Membrane effects of cocoa procyanidins in liposomes and jurkat T cells

We investigated the effects of the interaction between flavanols and related procyanidins (dimer to hexamer) with both cell and synthetic membranes, on bilayer fluidity and susceptibility to oxidation. Cocoa derived dimers (0.05 to 1 µg/ml) protected Jurkat T cells from AMVN-mediated oxidation and increased plasma membrane fluidity. These effects occurred in a concentration- and chain length-dependent manner. In liposomes, procyanidins prevented the Fe²+-induced permeabilization of the membrane. Together, these results support the hypothesis that procyanidins could interact with the polar headgroup of lipids, increasing membrane fluidity and also, preventing the access of molecules that could affect membrane integrity.

Oxidative damage induced by metals wihout redox capacity in biological systems

Results of our studies on several metals that have no redox capacity in biological systems, but can promete reactive oxygen species (ROS)-mediated reactions in in vivo and in vitro systems, will be presented. The experimental evidence indicates that the prooxidant effect of Al, Sc, Ga, In, Y, Be, La and Pb could be in part due to the interaction of metals with membranes, leading to changes in membrane physical properties, which include increase in lipid packing or lipid phase separation that can facilitate the initiation or propagation of lipid peroxidation in the presence of an initiator. The consequent relesse to the media of lipid peroxidation products could secondarily cause oxidative modifications of proteins and DNA. In vivo, Zn deficiency causes oxidative damage to lipids, proteins and DNA. This could be due to a decrease in the antioxidant actions of Zn per se or to the increase in iron tissue levels which occurs secondarily to Zn-deficiency.