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Oxygen Radical Disease in the Newborn Revisited: Oxidative Stress and Disease in the Newborn Period

机译:新生儿氧自由基病的再探讨:新生儿时期的氧化应激和疾病

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摘要

Thirty years ago, there was an emerging appreciation for the significance of oxidative stress in newborn disease. This prompted a renewed interest in the impact of oxygen therapy for the newborn in the delivery room and beyond, especially in premature infants. Today, the complexity of oxidative stress both in normal regulation and pathology is better understood, especially as it relates to neonatal mitochondrial oxidative stress responses to hyperoxia. Mitochondria are recipients of oxidative damage and have a propensity for oxidative self-injury that has been implicated in the pathogenesis of neonatal lung diseases. Similarly, both intrauterine growth restriction (IUGR) and macrosomia are associated with mitochondrial dysfunction and oxidative stress. Additionally, reoxygenation with 100% O2 in a hypoxic-ischemic newborn lamb model increased the production of pro-inflammatory cytokines in the brain. Moreover, the interplay between inflammation and oxidative stress in the newborn is better understood because of animal studies. Transcriptomic analyses have found a number of genes to be differentially expressed in murine models of bronchopulmonary dysplasia (BPD). Epigenetic changes have also been detected both in animal models of BPD and premature infants exposed to oxygen. Antioxidant therapy to prevent newborn disease has not been very successful; however, new therapeutic principles, like melatonin, are under investigation.
机译:30年前,人们逐渐认识到氧化应激在新生儿疾病中的重要性。这引起了人们对氧疗对分娩室及以后的新生儿,尤其是早产儿的影响重新产生兴趣。如今,人们已经更好地理解了正常调节和病理过程中氧化应激的复杂性,尤其是它与新生儿对高氧的线粒体氧化应激反应有关。线粒体是氧化损伤的接受者,并且具有氧化性自我伤害的倾向,这种倾向与新生儿肺部疾病的发病机制有关。同样,宫内生长受限(IUGR)和巨子症均与线粒体功能障碍和氧化应激相关。此外,在缺氧缺血性新生羔羊模型中用100%O2复氧会增加大脑中促炎性细胞因子的产生。此外,由于动物研究,对新生儿炎症和氧化应激之间的相互作用有了更好的了解。转录组学分析已经发现许多基因在支气管肺发育不良(BPD)的鼠模型中差异表达。在BPD的动物模型和暴露于氧气的早产儿中也都检测到表观遗传变化。预防新生儿疾病的抗氧化疗法不是很成功。然而,正在研究新的治疗原理,例如褪黑激素。

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