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Am J Physiol Lung Cell Mol Physiol 286: L1169-L1178, 2004. First published January 16, 2004; doi:10.1152/ajplung.00397.2003
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Interfacial phospholipids inhibit ozone-reactive absorption-mediated cytotoxicity in vitro

Lydia M. Connor,1 Carol A. Ballinger,2 Thomas B. Albrecht,3 and Edward M. Postlethwait2

1Human Biological Chemistry and Genetics and 3Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 77555; and 2Department of Environmental Health Sciences, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama 35294

Submitted 19 November 2003 ; accepted in final form 2 January 2004

The intrapulmonary distribution of inhaled ozone (O3) and induction of site-specific cell injury are related to complex interactions among airflow patterns, local gas-phase concentrations, and the rates of O3 flux into, and reaction and diffusion within, the epithelial lining fluid (ELF). Recent studies demonstrated that interfacial phospholipid films appreciably inhibited NO2 absorption. Because surface-active phospholipids are present on alveolar and airway interfaces, we investigated the effects of interfacial films on O3-reactive absorption and acute cell injury. Compressed films of dipalmitoyl-glycero-3-phosphocholine (DPPC) and rat lung lavage lipids significantly reduced O3-reactive absorption by ascorbic acid, reduced glutathione, and uric acid. Conversely, unsaturated phosphatidylcholine films did not inhibit O3 absorption. We evaluated O3-mediated cell injury using a human lung fibroblast cell culture system, an intermittent tilting exposure regimen to produce a thin covering layer, and nuclear fluorochrome permeability. Exposure produced negligible injury in cells covered with MEM. However, addition of AH2 produced appreciable (<50%) cell injury. Film spreading of DPPC monolayers necessitated the use of untilted regimens. Induction of acute cell injury in untilted cultures required both AH2 plus very high O3 concentrations. Addition of DPPC films significantly reduced cell injury. We conclude that acute cell injury likely results from O3 reaction with ELF substrates. Furthermore, interfacial films of surface-active, saturated phospholipids reduce the local dose of O3-derived reaction products. Finally, because O3 local dose and tissue damage likely correlate, we propose that interfacial phospholipids may modulate intrapulmonary distribution of inhaled O3 and the extent of site-specific cell injury.

surfactant; epithelial lining fluid; interfacial resistance; antioxidants


Address for reprint requests and other correspondence: E. M. Postlethwait, Dept. of Environmental Health Sciences, School of Public Health, Univ. of Alabama at Birmingham, RPHB 530, 1530 3rd Ave. South, Birmingham, AL 35294-0022 (E-mail: epostlethwait{at}ms.soph.uab.edu).






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