Schmidt H, Grune T, Müller R, Siems W G, Wauer R R
Children's Hospital Singen, Germany.
Pediatr Res. 1996 Jul;40(1):15-20. doi: 10.1203/00006450-199607000-00003.
For quantitative evaluation of lipid peroxidation after perinatal hypoxia in umbilical arterial cord blood samples from 109 healthy, acidotic, and asphyctic neonates with a gestational age ranging from 26 to 41 wk, the levels of aldehydic lipid peroxidation products malondialdehyde (MDA) and 4-hydroxynon-2-enal (HNE) were measured. Furthermore, the concentrations of oxidized and reduced glutathione (GSSH and GSH) and the purine compounds hypoxanthine and uric acid were determined. With increasing gestational age MDA and HNE levels increased. Furthermore, an increased level of GSH was also found. After perinatal hypoxia the concentrations of MDA and HNE rose distinctly (p < 0.001), reflecting sensitively the extent of in vivo lipid peroxidation. HNE is proposed to be a new parameter for quantitative evaluation of posthypoxic cellular damage in the perinatal period. HNE is a more specific parameter for estimation of lipid peroxidation processes in comparison with MDA. Additionally, HNE is cytotoxic and mutagenic at nanomolar concentrations. The increased levels of both MDA and HNE were accompanied by a strong decrease of GSH concentrations (p < 0.001), indicating the rapid consumption of GSH via a glutathione peroxidase reaction but additionally the high reactivity of HNE with sulfhydryl groups. During oxygen deficiency, increased levels of hypoxanthine (p < 0.01) and uric acid (p < 0.05) were due to the accelerated degradation of purine nucleotides. The rate of purine degradation including xanthine oxidase reactions characterizes the extent of an important radical source during oxygen deficiency, contributing to peroxidation of polyunsaturated fatty acids and the formation of peroxidation of polyunsaturated fatty acids and the formation of secondary aldehydic lipid peroxidation products.
为了定量评估109例胎龄为26至41周的健康、酸中毒和窒息新生儿脐动脉血样本围产期缺氧后的脂质过氧化情况，测定了醛类脂质过氧化产物丙二醛（MDA）和4-羟基壬-2-烯醛（HNE）的水平值。此外，还测定了氧化型和还原型谷胱甘肽（GSSH和GSH）以及嘌呤化合物次黄嘌呤和尿酸的浓度。随着胎龄增加，MDA和HNE水平升高。此外，还发现GSH水平有所增加。围产期缺氧后，MDA和HNE浓度明显升高（p<0.001），灵敏地反映了体内脂质过氧化的程度。HNE被认为是围产期缺氧后细胞损伤定量评估的一个新参数。与MDA相比，HNE是评估脂质过氧化过程的一个更具特异性的参数。此外，HNE在纳摩尔浓度下具有细胞毒性和致突变性。MDA和HNE水平的升高均伴随着GSH浓度的显著降低（p<0.001），这表明GSH通过谷胱甘肽过氧化物酶反应迅速消耗，但同时也表明HNE与巯基具有高反应性。缺氧期间，次黄嘌呤（p<0.01）和尿酸（p<0.05）水平升高是由于嘌呤核苷酸降解加速所致。包括黄嘌呤氧化酶反应在内的嘌呤降解速率表征了缺氧期间一个重要自由基来源的程度，这有助于多不饱和脂肪酸的过氧化以及二级醛类脂质过氧化产物的形成。
