The barrier function of the erythrocyte membrane, which is a vital prerequisite for the cell's survival, has long been known to be lost reversibly under the influence of biaxial stress during osmotic lysis. The processes occurring, on a molecular level, during lysis are, however, still essentially unknown [ 1, 21.More recent studies have demonstrated that uniaxial stress, particularly after minor oxidative alteration of membrane constituents [ 3 , 41 induces cation leakiness, leading to cell swelling and finally to lysis driven by a colloid-osmotic imbalance. More advanced states of membrane chemical damage, in particular by mild or aggressive oxidants, produce major leakiness to ions and nonelectrolytes even in the absence of additional shear stresses. Since our first observation of leak formation in erythrocytes treated with the mild SH-oxidant, diamide [5,6], we have studied a number of other examples of chemically induced leakiness, e.g. by SH-specific oxidants [7], by 0,-derived reactive species [ 8lo], by photo-oxidation [ l l ] , or by tellurite [12], and also following electroporation [ 131.Leaks induced by diamide and other mild oxidants are reversible following treatment with reducing agents, e.g. dithioerythritol (DTE). Leak formation can be suppressed by pretreatment of the cells with low concentrations of the SH alkylating agent N-ethylmaleimide (NEM). These findings indicate the involvement of SH groups. Leaks formed by electroporation are essentially stable at