Abstract
We have detailed two distinct mechanisms whereby membranes are damaged in the context of lethal cell injury. The first results from the insertion of proteins into the phospholipid bilayer. This is the mechanism by which viruses, both those that are directly and indirectly cytopathic, kill cells. It is suspected that there is at least one situation, the killing of thymocytes by glucocorticoids, in which the programed death of cells is the consequence of the insertion of a protein into the membrane.
The second mechanism is the loss of the unsaturated fatty acids of membrane phospholipids, an event that occurs as a result of either their peroxidative decomposition or the activation of a membrane-bound phospholipase. In each case, the loss of unsaturated fatty acids increases the molecular order of the membrane. As a result, there is the appearance of lateral domains of differing fluidity, the interfaces between which are believed to be sites of increased membrane permeability.
