Papp A, Németh I, Pelle Z
Szemészeti Klinika, Szent-Györgyi Albert Orvostudományi Egyetem, Szeged.
Orv Hetil. 1993 May 9;134(19):1021-6.
Oxygen radical injury may be one of the factors leading to Retinopathy of Prematurity. It occurs when the body's natural antioxidant capacity is overwhelmed by the free oxygen radicals produced during the perinatal period. Supposing, that premature infants may have defects in their antioxidant systems which can be detected later, even in childhood, a retrospective study of 36 patients of different ages (born prematurely) suffering from different stages of Retinopathy of Prematurity was carried out. According to our results, the signs of an acute oxidative stress could only be seen in the 3 month-old patients' erythrocyte glutathione redox system which was independent of the clinical severity of retinopathy. However, following an in vitro oxidative stress an increased susceptibility of erythrocytes was found in all our patient groups, which means, that the ratio of residual and original amounts of reduced glutathione was decreased and the amount of oxidated derivates of haemoglobin was increased. As selenium is an integral part of glutathione peroxidase enzyme, the very low selenium levels measured in all of our patient groups indicate a reduced glutathione peroxidase activity. The present study suggests, that selenium depletion even in Hungary might play an important role in the pathogenesis of Retinopathy of Prematurity.
氧自由基损伤可能是导致早产儿视网膜病变的因素之一。当围产期产生的游离氧自由基超过人体自然抗氧化能力时，就会发生这种损伤。假设早产儿的抗氧化系统可能存在缺陷，甚至在儿童期才能被检测到，我们对36例不同年龄（早产）且患有不同阶段早产儿视网膜病变的患者进行了一项回顾性研究。根据我们的结果，急性氧化应激的迹象仅在3个月大患者的红细胞谷胱甘肽氧化还原系统中可见，且与视网膜病变的临床严重程度无关。然而，在体外氧化应激后，我们所有患者组的红细胞敏感性均增加，这意味着还原型谷胱甘肽的残留量与原始量之比降低，血红蛋白氧化衍生物的量增加。由于硒是谷胱甘肽过氧化物酶的组成部分，我们所有患者组中测得的极低硒水平表明谷胱甘肽过氧化物酶活性降低。本研究表明，即使在匈牙利，硒缺乏可能在早产儿视网膜病变的发病机制中起重要作用。
