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臭氧暴露大鼠分离的II型肺细胞中磷脂酰胆碱的合成

Phosphatidylcholine synthesis in isolated type II pneumocytes from ozone-exposed rats.

作者信息

van Bree L, Haagsman H P, van Golde L M, Rombout P J

机构信息

Department of Inhalation Toxicology, National Institute of Public Health and Environmental Hygiene, Bilthoven, The Netherlands.

出版信息

Arch Toxicol. 1988 Jan;61(3):224-8. doi: 10.1007/BF00316638.

Abstract

Phosphatidylcholine (PC) synthesis by alveolar type II cells, as an indicator for the production of pulmonary surfactant, was studied after a 4-h exposure of rats to 4 mg ozone/m3 (2 ppm). Lung ravage fluid analysis after exposure revealed significant increases in proteins, which is indicative for pulmonary injury. When type II cells were isolated immediately and thereafter cultured for 20 h, the rate of PC synthesis in cells derived from ozone-exposed rats was not significantly different from that in cells from unexposed controls. Yet, a decreased rate of PC synthesis was observed when these cells were subsequently exposed to ozone in vitro. The activity of the enzyme glycerolphosphate acyltransferase (GPAT) was slightly enhanced in cultured type II cells isolated from ozone-exposed rats, while the lysophosphatidylcholine acyltransferase (LPCAT) activity was unchanged. However, ozone exposure of rats did result in a significant decrease of PC synthesis when measured in freshly prepared type II cell suspensions, although both GPAT and LPCAT activities were not affected. It is concluded that a decrease in pulmonary surfactant related PC synthesis after ozone exposure of rats can be demonstrated in freshly isolated type II pneumocytes. Cultured type II cells from exposed rats lack this effect and are therefore less useful to study changes in phospholipid biosynthesis after in vivo ozone exposure. The data on in vitro ozone exposure of cultured type II cells, however, support the view that ozone may impair pulmonary surfactant production.

摘要

将大鼠暴露于4毫克臭氧/立方米(2 ppm)环境4小时后,研究了肺泡II型细胞合成磷脂酰胆碱(PC)的情况,以此作为肺表面活性物质产生的指标。暴露后的肺灌洗液体分析显示蛋白质显著增加,这表明存在肺损伤。立即分离II型细胞并随后培养20小时,来自臭氧暴露大鼠的细胞中PC合成速率与未暴露对照组细胞中的合成速率无显著差异。然而,当这些细胞随后在体外暴露于臭氧时,观察到PC合成速率下降。从臭氧暴露大鼠分离的培养II型细胞中,甘油磷酸酰基转移酶(GPAT)的活性略有增强,而溶血磷脂酰胆碱酰基转移酶(LPCAT)的活性未改变。然而,在新鲜制备的II型细胞悬液中测量时,大鼠暴露于臭氧确实导致PC合成显著下降,尽管GPAT和LPCAT的活性均未受影响。得出的结论是,在新鲜分离的II型肺细胞中可以证明大鼠暴露于臭氧后与肺表面活性物质相关的PC合成减少。来自暴露大鼠的培养II型细胞缺乏这种效应,因此对于研究体内臭氧暴露后磷脂生物合成的变化不太有用。然而,关于培养II型细胞体外暴露于臭氧的数据支持这样的观点,即臭氧可能损害肺表面活性物质的产生。

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