Chemical protection against the long-term effects of a single whole-body exposure of mice to ionizing radiation. II. Causes of death

Male BALB/c or C57Bl mice were exposed to different doses of X rays. Certain groups were given a mixture of protectors or AET prior to irradiation; others served as controls. The animals were followed until spontaneous death, and the lethal diseases were classified as thymic lymphoma, nonthymic lymphoma, reticulosarcoma, myeloid leukemia, lung carcinoma, liver tumors, sarcoma, glomerulosclerosis, noncancerous lung lesions, and others. The data were evaluated by the method of competing risks. Death in nonirradiated BALB/c mice is largely caused by tumors, in particular by lung cancer and nonthymic lymphoma, whereas other causes predominate in the C57Bl strain. Radiation-induced life shortening of nonprotected mice is due to increased and advanced incidences of specific diseases, mainly thymic lymphoma in the medium dose range and glomerulosclerosis in the high dose range. Thymic lymphoma in BALB/c mice increases to a maximum at 650 R and declines thereafter. A shorter latency period is found for lung carcinoma, although the absolute incidence decreases because of the earlier deaths of the irradiated mice. After AET treatment the maximum incidence of thymic lymphoma in BALB/c mice is shifted to 1000 R but its height is unaltered, whereas treatment with a mixture not only displaces the maximum to a still higher dose but also decreases its frequency. Protection in BALB/c mice is also possible, although to a smaller extent, against myeloid leukemia, sarcoma, glomerulosclerosis, and noncancerous lung lesions but it is protection against the two latter diseases which contributes most to the prolonged survival in the high dose range. The protection in C57Bl mice resembles that in the BALB/c strain. Thus protection is effective against thymic lymphoma (possibly also against liver adenomas, all carcinomas, and myeloid leukemia) as well as against glomerulosclerosis and noncancerous lung lesions.