A number of investigations have revealed that very soon after exposure to ionizing radiation changes occur in the permeability of the plasma membrane of the very radiosensitive lymphocytes (1, 2) and ascites cells (3) as well as of the much more radioresistant erythrocytes (4-8). Brinkman and Lamberts (9) have observed rapid changes in the permeability of connective tissue membranes, and the increased permeability of the vascular system after irradiation has been known by radiologists for some time (10-12). The hypothesis has been put forward by Bacq and Alexander (13) that many of the deleterious effects of radiation on cells are caused by damage to the macromolecules constituting both the intracellular and intercellular membranes, resulting in the failure of their semipermeable characteristics and the consequent random diffusion of inorganic ions, enzyme cofactors, or even enzymes into and out of the cell. The object of this investigation was to determine if structural disturbances of the mitochondrion contribute to the death of mammalian cells. As has been known since 1888 (14), the mitochondrion is surrounded by a semipermeable membrane and consequently is capable of osmotic swelling. Mitochondria also exhibit selective permeability toward larger molecules such as diphosphopyridine nucleotide (DPN) and, as has recently been shown (15), toward the dye phenazine methosulfate. The internal localization of a number of mitochondrial dehydrogenases (16-20) coupled with the permeability barrier toward DPN provides a convenient tool for investigating the effect of ionizing radiation on mitochondrial permeability. Such alterations of permeability would be expected to precede morphological disintegration of the mitochondria as the result of radia-
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Scaife et al. (1961) studied this question.
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