Jain A, Mehta T, Auld P A, Rodrigues J, Ward R F, Schwartz M K, Mårtensson J
Division of Gastroenterology and Hepatology, Thomas Jefferson University, Philadelphia, PA 19107-5244, USA.
Pediatr Pulmonol. 1995 Sep;20(3):160-6. doi: 10.1002/ppul.1950200306.
Respiratory distress in premature newborns is associated with deficiency of surfactant in the bronchoalveolar lining fluid; this may be influenced by a local deficiency of antioxidants. Severe L-buthionine-S,R-sulfoximine-induced depletion of glutathione (GSH, a major antioxidant) in rodents is associated with lung type 2 cell lamellar body damage and decreased concentrations in lung and bronchoalveolar lavage fluid (BALF) of phosphatidyl choline (a major component of surfactant). At birth, prematurely born newborns (30-34 weeks) had lower peripheral venous plasma GSH concentrations than term (> 36 weeks) babies; these levels decreased further with increasing prematurity (< 27 weeks, with respiratory distress). On day 2, the peripheral venous plasma GSH concentrations reached a nadir, and the lowest levels were found in the most premature newborns. Lymphocyte GSH concentrations were lowest on day 2 and day 7, and in prematures (< 27 weeks, with respiratory distress) remained below adult lymphocyte GSH levels for at least 4 weeks. At birth, prematures (< 27 weeks, with respiratory distress) had a central plasma arterio-venous (A-V) GSH gradient across the lung (an estimate of lung uptake of GSH) of 0.72 +/- 0.15 (mean +/- SD) mumol/L; on day 2, the A-V gradient did not change significantly (0.49 +/- 0.09 mumol/L). At birth, these prematures had markedly decreased BALF GSH concentrations (compared with adult levels), and they were not significantly changed during the first 4 weeks of life. These results suggest that GSH deficiency is present in prematures and that it increases with the degree of prematurity. At birth, GSH deficiency will compromise the lungs' defense against oxidative stress injury. Oxidative stress is likely to increase if hyperoxic treatment is given for respiratory distress in these infants.
早产新生儿的呼吸窘迫与支气管肺泡衬液中表面活性剂缺乏有关；这可能受局部抗氧化剂缺乏的影响。啮齿动物中，严重的L-丁硫氨酸-S，R-亚砜亚胺诱导的谷胱甘肽（GSH，一种主要的抗氧化剂）耗竭与肺Ⅱ型细胞板层小体损伤以及肺和支气管肺泡灌洗液（BALF）中磷脂酰胆碱（表面活性剂的主要成分）浓度降低有关。出生时，早产新生儿（30 - 34周）外周静脉血浆GSH浓度低于足月儿（> 36周）；随着早产程度增加（< 27周，伴有呼吸窘迫），这些水平进一步降低。在出生后第2天，外周静脉血浆GSH浓度达到最低点，且在最早产的新生儿中发现最低水平。淋巴细胞GSH浓度在第2天和第7天最低，并且早产（< 27周，伴有呼吸窘迫）儿至少4周内淋巴细胞GSH水平仍低于成人淋巴细胞GSH水平。出生时，早产（< 27周，伴有呼吸窘迫）儿肺部中央血浆动静脉（A - V）GSH梯度（GSH肺摄取量的估计值）为0.72±0.15（平均值±标准差）μmol/L；在第2天，A - V梯度无显著变化（0.49±0.09 μmol/L）。出生时，这些早产儿BALF GSH浓度显著降低（与成人水平相比），且在出生后的前4周内无显著变化。这些结果表明早产儿存在GSH缺乏，且随着早产程度增加而加重。出生时，GSH缺乏会损害肺部对氧化应激损伤的防御能力。如果对这些婴儿因呼吸窘迫给予高氧治疗，氧化应激可能会增加。
