Merritt T A, Amirkhanian J D, Helbock H, Halliwell B, Cross C E
Division of Neonatology, University of California, Davis, Medical Center, Sacramento 95817.
Biochem J. 1993 Oct 1;295 ( Pt 1)(Pt 1):19-22. doi: 10.1042/bj2950019.
The reactive species hypochlorous acid (HOCl/OCl-) is a major product of the respiratory burst in activated neutrophils. We studied the effects of HOCl/OCl- on human surfactant and upon surfactants Survanta, KL4 and Exosurf, utilizing a pulsating surfactometer for measuring surface tension. HOCl/OCl- induced a marked dose-dependent decrease in the surface-tension-lowering activity of human surfactant. The surfactant containing surfactant proteins B and C (Survanta) was less sensitive; however, synthetic surfactants with or without peptides were not affected by HOCl/OCl- (KL4, Exosurf). Ascorbic acid and GSH protected human surfactant against inactivation by HOCl/OC1-. We suggest that HOCl/OCl- produced by activated phagocytes in the alveolar compartment of the lung could damage endogenous surfactant and affect the function of exogenously administered natural or other surfactants, especially if ascorbic acid and GSH levels in the lung lining fluids are subnormal, as is known to be the case in some inflammatory lung diseases.
活性物质次氯酸(HOCl/OCl-)是活化中性粒细胞呼吸爆发的主要产物。我们利用脉动表面张力仪测量表面张力,研究了HOCl/OCl-对人肺表面活性剂以及Survanta、KL4和Exosurf等表面活性剂的影响。HOCl/OCl-导致人肺表面活性剂降低表面张力的活性显著呈剂量依赖性下降。含有表面活性蛋白B和C的表面活性剂(Survanta)敏感性较低;然而,含或不含肽的合成表面活性剂不受HOCl/OCl-影响(KL4、Exosurf)。抗坏血酸和谷胱甘肽可保护人肺表面活性剂不被HOCl/OC1-灭活。我们认为,肺肺泡腔中活化吞噬细胞产生的HOCl/OCl-可能会损害内源性肺表面活性剂,并影响外源性天然或其他表面活性剂的功能,尤其是在肺衬液中抗坏血酸和谷胱甘肽水平低于正常时,正如某些炎症性肺病中所已知的情况。