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Relationship Between Oxidative Stress Markers and Endothelin-1 Levels in Newborns of Different Gestational Ages

机译:不同妊娠期新生儿氧化应激标记物和内皮素-1水平的关系

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Oxidative stress results from excessive reactive oxygen species formation and/or inadequate antioxidant defense. Premature and critically ill infants are especially susceptible due to an immature intrinsic antioxidant system that cannot fully compensate for a free radical load. Oxidative stress is also associated with endothelial dysfunction and alterations in Endothelin-1 (ET-1) signaling pathways. However, the effects of the complex interaction between oxidative stress and ET-1 in newborns are not well-understood. The objective of this pilot study was to determine the relationship between levels of common oxidative stress biomarkers [glutathione (GSH), malondialdehyde (MDA)] and ET-1 in newborns of different gestational ages. In a level IV NICU, 63 neonates were prospectively enrolled and divided into groups based on gestational age at birth: Early Preterm (24 0/7–30 6/7 weeks), Late Preterm (31 0/7–36 6/7 weeks), and Term (37 0/7–42 weeks). Umbilical cord (1.5 mL) and 24(±4) h of life (24 h) (1 mL) blood samples were collected for GSH, MDA, and ET-1 analyses. GSH, MDA, and ET-1 were determined using established methodology. Mean cord MDA levels for all age groups, Early Preterm (2.93 ± 0.08 pg/ml), Late Preterm (2.73 ± 0.15 pg/ml), and Term (2.92 ± 0.13 pg/ml), were significantly higher than those at 24 h of life ( p 0.05 and r 2 = 0.001, p 0.05, respectively) or 24 h of life (r 2 = 0.001, p 0.05 and r 2 = 0.03, p 0.05, respectively). Preterm neonates exposed to prenatal corticosteroids (1.87 ± 0.31 pg/ml) had lower cord MDA levels than non-exposed neonates (2.85 ± 0.12 pg/ml) ( p 0.05). Both cord and 24 h OS markers were significantly higher in neonates treated with oxygen therapy ( p 0.005 and p 0.05, respectively) than those who did not receive supplemental oxygen. Oxidative stress markers (MDA and GSH) and ET-1 levels act independently. MDA is higher in cord blood than at 24 h of life regardless of gestational age. In preterm neonates, ET-1 levels are higher in umbilical cord blood compared to 24 h of life.
机译:氧化应激由过量的反应性氧物种形成和/或不足的抗氧化剂防御。由于未成熟的内在抗氧化系统,婴儿的过早和严重的婴儿特别易于抑制自由基负荷。氧化应激也与内皮素-1(ET-1)信号传导途径中的内皮功能障碍和改变相关。然而,在新生儿之间氧化应激和ET-1之间的复杂相互作用的影响是不太理解的。该试点研究的目的是确定常见氧化应激生物标志物水平之间的关系[谷胱甘肽(GSH),丙二醛(MDA)]和ET-1在不同妊娠期的新生儿。在IV级尼卡苏级,在出生时期前瞻性年龄(24 0 / 7-30 6/7周),早期早产(31 0 / 7-36 6/7周6/7周)和术语(37 0/7-42周)。为GSH,MDA和ET-1分析收集寿命(24小时)(24小时)(24小时)(1mL)血液样品的脐带(1.5mL)和24(±4)H.使用已建立的方法确定GSH,MDA和ET-1。平均脊髓MDA水平适用于所有年龄组,早期早产(2.93±0.08 pg / ml),晚期早产(2.73±0.15pg / ml),术语(2.92±0.13pg / ml)显着高于24小时寿命(P 0.05和R 2 = 0.001,P> 0.05)或寿命24小时(R 2 = 0.001,P&GT; 0.05和R 2 = 0.03,P> 0.05)。暴露于产前皮质类固醇的早产儿(1.87±0.31pg / ml)具有比未暴露的新生儿(2.85±0.12pg / ml)的帘线MDA水平降低(P <0.05)。用氧疗法处理的新生儿(P <0.005和P <0.05分别)帘线和24小时OS标记显着高于未收到补充氧的那些。氧化应激标记物(MDA和GSH)和ET-1水平独立起作用。无论妊娠年龄如何,MDA都比脐带血高于生命的24小时。在早产新生儿中,脐带血中的ET-1水平较高,而生命的24小时则较高。

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