促氧化剂对早产儿支气管肺发育不良的危害

Mariana Ceahlau, Rodica Selevestru, Olga Tagadiuc, Svetlana Sciuca
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摘要

介绍。氧化应激可以定义为包括生命体(细胞器、细胞、器官/组织)在内的某一系统氧化还原状态失衡,过量产生活性氧和/或活性氮种(ROS/RNS),超过抗氧化防御系统的能力,具有减缓甚至阻止大分子氧化损伤的能力。氧化应激是包括肺部疾病在内的多种疾病的致病机制。材料和方法。81例早产儿被分为主组(支气管肺发育不良早产儿)和对照组(无支气管肺发育不良早产儿)。对对照组进行临床、仪器和实验室(TPA、促氧化-抗氧化平衡、一氧化氮代谢和丙二醛)的前瞻性评估。采用Microsoft Excel、MedCalc和SPSS对数据进行统计分析,并采用列联表分析(Contingency Table Analysis)来评价诊断试验的性能。结果。发现患有BPD的早产儿患病率降低了29% (p <0.001),促氧化-抗氧化平衡(PAB)和一氧化氮代谢物(NO)水平降低12% (p <0.001),与对照组相比。组织氧化损伤标志物评估显示显著62% (p <0.001)丙二醛(MDA)含量增加4.86倍(p <0.001)与对照组相比,支气管肺发育不良儿童的总抗氧化活性(TPA)增加。我们的研究证实,TPA、PAB、MDA和NO值是支气管肺发育不良儿童缺氧组织损伤的可靠指标,可推荐用于评估氧化应激强度。结论。肺支气管发育不良的特点是促氧化-抗氧化过程失衡,促氧化过程加剧,引发氧化/亚硝化应激和重要化合物的恶化。
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Harmfulness of prooxidants in bronchopulmonary dysplasia in preterm children
Introduction. Oxidative stress can be defined as the imbalance of the redox state of a certain system including living one (organelle, cell, organ/tissue), which excessively produces reactive oxygen and/or reactive nitrogen species (ROS/RNS) that exceed the capacity of the antioxidant defense system, which have the ability to slow down or even prevent the oxidative damage of macromolecules. Oxidative stress is a pathogenic mechanism of a large variety of diseases, including pulmonary one. Material and methods. 81 preterm born children included in the study were divided into the main group – preterm children with bronchopulmonary dysplasia (BPD), and the control group – preterm children without BPD. The comparison groups were prospectively evaluated clinical, instrumental and laboratory (TPA, prooxidant-antioxidant balance, nitric oxide metabolistes and MDA). Data were statistically analyzed using Microsoft Excel, MedCalc and SPSS and Contingency Table Analysis as a way to evaluate the performance of a diagnostic test. Results. In preterm children with BPD were found to be decreased by 29% (p < 0.001) the prooxidant-antioxidant balance (PAB) and the nitric oxide metabolistes (NO) level by 12% (p < 0.001) compared to children in the control group. The assessment of tissue oxidative damage markers revealed a significant 62% (p < 0.001) increase in malonic dialdehyde (MDA) content and a 4.86-fold (p < 0.001) increase in total prooxidant activity (TPA) in children with bronchopulmonary dysplasia compared to children in the control group. Our study confirms that TPA, PAB, MDA and NO values are reliable markers of hypoxic tissue damage at children with bronchopulmonary dysplasia and can be recommended for assessing the intensity of oxidative stress. Conclusions. Pulmonary bronchodysplasia is characterized by the imbalance of prooxidant-antioxidant processes with the exacerbation of prooxidant ones that trigger the oxidative/nitrosative stress and the deterioration of vital chemical compounds.
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