Tölle A, Kolleck I, Schlame M, Wauer R, Stevens P A, Rüstow B
Department of Neonatology, Charité Hospital, Medical School of Humboldt University, Berlin, Germany.
Biochim Biophys Acta. 1997 Jun 2;1346(2):198-204. doi: 10.1016/s0005-2760(97)00036-2.
Experimental and clinical studies have provided evidence for the involvement of oxygen free radicals in development of acute and chronic lung diseases. Hyperoxia is very often an indispensable therapeutic intervention which seems to impose oxidative stress on lung tissue. We measured the effect of hyperoxia (80% O2 for 20 h) (1) on the lipid composition of pulmonary surfactant treated in vitro, (2) on surfactant lipid synthesis and secretion of type II pneumocytes in primary culture, (3) on the lipid composition and on the SP-A content of rat lung lavages and (4) on the turnover of phospholipids, cholesterol, plasmalogens and vitamin E in type II pneumocytes, lamellar bodies and lavages of adult rat lungs. (1) Hyperoxia of lung lavages in vitro reduces the vitamin E content significantly but does not change the relative proportion of PUFA or the content of plasmalogens. (2) Hyperoxia does not affect the biosynthesis or secretion of surfactant lipids and plasmalogens by type pneumocytes in primary culture. (3) Hyperoxic treatment of rats increases the SP-A content and reduces the vitamin E content significantly but does not change the concentration of other lipid components of lung lavage. (4) The vitamin E turnover, measured in type II pneumocytes, lamellar bodies and lung lavages, is increased 2-fold in these fractions. In contrast, the turnover of surfactant cholesterol and surfactant lipids does not change. (5) Hyperoxia caused an increase of the vitamin E uptake by type II pneumocytes resulting in a vitamin E enrichment of lamellar bodies. From these results we conclude that type II pneumocytes are able to regulate the turnover of lipophilic constituents of the alveolar surfactant independently of each other. Hyperoxia caused type II pneumocytes to increase the vitamin E content of lamellar bodies. The lipid and SP-A content of alveolar fluid can be regulated independently each other.
实验和临床研究已为氧自由基参与急慢性肺部疾病的发展提供了证据。高氧常常是一种不可或缺的治疗干预措施，但似乎会给肺组织带来氧化应激。我们测定了高氧（80%氧气，持续20小时）对以下方面的影响：（1）体外处理的肺表面活性物质的脂质组成；（2）原代培养的II型肺细胞中表面活性物质脂质合成及分泌；（3）大鼠肺灌洗物的脂质组成及SP-A含量；（4）成年大鼠肺的II型肺细胞、板层小体和肺灌洗物中磷脂、胆固醇、缩醛磷脂和维生素E的周转。（1）体外高氧处理肺灌洗物可显著降低维生素E含量，但不会改变多不饱和脂肪酸的相对比例或缩醛磷脂含量。（2）高氧不影响原代培养的肺细胞合成及分泌表面活性物质脂质和缩醛磷脂。（3）高氧处理大鼠可显著增加SP-A含量并降低维生素E含量，但不会改变肺灌洗物中其他脂质成分的浓度。（4）在II型肺细胞、板层小体和肺灌洗物中测得的维生素E周转在这些组分中增加了2倍。相比之下，表面活性物质胆固醇和表面活性物质脂质的周转没有变化。（5）高氧导致II型肺细胞对维生素E的摄取增加，从而使板层小体中的维生素E富集。从这些结果我们得出结论，II型肺细胞能够相互独立地调节肺泡表面活性物质亲脂成分的周转。高氧使II型肺细胞增加板层小体中的维生素E含量。肺泡液的脂质和SP-A含量可相互独立调节。
