Monolayers and bilayers of lipid mixtures self-assembled on mercury form spontaneously gel-phase (solid ordered, s o ) and liquid-ordered (l o ) microdomains, thanks to the fluidity imparted to these films by the liquid metal support. The differential capacity of the hydrocarbon tail region of monolayers of mixtures of two lipid components of high and low transition temperature T m , increases during the transition from the liquid disordered (l d ) phase to the coexistence of l d and s o phases. Addition of cholesterol to this binary mixture causes a decrease in differential capacity. This behavior is explained by regarding the capacity as a measure of the total perimeter of the s o microdomains, due to the mismatch between these microdomains and the l d phase. Cholesterol removes this mismatch by converting the anisotropic s o microdomains into isotropic l o microdomains (rafts). This allows differential capacity measurements by electrochemical impedance spectroscopy to follow phase transitions in lipid mixtures. The coexistance of l d , l o and s o phases is confirmed by images of a distal lipid monolayer self-assembled on top of a thiolipid monolayer tethered to a mercury microcap, by using two-photon fluorescence lifetime imaging microscopy (2P-FLIM).

Hyperosmotic stresses represent one of the major constraints that adversely affect plants growth, development, and productivity. In this study, the focus was on early responses to hyperosmotic stress- (NaCl and sorbitol) induced reactive oxygen species (ROS) generation, cytosolic Ca2+ concentration ([Ca2+]cyt) increase, ion fluxes, and mitochondrial potential variations, and on their links in pathways leading to programmed cell death (PCD). By using BY-2 tobacco cells, it was shown that both NaCl- and sorbitol-induced PCD seemed to be dependent on superoxide anion (O2·–) generation by NADPH-oxidase. In the case of NaCl, an early influx of sodium through non-selective cation channels participates in the development of PCD through mitochondrial dysfunction and NADPH-oxidase-dependent O2·– generation. This supports the hypothesis of different pathways in NaCl- and sorbitol-induced cell death. Surprisingly, other shared early responses, such as [Ca2+]cyt increase and singlet oxygen production, do not seem to be involved in PCD.