Gerber Frédéric, Krafft Marie Pierre, Vandamme Thierry F
Institut Charles Sadron, UPR 22 CNRS, 6 rue Boussingault, 67083 Strasbourg Cedex, France; Laboratoire de Chimie Bioorganique, Faculté de Pharmacie, UMR 7514 CNRS, Université Louis Pasteur, 74 route du Rhin B.P.60024, 67401 Illkirch Cedex, France.
Biochim Biophys Acta. 2007 Mar;1768(3):490-4. doi: 10.1016/j.bbamem.2006.09.022. Epub 2006 Sep 30.
We have recently reported that fluorocarbon gases exhibit an effective fluidizing effect on Langmuir monolayers of dipalmitoyl phosphatidylcholine (DPPC), preventing them from crystallizing up to surface pressures of approximately 40 mN m(-1), i.e. well above the DPPC's equilibrium surface pressure. We now report that gaseous perfluorooctyl bromide (gPFOB) promotes the re-spreading of DPPC Langmuir monolayers compressed on a bovine serum albumin (BSA)-containing sub-phase. The latter protein is known to maintain a concentration-dependent surface pressure that can exceed the re-spreading pressure of collapsed monolayers. This phenomenon was proposed to be responsible for lung surfactant inactivation. Compression/expansion isotherms and fluorescence microscopy experiments were carried out to assess the monolayers' physical state. We have found that, during expansion under gPFOB-containing air, the surface pressure of a DPPC monolayer on a BSA-containing sub-phase decreased to much lower values than when the DPPC monolayer was expanded in the presence of BSA under air ( approximately 0 mN m(-1) vs. approximately 7.5 mN m(-1) at 120 A(2), respectively). Moreover, fluorescence images showed that, during expansion, the BSA-coupled DPPC monolayers, in contact with gPFOB, remained in the liquid-expanded state for surface pressures lower than 10 mN m(-1), whereas they were in a liquid-condensed semi-crystalline state, even at large molecular areas (120 A(2)), when expanded under air. The re-incorporation of the PFOB molecules in the DPPC monolayer during expansion thus competes with the re-incorporation of BSA, thus preventing the latter from penetrating into the DPPC monolayer. We suggest that combinations of DPPC and a fluorocarbon gas may be useful in the treatment of lung conditions resulting from a deterioration of the native lung surfactant function due to plasma proteins, such as in the acute respiratory distress syndrome.
我们最近报道，碳氟化合物气体对二棕榈酰磷脂酰胆碱（DPPC）的朗缪尔单分子层表现出有效的流化作用，可防止它们在高达约40 mN m⁻¹的表面压力下结晶，即远高于DPPC的平衡表面压力。我们现在报道，气态全氟辛基溴（gPFOB）可促进在含牛血清白蛋白（BSA）的亚相中压缩的DPPC朗缪尔单分子层的重新铺展。后一种蛋白质已知可维持浓度依赖性的表面压力，该压力可能超过塌陷单分子层的重新铺展压力。有人提出这种现象是肺表面活性剂失活的原因。进行压缩/膨胀等温线和荧光显微镜实验以评估单分子层的物理状态。我们发现，在含gPFOB的空气中膨胀期间，含BSA的亚相上DPPC单分子层的表面压力降至比在空气中含BSA的情况下DPPC单分子层膨胀时低得多的值（分别在120 Ų时约为0 mN m⁻¹对约7.5 mN m⁻¹）。此外，荧光图像显示，在膨胀过程中，与gPFOB接触的与BSA偶联的DPPC单分子层在表面压力低于10 mN m⁻¹时保持在液体膨胀状态，而在空气中膨胀时，即使在大分子面积（120 Ų）时，它们也处于液体凝聚的半结晶状态。因此，在膨胀过程中PFOB分子重新掺入DPPC单分子层与BSA的重新掺入相互竞争，从而阻止后者渗透到DPPC单分子层中。我们认为，DPPC和碳氟化合物气体的组合可能有助于治疗由于血浆蛋白导致天然肺表面活性剂功能恶化而引起的肺部疾病，例如急性呼吸窘迫综合征。
