The Nature of the Membrane Injury in Irradiated Human Erythrocytes

The mechanism of the radiation-induced increase in sodium accumulation of erythrocytes was studied by chemically altering the cell surface and the cell interior. Agents such as PCMBS and GED, 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 (${\rm CrO}_{4}{}^{-}$) 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 and MEG and correlated with the removal by these agents of a small amount of the PCMBS from the cells. Reversal of of radiation effect on sodium accumulation was observed with BAL. Radiation increased accumulation of other monovalent 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 erythrocyte Na-K permeability, that aleration 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.