Role Of Membrane Fluidity Research Articles

Temperature dependence of ultrasound-induced cell killing: the role of membrane fluidity.

Chinese hamster cells in suspension were exposed to 20 kHz ultrasound (US) at 54 W/cm2 and various temperatures between 2 and 44 degrees C. Activation energies were 2.6 and 24 kcal/mole below and above 35 degrees C, respectively. Procaine, a local anaesthetic drug known to increase membrane fluidity, enhanced cellular inactivation by US above 41 degrees C, increasing the activation energy to 62 kcal/mole. The inactivation of the bacterium Salmonella typhimurium by US was also dependent on the exposure temperature, with an activation energy of 2.9 kcal/mole between 2 and 44 degrees C. These data are most simply explained by the hypothesis that membranes are a major target for cellular inactivation by US and that the fluidity of the membranes is important in this respect.

Radiation killing of E. coli K1060: role of membrane fluidity, hypothermia and local anaesthetics.

The enhancement of killing by gamma-irradiation, which is seen when E. coli K1060 are cooled below the transition temperature of their membrane lipids, is blocked by procaine-HCl. These data are consistent with the hypothesis that increased killing associated with irradiation at 0 degree C is the result of membrane microviscosity increases, since procaine is known to fluidize membranes. A cooling enhancement ratio (c.e.r.) is defined as the ratio of radiation D0 at 22 degrees C to its value at 0 degree C. The c.e.r. for oxygen-bubbled cells is 1.5 and for nitrogen-bubbled cells is 2.1. In the presence of 25 mM procaine the respective c.e.r. values are 1.08 and 1.29. The oxygen enhancement ratio (o.e.r.) at 22 degree C is 3.43 and at 0 degree C is 2.45. The addition of procaine does not change the o.e.r. Thus, the temperature effect on o.e.r. does not appear to be related to membrane fluidity.

Receptor Mobility and its Cooperative Restriction by Ligands

The functional significance of membrane fluidity and receptor mobility in lymphoid cells has been studied in the recent literature. Although far from clarified, the role of membrane fluidity in achieving control over cell activity is probably important; it allows cooperative interactions over long distances. Here, the emphasis is put on the phenomenon of restriction of receptor mobility by ligands such as Concanavalin A, a phenomenon discovered in recent years using morphological techniques. We discuss in some detail our own approach for studying this phenomenon. This consists of quantitatively measuring the active sites on cell-bound lectin molecules by subsequent fixation of horse-radish peroxidase. This study has shown a cooperative binding of Concanavalin A to cells which corresponds to a modification of the membrane, leading to the recruitment of new receptors. The existence of a post-binding event, that we have called micro-redistribution, has been shown at 4 degrees C, through the use of peroxidase binding to cell-bound lectin. A cooperative restriction of receptor microredistribution is observed when the cooperative recruitment of receptors induced by increasing concentrations of Concanavalin A occurs. Both phenomena were shown to be modulated by drugs such as colchicine and cytochalasin B. The characteristics of this modulation suggest that density and distribution of receptors are dependent upon the state of a multimeric submembrane structure which is still functional at 4 degrees C.