrease in superoxide anion and hydrogen peroxide and IL-6 and TNF-α production. Oxidative damages in lipids and proteins were significantly decreased after ASTA-treatment. CONCLUSIONS: Taken together our results are supportive to a beneficial effect of astaxanthin-treatment on human neutrophils function as demonstrated by increased phagocytic and fungicide capacity as well as by the reduced superoxide anion and hydrogen peroxide production, however, without affecting neutrophils capacity to kill C. albicans. This process appears to be mediated by calcium released from intracellular storages as well as nitric oxide production.


Assuntos
Antioxidantes/farmacologia , Neutrófilos/efeitos dos fármacos , Fagocitose/efeitos dos fármacos , Antioxidantes/toxicidade , Cálcio/metabolismo , Candida albicans/efeitos dos fármacos , Catalase/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Citocinas/metabolismo , Dimetil Sulfóxido/farmacologia , Dimetil Sulfóxido/toxicidade , Glutationa Peroxidase/metabolismo , Glutationa Redutase/metabolismo , Humanos , Sistema Imunitário/efeitos dos fármacos , Neutrófilos/metabolismo , Neutrófilos/fisiologia , Óxidos de Nitrogênio/metabolismo , Estresse Oxidativo , Espécies Reativas de Oxigênio/metabolismo , Superóxido Dismutase/metabolismo , Xantofilas/farmacologia , Xantofilas/toxicidade
2.
Cell Biol Toxicol ; 26(5): 457-67, 2010 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-20229275

RESUMO

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 (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.


Assuntos
Antioxidantes/farmacologia , Linfócitos/efeitos dos fármacos , Linfócitos/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Adulto , Apoptose , Catalase/metabolismo , Dimetil Sulfóxido/farmacologia , Feminino , Humanos , Peróxido de Hidrogênio/metabolismo , Peróxido de Hidrogênio/farmacologia , Iridoviridae , Masculino , Mitógenos/farmacologia , NF-kappa B/metabolismo , Óxido Nítrico/metabolismo , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Transdução de Sinais , Superóxido Dismutase/metabolismo , Xantofilas/farmacologia
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