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中性粒细胞对缺氧/复氧诱导的氧化应激的耐受性。

Neutrophil tolerance to oxidative stress induced by hypoxia/reoxygenation.

作者信息

Sureda Antoni, Batle Joan M, Tauler Pere, Cases Nuria, Aguiló Antoni, Tur Josep A, Pons Antoni

机构信息

Laboratori de Ciències de l'Activitat Física, Departament de Biologia Fonamental i Ciències de la Salut, Universitat de les Illes Balears, Campus Universitari, Crtra. Valldemossa, Km 7.5, E-07122-Palma de Mallorca, Illes Balears, Spain.

出版信息

Free Radic Res. 2004 Sep;38(9):1003-9. doi: 10.1080/10715760400000984.

Abstract

Repetitive episodes of hypoxia/reoxygenation induce cellular adaptations resulting in a tolerance process against oxidative stress. We studied the effects of chronic episodes of hypoxia/reoxygenation on neutrophil antioxidant defenses, neutrophil oxidative capability, and oxidative damage induced in neutrophils and plasma. Seven professional apnea divers participated in the study. Blood samples were taken under basal conditions, after a diving apnea session, and under basal conditions after five consecutive days of diving apnea sessions (basal post-diving). Chronic episodes of hypoxia/reoxygenation increased malondialdehyde (MDA), carbonyl derivates and creatine kinase (CPK) in plasma. Neutrophil catalase (CAT) levels were higher in basal post-diving. Neutrophil oxidative burst was maintained after diving, although the maximum response was delayed in basal post-diving. Neutrophil thioredoxin reductase (TR) activity increased in basal post-diving, and glutathione reductase (GR) activity was maintained. Chronic, repetitive episodes of diving apnea induce neutrophil adaptations in order to delay the oxidative burst response and to facilitate protein reduction. Diving apnea could be a good model to study tolerance to the oxidative stress generated by hypoxia/ reoxygenation.

摘要

反复的缺氧/复氧发作会诱导细胞适应性变化,从而产生针对氧化应激的耐受过程。我们研究了慢性缺氧/复氧发作对中性粒细胞抗氧化防御、中性粒细胞氧化能力以及中性粒细胞和血浆中诱导的氧化损伤的影响。七名专业潜水憋气者参与了该研究。在基础条件下、一次潜水憋气后以及连续五天潜水憋气后(潜水后基础状态)采集血样。慢性缺氧/复氧发作会使血浆中的丙二醛(MDA)、羰基衍生物和肌酸激酶(CPK)升高。潜水后基础状态下中性粒细胞过氧化氢酶(CAT)水平更高。潜水后中性粒细胞氧化爆发得以维持,尽管在潜水后基础状态下最大反应有所延迟。潜水后基础状态下中性粒细胞硫氧还蛋白还原酶(TR)活性增加,谷胱甘肽还原酶(GR)活性得以维持。慢性、反复的潜水憋气发作会诱导中性粒细胞适应性变化,以延迟氧化爆发反应并促进蛋白质还原。潜水憋气可能是研究对缺氧/复氧产生的氧化应激耐受性的良好模型。

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