Gunnison A F, Finkelstein I
Nelson Institute of Environmental Medicine, New York University Medical Center, New York 10016, USA.
Lung. 1997;175(2):127-37. doi: 10.1007/pl00007560.
Our laboratory has demonstrated recently that pulmonary inflammation induced by acute ozone exposure is much more severe in late stage pregnant and lactating rats than in postlactating rats or age-matched virgin females. It is currently widely believed that such pulmonary damage results, at least in part, from the reaction of ozone at sites of unsaturation in phospholipid fatty acid (PLFA) molecules located in the epithelial fluid layer lining the lung surfaces and/or the plasma membranes of epithelial cells underlying this fluid layer. The objective of this study was to compare the PLFA composition of lung tissue and surfactant from ozone-sensitive late stage pregnant and lactating rats with comparable tissue from relatively ozone-insensitive age-matched prepregnant (virgin female) rats to explore the possibility that changes in lung PLFA composition during pregnancy and/or lactation contribute to the enhanced sensitivity of these physiologic states to ozone. In addition, the correlation of changes in plasma PLFA composition with those in lung was investigated. There were minor differences in the composition of lung tissue and surfactant PLFAs between prepregnant rats and pregnant rats at day 17 of gestation and only slightly greater differences between prepregnant and lactating rats. Changes from the prepregnant state in the PLFA composition of lung tissue, but not surfactant, correlated with changes in the plasma only in lactating rats and not in pregnant rats. Overall, the double bond index of PLFAs in surfactant and lung tissue was decreased in pregnant and lactating rats compared with prepregnant rats. Thus, the increased sensitivity of pregnant and lactating rats to ozone-induced lung injury cannot be attributed to an increased availability of unsaturated fatty acids. In addition, the arachidonic acid composition of phospholipids did not appear to explain differences between prepregnant rats and pregnant or lactating rats in their inflammatory response to ozone. In conclusion, there is no evidence that the relatively minor changes in lung tissue PLFA composition which occur during pregnancy and lactation predispose rats in these physiologic states to ozone-induced pulmonary toxicity.
我们实验室最近证实，急性臭氧暴露诱发的肺部炎症在妊娠后期和哺乳期大鼠中比在哺乳期后大鼠或年龄匹配的未孕雌性大鼠中更为严重。目前普遍认为，这种肺部损伤至少部分是由于臭氧与位于肺表面内衬上皮液层和/或该液层下方上皮细胞质膜中的磷脂脂肪酸（PLFA）分子不饱和位点发生反应所致。本研究的目的是比较臭氧敏感的妊娠后期和哺乳期大鼠的肺组织和表面活性剂的PLFA组成与相对臭氧不敏感的年龄匹配的未孕（未育雌性）大鼠的相应组织，以探讨妊娠和/或哺乳期肺PLFA组成的变化是否导致这些生理状态对臭氧的敏感性增强。此外，还研究了血浆PLFA组成变化与肺中变化的相关性。未孕大鼠与妊娠第17天的妊娠大鼠之间肺组织和表面活性剂PLFAs的组成存在微小差异，未孕大鼠与哺乳期大鼠之间的差异仅略大。肺组织而非表面活性剂的PLFA组成从未孕状态的变化仅在哺乳期大鼠中与血浆变化相关，而在妊娠大鼠中则不相关。总体而言，与未孕大鼠相比，妊娠和哺乳期大鼠表面活性剂和肺组织中PLFAs的双键指数降低。因此，妊娠和哺乳期大鼠对臭氧诱导的肺损伤敏感性增加不能归因于不饱和脂肪酸可用性的增加。此外，磷脂的花生四烯酸组成似乎无法解释未孕大鼠与妊娠或哺乳期大鼠对臭氧炎症反应的差异。总之，没有证据表明妊娠和哺乳期肺组织PLFA组成的相对微小变化会使处于这些生理状态的大鼠易患臭氧诱导的肺毒性。
