1. Ca2+ (0.4-16 mM) had no detectable action on the agglutination of hen erythrocytes by Sendai virus. 2. Pretreatment of the cells with Ca2+ (0.1-8 mM) in the presence of the bivalent cation ionophore A23187 led, however, to a significant decrease in the subsequent agglutination of the cells by the virus. 3. It thus appears that the entry of Ca2+ into the interior of these cells decreases cellular agglutination by Sendai virus; possible interpretations of this phenomenon are discussed in terms of the movement of intramembranous particles. 4. With a small number of virions, maximum cell fusion by Sendai virus occurred in the presence of EGTA [ethanedioxybis(ethylamine)tetra-acetate]. 5. Virus-induced cell fusion was significantly decreased by Ca2+, even at a concentration of 0.2 mM; it is suggested that this may result from diminished interactions between virus particles and erythrocyte membranes.

1. The ability of a number of carboxylic acids, their esters, retinol and α-tocopherol to induce fusion of hen erythrocytes in vitro was investigated. 2. Some 30 different fat-soluble substances (100μg/ml) were found to cause the formation of multinucleated erythrocytes with a suspension of 3×10 8 erythrocytes/ml. The most effective agents induced fusion within 5–10min at 37°C; some substances required about 1h. 3. Inclusion of Dextran 60C in the test medium minimized colloid osmotic lysis caused by exogenous lipids that induce cell fusion. 4. Cell swelling, followed by cell adhesion, was then seen to precede cell fusion. 5. Fusion occurred with C 10 –C 14 saturated carboxylic acids, with unsaturated, longer-chain carboxylic acids and their mono-esters; retinol, and to a lesser extent α-tocopherol, also caused cell fusion. 6. C 6 –C 9 , C 15 , C 16 and C 18 saturated carboxylic acids did not induce fusion within 4h; glyceryl dioleate was only weakly active, and glyceryl trioleate was inactive in the test system. 7. Fusion was facilitated by a high ratio of chemical agents to cell number and by incubation between pH5 and 6. It was inhibited by EDTA and by serum albumin. 8. Glyceryl mono-oleate caused both a similar fusion of several species of mammalian erythrocyte and the interspecific fusion of human and chicken erythrocytes. 9. The term ‘fusogenic’ is proposed to describe chemical, viral and physical agents that cause membranes to fuse. 10. The biochemical mechanisms involved and the possible biological significance of membrane fusion by fusogenic lipids are discussed.

1. The behaviour of retinol in aqueous colloidal dispersions has been studied because, if membranes are a physiological site of action of vitamin A, the reactions of colloidal retinol may be relevant to the functions of the vitamin in vivo . 2. Dispersions of retinol in NaCl exhibit characteristic spectral changes, and they consume O 2 , within minutes of preparation. 3. The maximum rate of O 2 uptake is approximately linearly dependent on the concentration of O 2 . 4. At limiting concentrations of O 2 , the spectral changes are accelerated by catalase, indicating that H 2 O 2 is one of the reaction products. 5. The autoxidation, which is relatively unaffected by light, has the characteristics of a radical-catalysed reaction. O 2 uptake is preceded by an exceptionally short induction period; the reaction is catalysed by Fe 2+ ions and is inhibited by diphenylpicrylhydrazyl. 6. The maximum rate of autoxidation, which is less in water or sucrose solution than in saline, depends on the degree of aggregation of retinol molecules induced by cations. 7. In the absence of O 2 , the cation-induced aggregates exhibit a spectral red-shift, which difference-spectra indicate is caused by formation of a species with λ max. 370–380nm. 8. This species, from which retinol can be quantitatively recovered, is apparently the oxygen-sensitive form of retinol that initiates the rapid autoxidation. 9. The possible biological significance of the production of a highly reactive form of retinol in micellar aggregates is discussed.