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J Clin Invest. 1974 Mar;53(3):705-9. doi: 10.1172/JCI107608.
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本文引用的文献

1
A morphologic and cytochemical study on the great alveolar cell.关于肺泡大细胞的形态学和细胞化学研究。
J Histochem Cytochem. 1966 Dec;14(12):884-97. doi: 10.1177/14.12.884.
2
Protein measurement with the Folin phenol reagent.使用福林酚试剂进行蛋白质测定。
J Biol Chem. 1951 Nov;193(1):265-75.
3
GRANULAR PNEUMOCYTES: ELECTRON MICROSCOPIC EVIDENCE OF THEIR EXOCRINIC FUNCTION.颗粒性肺细胞:其外分泌功能的电子显微镜证据
Science. 1964 Sep 18;145(3638):1318-9. doi: 10.1126/science.145.3638.1318-a.
4
The pulmonary alveolar mucoid film and the pneumonocytes.肺泡黏液膜和肺上皮细胞。
Lancet. 1954 May 29;266(6822):1099-1104. doi: 10.1016/s0140-6736(54)92154-6.
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Alveolar cells: incorporation of carbohydrate into protein and evidence for intracellular protein transport.肺泡细胞:碳水化合物掺入蛋白质及细胞内蛋白质转运的证据
J Clin Invest. 1968 Feb;47(2):366-74. doi: 10.1172/JCI105733.
6
Metabolic factors affecting protein synthesis by lung in vitro.体外影响肺蛋白质合成的代谢因素。
J Appl Physiol. 1971 Jan;30(1):1-6. doi: 10.1152/jappl.1971.30.1.1.
7
In vitro synthesis of different categories of specific protein by membrane-bound and free ribosomes.膜结合核糖体和游离核糖体在体外合成不同类别的特定蛋白质。
Proc Natl Acad Sci U S A. 1969 Aug;63(4):1370-6. doi: 10.1073/pnas.63.4.1370.
8
The cellular origin of pulmonary surfactant.肺表面活性物质的细胞起源。
Lab Invest. 1971 Sep;25(3):260-8.
9
Granular pneumocytes. Electron microscopic radioautographic evidence of intracellular protein transport.颗粒性肺细胞。细胞内蛋白质转运的电子显微镜放射自显影证据。
Am Rev Respir Dis. 1972 Jun;105(6):927-31. doi: 10.1164/arrd.1972.105.6.927.
10
Pathogenesis and reversibility of the pulmonary lesions of oxygen toxicity in monkeys. II. Ultrastructural and morphometric studies.猴子氧中毒肺部病变的发病机制与可逆性。II. 超微结构与形态计量学研究。
Lab Invest. 1969 Jan;20(1):101-18.

对高氧的适应。对肺蛋白质合成及颗粒性肺细胞超微结构的影响。

Adaption to hyperoxia. Influence on protein synthesis by lung and on granular pneumocyte ultrastructure.

作者信息

Massaro G D, Massaro D

出版信息

J Clin Invest. 1974 Mar;53(3):705-9. doi: 10.1172/JCI107608.

DOI:10.1172/JCI107608
PMID:4405905
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC333050/
Abstract

We studied the influence of prolonged exposure to hyperoxia (O(2) > 98%) on protein synthesis and on the ultrastructure of the granular pneumocyte. To study protein synthesis, as indicated by l-[U-(14)C]-leucine incorporation into protein, lung slices were incubated with radioactive leucine and a surface-active fraction was obtained by ultracentrifugation of lung homogenates. We found that, following an initial depression in protein synthesis after 48 h of hyperoxia, protein synthesis in rats exposed to oxygen for 96 h rose to greater than control levels. This increase in protein synthesis was noted in whole lung protein and in protein present in the surface-active fraction. Stereologic ultrastructural analysis of granular pneumocytes revealed that the lamellar bodies occupy the same percentage of cytoplasmic volume in oxygen-exposed and control rats after 96 h; a previous study had shown lamellar bodies of oxygen-exposed rats to occupy less volume than those of control rats after 48 h of exposure at which time protein synthesis was also depressed. After 96 h of exposure there is a greater amount of rough endoplasmic reticulum in the granular pneumocytes of oxygen-exposed rats. These studies show that after 96 h of hyperoxia the lung has recovered its ability to synthesize protein including protein in the surface-active fraction and that these biochemical changes are associated with consistent ultrastructural alterations in the granular pneumocyte.

摘要

我们研究了长时间暴露于高氧环境(O₂>98%)对蛋白质合成及颗粒性肺细胞超微结构的影响。为研究蛋白质合成情况,以l-[U-(¹⁴)C]-亮氨酸掺入蛋白质来表示,将肺切片与放射性亮氨酸一起孵育,然后通过对肺匀浆进行超速离心获得表面活性部分。我们发现,在高氧暴露48小时后蛋白质合成最初出现下降之后,暴露于氧气96小时的大鼠的蛋白质合成上升至高于对照水平。这种蛋白质合成的增加在全肺蛋白质以及表面活性部分中的蛋白质中均有体现。对颗粒性肺细胞进行的体视学超微结构分析显示,在暴露于氧气和对照的大鼠中,96小时后板层小体在细胞质体积中所占百分比相同;之前的一项研究表明,暴露于氧气的大鼠在暴露48小时后板层小体所占体积比对照大鼠的小,而此时蛋白质合成也受到抑制。暴露96小时后,暴露于氧气的大鼠的颗粒性肺细胞中存在更多的粗面内质网。这些研究表明,高氧暴露96小时后,肺恢复了其合成蛋白质的能力,包括表面活性部分中的蛋白质,并且这些生化变化与颗粒性肺细胞中一致的超微结构改变相关。