Suspensions of lymph node cells from dinitrophenylated bovine gamma globulin (DNP-BGG)-immune LBN F 1 hybrid rats (Lewis × Brown Norway) were prepared, irradiated, and injected intravenously into unirradiated syngeneic intermediate hosts and irradiated syngeneic adoptive controls. After allowance of 24 hr for homing to occur, the intermediate hosts were killed and cell preparations from the lymph nodes and spleen were injected intravenously into separate irradiated LBN final host groups. All control and experimental groups were challenged (DNP-BGG saline iv) 24 hr after the injection of the lymphoid cells. Rats were bled on Days 7, 11, and 14 after challenge and the antigen-binding capacity (ABC) of the serum was determined. After correction for the fraction of the total cell population transferred from the intermediate host, the peak ABC of the final hosts was related to the number of memory cells present. It was thus possible to determine the relative distribution of the memory cell population to the spleen and lymph nodes of the intermediate hosts. In the intermediate control animals, irradiated memory cells provided a secondary antibody response which was delayed but not suppressed when compared to unirradiated cells. In intermediate hosts, the homing of lymph node memory cells to the spleen and lymph nodes was significantly reduced by an exposure to 200 R of X radiation.

Mice containing log phase S-180 (Sarcoma 180) ascites tumor cells were given whole-body X-irradiation (50, 100, 200, 400 R) to produce mitotic inhibition (block in G 2 ). The effect of caffeine (1.9, 19, 194, 1942 μg) was studied by administration to the mice before X-irradiation (5, 10, 20, 40 min). The dose-related period of mitotic arrest was reduced when caffeine was administered 5 or 10 min prior to X-irradiation. This effect of caffeine was no longer evident when the period before X-irradiation was extended to 20 min. There was no such caffeine effect when administered after X-irradiation. The duration of mitotic inhibition was diminished at all concentrations of caffeine employed.

Mouse ascites tumor cells were irradiated in vivo and the delay in cell division determined by periodic examination of mitotic index. Fractional exposures of 200 R were given eight times for a total of 1600 R. The effect on survival was determined 9 days after an inoculation of 4000 cells which had been removed from the irradiated animal. Survival was determined by counting the cells and was expressed as percentage of controls. It was found that fraction intervals of 0.5 and of 1 hour gave minimal delay and maximal survival. As the fractional interval was increased to 3 and to 4.8 hours, the delay became directly proportional to total radiation exposure and there was little recovery from lethal action as compared to the effect of other methods of exposure. It appeared that fractionation at 4.8-hour intervals tended to partially synchronize cells into later stages of the generation cycle; increased mitotic delay; and reduced survival as compared with effects of shorter fraction intervals.

Topical ocular application of DMSO prior to head-only irradiation of mice prevented complete cataract formation. While some degree of radiation damage was detected in these lenses, it did not progress to complete lenticular opacity as occurred in the irradiated control animals. The minimum effective DMSO concentration was about 10%. One hundred percent DMSO was effective when applied only one minute prior to exposure. The drug protected against exposures up to 1400 R; 1800 R was lethal. It was not effective when administered following irradiation. The mechanism of DMSO protection may involve hypertonicity to some extent and may involve alteration in epithelial cell metabolism. DMSO, as administered in these experiments, did not result in systemic radioprotection. In the same animals wherein DMSO (in high concentration) protected against radiation cataract, it resulted in radiosensitization of the cornea. This action of DMSO may be due to a nonspecific stress on the irradiated cornea. No corneal lesions were observed in the DMSO treated unirradiated control animals. The reason for the dichotomy between DMSO effect on radiation damage to lens and cornea remains abscure.

The effect of whole-body X-irradiation with an exposure of 1000 R on thyroid function in mice was studied. The rate of thyroid 131 I uptake in the irradiated animals was lower than that in the controls on the second day postirradiation. The radiochromatographic study of thyroid tissue hydrolyzates showed gradual suppression of thyroid hormone synthesis after irradiation. The initial 6-hour conversion ratio of plasma 131 I was lower in the irradiated animals than in the controls. There was a temporary retardation in the thyroid hormone secretion after irradiation. From these experiments, with the additional support from the previous literature, it was concluded that a whole-body exposure of mice with 1000 R of X-rays acted as a stressor to reduce the various aspects of thyroid function during 6 to 48 hours after the exposure.

The effect of X-irradiation on <tex-math>$\text{glycine-}1\text{-}{}^{14}{\rm C}$</tex-math> transport in Ehrlich ascites tumor cells was investigated immediately after in vitro radiation exposure in the presence and absence of oxygen, in the presence and absence of bovine serum albumin, and at different cell concentrations. The effect (reduction of transport capability) was more pronounced when the cells were irradiated as a 1:500 suspension than as a 1:10 suspension. There was an oxygen enhancement in both the 1:500 and the 1:10 experiments. Bovine serum albumin exerted a protective influence when present (1:500 cells) during irradiation. Neither the "passive" permeability to glycine (measured at 0°C) nor the fraction of viable cells in the incubation population (measured by aqueous eosin staining) was significantly different from control. Irradiation of the medium prior to addition of cells was without effect within the experimental period. The effect on transport probably involved the indirect action on the plasma membrane, since (1) it was immediate, (2) it was influenced by the volume ratio of cells to irradiation medium, and (3) a nonpenetrating substance afforded protection when it was present during irradiation.