title: Astaxanthin addition improves human neutrophils function: in vitro study.
abstract: OBJECTIVE
  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.
authors.affiliation: Postgraduate Program, Health Science, CBS, Cruzeiro do Sul University, Avenida Regente Feijó, 1295. Tatuapé, São Paulo, SP CEP 03342-000, Brazil.
authors.forename: Rita C
authors.initials: RC
authors.lastname: Macedo
authors.forename: Anaysa P
authors.initials: AP
authors.lastname: Bolin
authors.forename: Douglas P
authors.initials: DP
authors.lastname: Marin
authors.forename: Rosemari
authors.initials: R
authors.lastname: Otton
mesh_terms: D000975:Antioxidants / Q000494:pharmacology* / Q000633:toxicity; D002118:Calcium / Q000378:metabolism; D002176:Candida albicans / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D004121:Dimethyl Sulfoxide / Q000494:pharmacology / Q000633:toxicity; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006801:Humans; D007107:Immune System / Q000187:drug effects; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D009589:Nitrogen Oxides / Q000378:metabolism; D018384:Oxidative Stress; D010587:Phagocytosis / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D024341:Xanthophylls / Q000494:pharmacology / Q000633:toxicity
chemical_list: D000975:Antioxidants; D016207:Cytokines; D009589:Nitrogen Oxides; D017382:Reactive Oxygen Species; D024341:Xanthophylls; C005948:astaxanthine; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D002118:Calcium; D004121:Dimethyl Sulfoxide