Rosenfeld W, Concepcion L
J Free Radic Biol Med. 1986;2(4):295-8. doi: 10.1016/s0748-5514(86)80013-7.
Deficiencies of antioxidant defenses have been postulated as possible mechanisms in the development of bronchopulmonary dysplasia (BPD). Neonates, especially prematures with respiratory distress syndrome (RDS), are exposed to high oxygen tensions for prolonged periods. To evaluate the neonates' ability to respond to an oxygen challenge with increased superoxide dismutase (SOD), 9 prematures were studied immediately at birth and on days 1, 3, 5, and 7. An increase in plasma levels was noted during the first week of life in the patients who were exposed to oxygen. The mean endogenous SOD level at birth was 1.28 microgram/ml. On day 1, plasma SOD rose to 1.53 microgram/ml and to 2.25 micrograms/ml on day 3 (P = .003). This trend continued into the fifth and seventh days. Whether this increase in SOD has clinical significance in the prevention of BPD requires further investigation.
抗氧化防御机制的缺陷被认为是支气管肺发育不良(BPD)发病的可能机制。新生儿,尤其是患有呼吸窘迫综合征(RDS)的早产儿,长时间暴露于高氧环境中。为了评估新生儿通过增加超氧化物歧化酶(SOD)来应对氧挑战的能力,对9名早产儿在出生时及出生后第1、3、5和7天进行了即时研究。在暴露于氧气的患者中,出生后第一周血浆水平有所升高。出生时内源性SOD的平均水平为1.28微克/毫升。第1天,血浆SOD升至1.53微克/毫升,第3天升至2.25微克/毫升(P = 0.003)。这种趋势持续到第5天和第7天。SOD的这种增加在预防BPD方面是否具有临床意义尚需进一步研究。