Molecular aggregation of the slow reacting hemolytic lysolecithin analog 1-octadecyl-2-benzyl-glycero-3-phosphorylcholine in aqueous solution.

An attempt has been made to relate the retarded adsoprtion to red cells of the slow reacting hemolytic phosphatide Rac. 1-octadecyl-2-benzyl-glycero-3-phosphorylcholine (benzyl-lysolecithin) to its aggregation status in aqueous solution. Light scattering measurements indicate a critical micelle concentration at 37 degrees of less than 2 X 10(-6) M. The micellar weight as determined by angle dependent light scattering is 6 X 10(7) with about 97 000 molecules per micells. The aggregates, which according to electron-microscopic observations are more similar to lecithin-liposomes than to usual lysolecithin-micelles, undergo a phase transition at 14 degrees from a tightly packed liquid-crystalline state to the more loose structure of a gel phase with increased mobility of the aliphatic chains. The enthalpy of transition is 4.2 kcal/mole. These changes of the micellar structure are reflected in the binding kinetics of benzyl-lysolecithin to red cells in that the binding rate is rather constant below, but strongly increasing above the transition temperature. It is concluded that the unusual micellar structure is responsible for the retarded adsorption of this lysolecithin analog to red cells and that the rate of adsorption is probably determined by the rate of escape of single lysophosphatide molecules from the micelles.

Regulation of guanylate and adenylate cyclase activities by lysolecithin.

The guanylate cyclase activity [GTP pyrophosphate-lyase (cyclizing), EC 4.6.1.2] in membrane preparations from 3T3 mouse fibroblasts is stimulated approximately 5-fold by lysolecithin at concentrations of 100 mug/ml and above.

Adjuvant effect of lysolecithin analogues on the development of contact sensitivity in mice.

The influence of two lysolecithin analogues on the development of contact sensitivity (CS) to picryl chloride in mice was studied. Both substances were shown to have an adjuvant effect on the primary CS response, but depending on dosage of adjuvant and antigen, the timing of adjuvant injection, and the strain of mice employed, the relative activities of the two substances varied considerably. Large amounts of one of the adjuvants were less stimulatory than small amounts. Both substances had a suppressive effect on the development of CS following repeated administration of picryl chloride. The results are discussed in relation to hypotheses on the cellular targets for, and mode of action of, immunological adjuvants.