Surface Pressure-surface Area Research Articles

Surface pressure hysteresis of mixed lipid/protein monolayers: applications to the alveolar dynamics.

Experimental data on surface pressure-surface area hysteresis of mixed serum albumin/dipalmitoyl lecithin/sphingomyelin monolayers in the Langmuir trough are presented. Several possible physicochemical mechanisms of the hysteresis are discussed: Marangoni effect, surface pressure relaxations, bulk-to-surface diffusion interchange, and collapse. Depending on the concrete conditions each of these mechanisms can be important. Possible applications of these results to the alveolar dynamics are presented and discussed on the basis of the balloon model of the alveolus. The main conclusions of biological importance are that 1) the alveolar stability depends on the DPL/SM ratio as well as on the protein content. Under normal breathing conditions the surface pressure hysteresis is small and does not play a decisive role in the alveolar dynamics. 2) At large extent of compression the collapse predominates in determining the hysteretic behavior of the alveolar surface.

Effect of Lipids on Enzymatic Activity of Pig Heart Mitochondrial Malate Dehydrogenase Monomolecular Films

The effect of various lipids on the enzymatic activity of pig heart mitochondrial malate dehydrogenase monomolecular films was studied using the subphase exchange technique described previously. Surface pressure-surface area (π–A) curves of mixed films of the enzyme with dipalmitoyllecithin, egg lecithin, cholesterol, and phospholipids extracted from pig hearts showed that the enzyme interacted with all of the lipids and that the enzyme remained in the film at pressures well above the collapse pressure of malate dehydrogenase in the absence of lipid. The surface enzyme activity was dependent on surface pressure for each lipid; in all cases, the lipids greatly broadened the range of surface pressures where surface enzyme activity was observed. The π–A and enzyme activity data showed good correlation. Although the simple model system employed does not simulate the complexity of the biological membrane, it gives some evidence for the role of lipids in the stability of membrane-bound enzymes.

Equilibrium and metastable states in lecithin films

We have considered whether lecithin surface films below the gel-liquid crystal transition temperature, Tc, are in unique physical states. In general, below Tc, equilibrium films do not exist when surface pressures, pi, exceed about 0.1 dyn/cm. Since surface pressure-surface area isotherms of lecithin films below Tc always encompass pi's much greater than 0.1 dyn/cm, the film states are metastable. We show that the film properties under these conditions depend strongly on the history of the film, particularly the method of film formation. Lecithin surface films below Tc are thus in arbitrary metastable states, so that pi-area isotherms are difficult to interpret. The physical significance of such isotherms remains to be determined. The utility of pure lecithin surface layers below Tc as models for biological systems is also challenged by our results.

Anesthetic interaction with a model cell membrane: expansion, phase transition, and melting of the lecithin monolayer.

A synthetic L-α-dipalmitoyl lecithin monolayer at an air-water interface was used as a model to study the effects of volatile anesthetics on cell membranes. Methoxyflurane, chloroform, halothane, enflurane and fluroxene were used in this study. When the surface pressure of the monolayer was kept constant, anesthetics at clinically effective tensions expaned the area 0.5 per cent When the area of the monolayer was kept constant, the surface pressure was increased about 1.0 dyn/cm by anesthetics. This increase of the surface energy was caused by the addition of 2.70 x 1013 anesthetic molecules to one square cm of the interface. The surface pressure-surface area curve shows a discontinuity, and a transition from liquid-expanded phase to liquid-condensed phase occurs at this point The liquid-expanded phase is regarded as the “melted” state of the monolayer. Anesthetics shifted the phase transition point towards a more condensed region, indicating melting of the monolayer membrane. Anesthetics decreased the latent heat and entropy change of the phase transition, implying that anesthetics facilitate the melting of the membrane. The compressional modulus, a measure of the rigidity of the monolayer, was decreased by anesthetics. This decrease of rigidity, or increase of fluidity, was also disclosed by analysis of the hysteresis curve (surface pressure-surface area) obtained by compression and expansion of the monolayer. The results support the unfolding theory of anesthesia which postulates that disordering and

Interaction of 3,4-Benzpyrene with Monomolecular Films

The interactions of the carcinogenic hydrocarbon, 3,4-benzpyrene [benz(a)pyrene], with cholesterol, phospholipid, protein, and lipid-protein films were investigated. Whereas the interaction between 3,4-benzpyrene and cholesterol was weak, the interaction between the carcinogen and dipalmitoyl lecithin was very strong, as determined from surface pressure-surface area data. The extent of the interaction between the phospholipid and 3,4-benzpyrene was dependent on the mole fraction of each component in the film. 3,4-Benzpyrene was shown also to interact strongly with protein films and mixed lipid-protein films. In the case of the latter films, the extent of interaction was dependent on whether or not the lipid was first allowed to interact with the protein before the carcinogen was added. The biological significance of these data is discussed.

Identification of cholesteryl nitrate as a product of the reaction between NO 2 and cholesterol monomolecular films

The effects of exposure of monomolecular films of cholesterol, dihydrocholesterol, 5-cholesten-3-one, 7-hydroxycholesterol, and 7-ketocholesterol to air and NO 2 were studied. Whereas exposure to air resulted in expansion of the films in all cases, exposure to NO 2 resulted in condensation of all of the films with the exception of 5-cholesten-3-one. The expansion effects were determined to be the result of the formation of various autoxidation products of cholesterol. The condensation effects were caused by the formation and subsequent desorption of cholesteryl nitrate. Identification of the products was based on surface pressure-surface area and thin layer chromatographic evidence.