The lethal and other biological effects of X-rays can be reduced by the prior administration of certain substances. The elucidation of the mechanism of such action is difficult to approach directly, since ionizing radiations initiate many different effects and it is not even known which of these is responsible for death. Thus, with different animals, post-mortem examination indicates quite different physiological changes, and hemorrhages at different sites as well as infection have been given as cause of death (1). Despite these different end effects, it is not reasonable to infer that there is no common primary effect or effects of X-rays initiating the processes causing death. Many biological experiments have been made (cf. Patt, 2) to elucidate the mechanism by which the protective agents function, but because of the complexities involved little progress has been made. A large number of chemically dissimilar substances can protect mice against a dose of X-rays which would otherwise be fatal within 2 weeks. A number of different mechanisms have been proposed for the action of protectors, and comprehensive reviews have been published (2, 3). The first protectors shown to be active in animals were cyanide (4) and cysteine (5). The latter was tried after the finding of Barron (6) that SH enzymes in vitro were readily inactivated by X-rays by oxidation to the -S-Sform, and that a subsequent treatment with -SH compounds such as cysteine or glutathione restored the activity. These results cannot, however, be extrapolated to whole-body irradiations, for which there is no evidence of inactivation of sulfhydryl enzymes. Moreover, the facile reconstitution of the enzyme suggests that the reducing capacity of the body would immediately reverse this effect (7). Also, since these active chemicals have no known pharmacological effect in common and have to be administered before irradiation, it seems reasonable that they interfere with one of the primary reactions induced by X-rays and do not treat the radiation syndrome.