Environmental tobacco smoke effects on lung surfactant film organization.

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 h 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 microm to approximately 2 microm, 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.

A novel optical approach to achieving tooth whitening.

OBJECTIVE: To investigate a new optical approach to tooth whitening by enhancing the measurement and perception of tooth whiteness using blue coloured materials deposited onto the tooth surface. METHODS: Salivary pellicle coated human extracted teeth or polished enamel specimens were used as substrates and their colour was measured using a colorimeter in the CIELAB mode. Whole teeth were treated with a range of blue dyes and pigments and the colour measured following rinsing with water. Whole teeth were treated with Blue Covarine for 30 s, rinsed with water and colour changes assessed via colorimetric and visual assessment with a Vita Shade guide under controlled lighting (D65). Deposition of Blue Covarine onto cut enamel specimens was investigated using time-of-flight secondary ion mass spectrometry (TOF-SIMS). Tooth colour changes were also investigated following brushing for 1 min with toothpaste formulations containing Blue Covarine. RESULTS: Blue Covarine gave a significantly greater deltab* shift (p < 0.0001) compared to water. Blue Covarine gave a mean Vita Shade change of 1.18 compared to the water control (-0.03) (p <0.0001) and an increase in objectively measured whiteness index (WIO) (p <0.0001). Blue Covarine was chemically detected on enamel surfaces using TOF-SIMS. Toothpaste formulations containing Blue Covarine gave improvements in tooth whiteness. CONCLUSIONS: Blue Covarine has been identified as a new approach to tooth whitening. Its mode of action involves deposition and retention on tooth surfaces where it alters the optical properties of the tooth. This gives rise to an increase in the overall measurement and perception of tooth whiteness.

A brief review of the relationships between monolayer viscosity, phase behavior, surface pressure, and temperature using a simple monolayer viscometer.

The two-dimensional surface shear viscosity, eta, of fatty acid monolayers of different chain lengths, measured using a simple magnetic needle viscometer, strongly correlates with the molecular organization in condensed phases and the absolute temperature. eta can increase by orders of magnitude at phase boundaries associated with tilted to untilted molecular order, providing the underlying order is semicrystalline. Hence, untilted, long-range ordered CS phases are the most viscous films. However, despite being untilted, the LS rotator phase is less viscous than certain laterally ordered tilted phases, suggesting a decrease of the van der Waals interactions due to molecular rotation. In certain regions of the L2 phase, eta reaches a maximum before the L2-LS transition, an anomalous behavior correlated with the change in the lattice symmetry of the headgroup. Surface shear viscosity, even when measured with a macroscopic probe, is particularly sensitive to the microscopic organization of monolayers.

Inhibition of pulmonary surfactant adsorption by serum and the mechanisms of reversal by hydrophilic polymers: theory.

A theory based on the Smolukowski analysis of colloid stability shows that the presence of charged, surface-active serum proteins at the alveolar air-liquid interface can severely reduce or eliminate the adsorption of lung surfactant from the subphase to the interface, consistent with the observations reported in the companion article (pages 1769-1779). Adding nonadsorbing, hydrophilic polymers to the subphase provides a depletion attraction between the surfactant aggregates and the interface, which can overcome the steric and electrostatic resistance to adsorption induced by serum. The depletion force increases with polymer concentration as well as with polymer molecular weight. Increasing the surfactant concentration has a much smaller effect than adding polymer, as is observed. Natural hydrophilic polymers, like the SP-A present in native surfactant, or hyaluronan, normally present in the alveolar fluids, can enhance adsorption in the presence of serum to eliminate inactivation.

Inactivation of pulmonary surfactant due to serum-inhibited adsorption and reversal by hydrophilic polymers: experimental.

The rate of change of surface pressure, pi, in a Langmuir trough following the deposition of surfactant suspensions on subphases containing serum, with or without polymers, is used to model a likely cause of surfactant inactivation in vivo: inhibition of surfactant adsorption due to competitive adsorption of surface active serum proteins. Aqueous suspensions of native porcine surfactant, organic extracts of native surfactant, and the clinical surfactants Curosurf, Infasurf, and Survanta spread on buffered subphases increase the surface pressure, pi, to approximately 40 mN/m within 2 min. The variation with concentration, temperature, and mode of spreading confirmed Brewster angle microscopy observations that subphase to surface adsorption of surfactant is the dominant form of surfactant transport to the interface. However (with the exception of native porcine surfactant), similar rapid increases in pi did not occur when surfactants were applied to subphases containing serum. Components of serum are surface active and adsorb reversibly to the interface increasing pi up to a concentration-dependent saturation value, pi(max). When surfactants were applied to subphases containing serum, the increase in pi was significantly slowed or eliminated. Therefore, serum at the interface presents a barrier to surfactant adsorption. Addition of either hyaluronan (normally found in alveolar fluid) or polyethylene glycol to subphases containing serum reversed inhibition by restoring the rate of surfactant adsorption to that of the clean interface, thereby allowing surfactant to overcome the serum-induced barrier to adsorption.

Keeping lung surfactant where it belongs: protein regulation of two-dimensional viscosity.

Lung surfactant causes the surface tension, gamma, in the alveoli to drop to nearly zero on exhalation; in the upper airways gamma is approximately 30 mN/m and constant. Hence, a surface tension gradient exists between alveoli and airways that should lead to surfactant flow out of the alveoli and elimination of the surface tension gradient. However, the lung surfactant specific protein SP-C enhances the resistance to surfactant flow by regulating the ratio of solid to fluid phase in the monolayer, leading to a jamming transition at which the monolayer transforms from fluidlike to solidlike. The accompanying three orders of magnitude increase in surface viscosity helps minimize surfactant flow to the airways and likely stabilizes the alveoli against collapse.

Modifying calf lung surfactant by hexadecanol.

Monolayer properties such as phase behavior, collapse pressure, and surface viscosity are determined by monolayer composition. Learning how to control these properties through simple additives is important to understanding lung surfactant monolayers and to designing optimal replacement surfactants for treatment of disease. The properties of Infasurf, a replacement lung surfactant derived from calf lung lavage organic extract, can be modified in a controlled fashion by adding hexadecanol (HD). Grazing incidence X-ray diffraction shows that the HD preferentially interacts with dipalmitoylphosphatidylcholine (DPPC), the main phospholipid component of Infasurf, in the same way as in binary mixtures of DPPC and HD. HD intercalates between the DPPC chains, which leads to a tighter packing of the two-dimensional lattice and greater stability of the solid phase. This molecular reorganization triggers changes at the macroscopic scale, leading to a greatly increased solid-phase fraction at a given surface pressure and order of magnitude increases in the surface shear viscosity. However, the collapse pressure decreases, and, hence, the minimum surface tension of the film increases.

More than a monolayer: relating lung surfactant structure and mechanics to composition.

Survanta, a clinically used bovine lung surfactant extract, in contact with surfactant in the subphase, shows a coexistence of discrete monolayer islands of solid phase coexisting with continuous multilayer "reservoirs" of fluid phase adjacent to the air-water interface. Exchange between the monolayer, the multilayer reservoir, and the subphase determines surfactant mechanical properties such as the monolayer collapse pressure and surface viscosity by regulating solid-fluid coexistence. Grazing incidence x-ray diffraction shows that the solid phase domains consist of two-dimensional crystals similar to those formed by mixtures of dipalmitoylphosphatidylcholine and palmitic acid. The condensed domains grow as the surface pressure is increased until they coalesce, trapping protrusions of liquid matrix. At approximately 40 mN/m, a plateau exists in the isotherm at which the solid phase fraction increases from approximately 60 to 90%, at which the surface viscosity diverges. The viscosity is driven by the percolation of the solid phase domains, which depends on the solid phase area fraction of the monolayer. The high viscosity may lead to high monolayer collapse pressures, help prevent atelectasis, and minimize the flow of lung surfactant out of the alveoli due to surface tension gradients.

Linear dependence of surface drag on surface viscosity.

Flow at an air-water interface is limited by drag from both the two-dimensional surface and three-dimensional subphase. Separating these contributions to the interfacial drag is necessary to measure surface viscosity as well as to understand the influence of the interface on flow. In these experiments, a magnetic needle floating on a monolayer-covered air-water interface is put in motion by applying a constant magnetic force, F(m). The needle velocity varies exponentially with time, reaching a terminal velocity F(m)/C, in which C is the drag coefficient. C is shown to be linearly proportional to the monolayer surface viscosity, eta(s), for dipalmitoylphosphatidylcholine monolayers in the condensed phase by comparison to surface viscosity measured by channel viscometry.