The Nature of the Membrane Injury in Irradiated Human Erythrocytes

Abstract

The mechanism of the radiation-induced increase in Na accumulation of erythrocytes was studied by chemically altering the cell surface and the cell interior. Agents such as PCMBS [p-chloromercuribenzene sulfonate] and GED [bis(2-guanidoethyldi-sulfide], which block surface sulfhydryl groups, mimicked the radiation effect but, when employed with radiation, reduced the radiation effect. Papain, which increased the surface sulfhydryl groups, increased the radiation effect. Trypsin and neuraminidase, which did not alter surface sulfhydryl groups, did not alter the radiation effect. Agents that altered the heme (nitrite, carbon monoxide, nitrogen) or globin (CrO4[long dash]) of hemoglobin inside the cells did not alter the radiation effect. The measurement of sulfhydryl groups on the cells showed decrease on irradiation. Reversal of PCMBS effect on sodium accumulation was observed with GSH [reduced glutathione] and MEG [2-mercaptoethylguanidine] and correlated with the removal by these agents of a small amount of the PCMBS from the cells. Reversal of radiation effect on Na accumulation was observed with BAL [2,3-di-mercaptopropanol]. Radiation increased accumulation of other mono-valent cations besides Na but did not affect accumulation of divalent cations, anions, or nonionic substances. The results indicate that the sulfhydryl group is the major target in radiation alteration of erythro-cyte Na-K permeability, that alteration of only a small number of sulfhydryl groups on the cell surface creates most of the effect, and that the result is not the production of a membrane hole but the induction of a very specific chemical change in the membrane affecting only monovalent cation permeability.