Kafoury R M, Pryor W A, Squadrito G L, Salgo M G, Zou X, Friedman M
Section of Pulmonary Diseases, Critical Care and Environmental Medicine, and Tulane/Xavier Center for Bioenvironmental Research, Tulane University Medical Center, New Orleans, LA 70112, USA.
Am J Respir Crit Care Med. 1999 Dec;160(6):1934-42. doi: 10.1164/ajrccm.160.6.9902025.
We have proposed that exposure of epithelial cell membrane lipids in the lung (mainly phospholipids) to ozone will generate lipid ozonation products (LOP), which could be responsible for the proinflammatory effects of ozone. The ozonation of phosphocholine, the principal membrane phospholipid, produces a limited number of LOP, including hydroxyhydroperoxides and aldehydes. We now report that exposure of cultured human bronchial epithelial cells to the ozonized 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) product, 1-palmitoyl-2-(9-oxononanoyl)-sn-glycero-3-phosphocholine (PC-ALD), a phospholipase A(2) (PLA(2))-stimulatory LOP, resulted in a 113 +/- 11% increase in the amounts of tritiated platelet-activating factor ((3)H-PAF) released apically. (3)H-PAF release was also induced by 1-hydroxy-1-hydroperoxynonane of ozonized POPC (HHP-C9), a phospholipase C (PLC)- stimulatory LOP (134 +/- 40% increase in (3)H-PAF). PC-ALD at 10 microM, but not HHP-C9, induced a 127 +/- 24% increase in prostaglandin E(2) (PGE(2)) release (n = 6, p < 0.05). In contrast, HHP-C9, but not PC-ALD, induced interleukin (IL)-6 release (178 +/- 23% increase, n = 6, p < 0.05) and IL-8 release (101 +/- 23% increase, n = 8, p < 0. 05). These results suggest that LOP-dependent release of proinflammatory mediators may play an important role in the early inflammatory response seen during exposure to ozone.
我们已经提出，肺部上皮细胞膜脂质（主要是磷脂）暴露于臭氧会产生脂质臭氧化产物（LOP），这可能是臭氧促炎作用的原因。主要的膜磷脂磷脂酰胆碱的臭氧化产生了数量有限的LOP，包括羟基氢过氧化物和醛类。我们现在报告，将培养的人支气管上皮细胞暴露于经臭氧处理的1-棕榈酰-2-油酰-sn-甘油-3-磷酸胆碱（POPC）产物1-棕榈酰-2-（9-氧代壬酰基）-sn-甘油-3-磷酸胆碱（PC-ALD），一种磷脂酶A2（PLA2）刺激的LOP，导致顶端释放的氚化血小板活化因子（3H-PAF）量增加了113±11%。经臭氧处理的POPC的1-羟基-1-氢过氧壬烷（HHP-C9），一种磷脂酶C（PLC）刺激的LOP，也诱导了3H-PAF的释放（3H-PAF增加了134±40%）。10μM的PC-ALD，但不是HHP-C9，诱导前列腺素E2（PGE2）释放增加了127±24%（n = 6，p < 0.05）。相反，HHP-C9，但不是PC-ALD，诱导白细胞介素（IL）-6释放（增加了178±23%，n = 6，p < 0.05）和IL-8释放（增加了101±23%，n = 8，p < 0.05）。这些结果表明，依赖LOP的促炎介质释放可能在臭氧暴露期间出现的早期炎症反应中起重要作用。
