Miles P R, Bowman L, Reasor M J
Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Morgantown, West Virginia, USA.
J Toxicol Environ Health. 1996 Dec 6;49(5):511-23. doi: 10.1080/009841096160727.
Previous studies have shown that vitamin E may be an integral part of lung surfactant and may function to protect this material from oxidant damage. Therefore, we measured the vitamin E levels in alveolar lavage materials from rats exposed to crystalline silica or treated with chlorphentermine (CP), two treatments that are known to increase surfactant phospholipids (PL) by different mechanisms. Silica exposure leads to increased PL synthesis, and CP treatment causes a reduction in PL degradation. Two different silica preparations, HCL-washed and unwashed silica, were used because exposure to each of them leads to different degrees of phospholipidosis. Exposure to HCL-washed silica results in a more than 17-fold increase in lavage PL and protein levels and a 12.2-fold increase in the amount of vitamin E. Exposure to unwashed silica leads to an approximately 7-fold increase in PL and proteins and a 5.8-fold increase in lavage vitamin E. Following treatment of rats with CP, there is a 15- to 19-fold increase in lavage PL and proteins and a 13.6-fold increase in vitamin E. When the results are expressed as micrograms vitamin E per milligram of lavage PL or protein, there is not much difference between controls and each treatment group. Because surfactant synthesis occurs in the endoplasmic reticulum, we also measured vitamin E in lung microsomes. Both silica exposure and CP treatment also lead to 1.8- to 2.5-fold increases, respectively, in the lung microsomal levels of vitamin E. These results demonstrate that alveolar lavage vitamin E levels are elevated along with lavage PL and proteins, and lung microsomal vitamin E levels are increased following exposure of rats to silica or treatment of the animals with CP.
先前的研究表明，维生素E可能是肺表面活性剂的一个组成部分，并且可能起到保护这种物质免受氧化损伤的作用。因此，我们测量了暴露于结晶二氧化硅或用氯苯丁胺（CP）处理的大鼠肺泡灌洗材料中的维生素E水平，这两种处理方式已知会通过不同机制增加表面活性剂磷脂（PL）。接触二氧化硅会导致PL合成增加，而CP处理会使PL降解减少。使用了两种不同的二氧化硅制剂，即盐酸洗涤过的二氧化硅和未洗涤的二氧化硅，因为接触它们中的每一种都会导致不同程度的磷脂沉着症。接触盐酸洗涤过的二氧化硅会使灌洗PL和蛋白质水平增加超过17倍，维生素E含量增加12.2倍。接触未洗涤的二氧化硅会使PL和蛋白质增加约7倍，灌洗维生素E增加5.8倍。用CP处理大鼠后，灌洗PL和蛋白质增加15至19倍，维生素E增加13.6倍。当结果以每毫克灌洗PL或蛋白质中维生素E的微克数表示时，对照组与每个处理组之间没有太大差异。由于表面活性剂合成发生在内质网中，我们还测量了肺微粒体中的维生素E。二氧化硅暴露和CP处理也分别导致肺微粒体维生素E水平增加1.8至2.5倍。这些结果表明，随着灌洗PL和蛋白质的增加，肺泡灌洗维生素E水平升高，并且大鼠暴露于二氧化硅或用CP处理动物后，肺微粒体维生素E水平增加。
