title: Carbonyl stress and a combination of astaxanthin/vitamin C induce biochemical changes in human neutrophils.
abstract: The purpose of the present study was to find out whether co-treatment of human neutrophils with high glucose and methylglyoxal (MGO) can alter the biochemical parameters of human neutrophils. We also examined if astaxanthin associated with vitamin C can improve those biochemical parameters. Neutrophils from healthy subjects were treated with 20mM of glucose and 30 μM MGO followed or not by the addition of the antioxidants astaxanthin (2 μM) and vitamin C (100 μM). MGO/high glucose treatment reduced the phagocytic capacity and the G6PDH, total/SOD and GR activities. Additionally, there was an increase in the activity of myeloperoxidase (MPO) with consequent increase in the hypochlorous acid production, CAT activity and in the release of IL-6 cytokine without changes in intracellular calcium mobilization. Our study also shows that the association of astaxanthin with vitamin C greatly improved neutrophil phagocytic capacity, decreasing all reactive oxygen species measured, pro-inflammatory IL-1β and TNF-α release, MPO activity and HClO production. The combination of astaxanthin with vitamin C alone has more antioxidant and anti-inflammatory effects than when they were in the presence of MGO/high glucose. Injury to the function of neutrophils due to high glucose and methylglyoxal appears not to involve oxidative stress or calcium release. The association of antioxidants astaxanthin and vitamin C promoted a significant improvement in the function of neutrophils and in the redox status.
authors: Postgraduate Program, Health Sciences, CBS, Universidade Cruzeiro do Sul, 03342000 São Paulo, SP, Brazil.
authors: B A
authors: BA
authors: Guerra
authors: A P
authors: AP
authors: Bolin
authors: R
authors: R
authors: Otton
mesh_terms: D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D002462:Cell Membrane / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004338:Drug Combinations; D005260:Female; D005343:Fibrinolytic Agents / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D009195:Peroxidase / Q000378:metabolism; D010587:Phagocytosis / Q000187:drug effects; D050050:Protein Carbonylation / Q000187:drug effects; D011765:Pyruvaldehyde / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D024341:Xanthophylls / Q000494:pharmacology; D055815:Young Adult
chemical_list: D000975:Antioxidants; D004338:Drug Combinations; D005343:Fibrinolytic Agents; C508600:IL6 protein, human; D015850:Interleukin-6; D017382:Reactive Oxygen Species; D024341:Xanthophylls; D011765:Pyruvaldehyde; C005948:astaxanthine; D005954:Glucosephosphate Dehydrogenase; D002374:Catalase; D009195:Peroxidase; D013482:Superoxide Dismutase; D005947:Glucose; D001205:Ascorbic Acid