Environmental tobacco smoke effects on lung surfactant film organization

Abstract

Adsorption of the clinical lung surfactants (LS) Curosurf or Survanta from aqueous suspension to the air-water interface progresses from multi-bilayer aggregates through multilayer films to a coexistence between multilayer and monolayer domains. Exposure to environmental tobacco smoke (ETS) alters this progression as shown by Langmuir isotherms, fluorescence microscopy and atomic force microscopy (AFM). After 12 hours of LS exposure to ETS, AFM images of Langmuir-Blodgett deposited films show that ETS reduces the amount of material near the interface and alters how surfactant is removed from the interface during compression. For Curosurf, ETS prevents refining of the film composition during cycling; this leads to higher minimum surface tensions. ETS also changes the morphology of the Curosurf film by reducing the size of condensed phase domains from 8–12 μm to ~ 2μm, suggesting a decrease in the line tension between the domains. The minimum surface tension and morphology of the Survanta film are less impacted by ETS exposure, although the amount of material associated with the film is reduced in a similar way to Curosurf. Fluorescence and mass spectra of Survanta dispersions containing native bovine SP-B treated with ETS indicate the oxidative degradation of protein aromatic amino acid residue side chains. Native bovine SP-C isolated from ETS exposed Survanta had changes in molecular mass consistent with deacylation of the lipoprotein. Fourier Transform Infrared Spectroscopy (FTIR) characterization of the hydrophobic proteins from ETS treated Survanta dispersions show significant changes in the conformation of SP-B and SP-C that correlate with the altered surface activity and morphology of the lipid-protein film.

Interplay of mycolic acids, antimycobacterial compounds and pulmonary surfactant membrane: A biophysical approach to disease

“…The secondary structure of the proteins changes upon interaction with: MAs, RFB, RFB2 and with both compounds when MAs are present. Since the antimycobacterial compounds and the MAs alter the structure of the proteins in the plateau region, the way how the material is removed from the interface also changes and this could have negative effects in the lung function and alter the normal breathing process [53,62]. Moreover, the hysteresis of the PS monolayer when both antimycobacterial compounds and MAs are present does not increase relatively to the hysteresis of the PS monolayer when MAs are present in the absence of the antimycobacterial compounds, suggesting that the RFB and its derivate might reduce the amount of bacteria that is able to reach the alveolar macrophages and the bloodstream.…”

“…If the band appears as two components: one at the β-sheet position and another as a shoulder at 1682-1710 cm −1 it is indicative of an antiparallel β-sheet. The parallel β-sheet is predicted to have higher frequency for the lower component [62,64,65]. The disorder of random coils (unstructured) occurs at the same wavenumbers of the α-helices (1637-1650 cm −1 ), originating from the former broader and less intense bands compared to the α-helices [62,64,66].…”

“…It is well known that the secondary structure of the SP-B and SP-C is related with the normal functions of these hydrophobic proteins, and changes in their structure might have a negative implication by inducing changes in the PS surface activity [62]. Accordingly, besides analyzing the lipidic portion of the PS monolayer, we have also used PM-IRRAS to study the secondary structure of the SP-B and SP-C at the dynamic inspiratory tension.…”

Enhanced phospholipase B activity and alteration of phospholipids and neutral lipids in Saccharomyces cerevisiae exposed to N-nitrosonornicotine

“…The functions of membrane is inherently linked to the type of phospholipids present in the cell membrane, and their interactions with each other. Environmentally induced alterations in phospholipid composition can lead to changes in membrane integrity, permeability, membrane cell injury and even death (Stenger et al 2009). This is especially true with toxic substances because they easily generate reactive oxygen species (ROS) which in turn interact with cell membrane (Nachiappan et al 1994).…”

Vibrational spectroscopy for probing molecular-level interactions in organic films mimicking biointerfaces

“…Dieudonne et al [129] used IRRAS to probe structurefunction relationships and protein-lipid interaction in bulk phase and monolayer for three peptides with amino acid sequences based on the pulmonary surfactant protein SP-B (SP-B 1-20 , SP-B 9-36a and SP-B 40-60A ), with substantial differences being observed in peptide surface activity. The influence of tobacco smoke in clinical lung surfactants has been studied by using FTIR [130], where hydrophobic proteins from tobacco smoke-treated Survanta (a specific lung surfactant) affected the conformation of SP-B and SP-C.…”