Hypoxia/reoxygenation and vitamin c intake influence no synthesis and antioxidant defenses of neutrophils

Oxidative stress induced by hypoxia/reoxygenation mediates the pathophysiological consequence of ischemia/reperfusion and human diseases. Diving apnea could be a good model of oxidative stress induced by hypoxia/reoxygenation. We studied the influence of vitamin C diet supplementation on the respons...

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Veröffentlicht in:Free radical biology & medicine 2004-12, Vol.37 (11), p.1744-1755
Hauptverfasser: Sureda, Antoni, Batle, Joan M., Tauler, Pedro, Aguiló, Antoni, Cases, Nuria, Tur, Josep A., Pons, Antoni
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Sprache:eng
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Zusammenfassung:Oxidative stress induced by hypoxia/reoxygenation mediates the pathophysiological consequence of ischemia/reperfusion and human diseases. Diving apnea could be a good model of oxidative stress induced by hypoxia/reoxygenation. We studied the influence of vitamin C diet supplementation on the response of neutrophil antioxidant defenses, NO production, and redox status to diving apnea. Seven professional apnea divers participated in a double-blind cross study. Divers were assigned to either vitamin C-supplemented (1 g/d for a week) or placebo groups. Blood samples were taken under basal conditions, immediately after diving apnea for 4 h and after 1 h of recovery. Plasma vitamin C increased only in the supplemented group after diving and was maintained high in recovery. Diving apnea decreased neutrophil GSH/GSSG ratio in both groups, but maintained protein carbonyl derivates. Neutrophil catalase activity and levels and glutathione peroxidase activity were lower in the supplemented group than in the placebo group after diving. iNOS and nitrite levels decreased only in the supplemented group after diving and recovery. Diving apnea induced oxidative stress and initiated neutrophil reactions that resemble the acute-phase immune response with increased myeloperoxidase activity in neutrophils. Diet supplementation with vitamin C reduced neutrophil iNOS levels and NO production.
ISSN:0891-5849
1873-4596
DOI:10.1016/j.freeradbiomed.2004.07.033