Cultured mouse (C3H IOTI/2) cells in contact-inhibited state were subjected to protracted exposure at 4°C or 37°C to either β-rays from HTO or ⁶⁰Co γ-rays. The duration of exposure was 20 h and the total dose was varied by changing the dose-rate.
The dose-survival and dose-transformation curves for γ-irradiation at 4°C were close to those obtained after a single acute X-ray dose (0.5 Gy/min). When γ-irradiation was administered at 37°C, both the lethality and transformation induction were lower than those after the corresponding doses at 4°C, presumably owing to repair of lethal and transformational damage during γ-irradiation at 37°C. The same effect of temperature was observed in the case of HTO exposure, indicating again the existence of repair of damage during β-irradiation at 37°C but not at 4°C. These facts strongly suggest that when irradiated at a low temperature such as 4°C, both the dose-lethality and dose-transformation induction relationships were independent of the dose-rate for either γ- or β-exposure, at least at the dose-rates used in this experiment.
Thus, the comparison of radiation effectiveness between β- and γ-exposures at 4°C gave reliable values of relative biological effectiveness (RBE) of tritium β-rays which were ca. 1.4 at the D₀ for lethality and 1.6 for cell transformation within the dose range examined (1 to 6 Gy of β-rays). The comparison between exposures at 37°C resulted in RBE values (1.4 and 1.7, respectively) very close to those at 4°C.

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Effects of microwave-induced whole-body hyperthermia (WBH) on the mouse kidney were examined histologically for acute and late effects up to 150 days after WBH treatment at 43.5°C (rectal temperature) for 20 min or 42°C for 40 min. As a whole the damage could be divided into two types. One was the damage to distorted epithelial cells in the subcapsular region. This lesion was common in most animals, possibly caused by direct hyperthermic effect of microwave. The other was general renal atrophy accompanied with aqueous or protein-rich cysts due to a chain of physiological reactions of the whole body to WBH. The first reaction was characterized by general stasis of the blood stream in all parts of the kidney, which resulted in acute ischemia of some tissues. This was seen immediately by dilatation of the renal and interlobular veins as well as the bundles of capillaries in the medulla region. The subsequent event was rather specific cell necrosis of distal and collecting tubular epithelium as compared to proximal tubules. The cell destruction induced cell proliferation of the proximal tubular epithelia after two days. Later on, in accord with the recovery of the blood circulation, the proliferated cells were carried away into the lumen, these processes then resulting in obstruction of tubules through formation of protein casts in the lumen. The block incidentally led to the destruction of nephrons. The degenerated area sometimes consisted of aqueous or protein-rich cysts of various sizes after 7 to 30 days. Thereafter these cysts degenerated, decreasing in both number and size. Thus irreversible atrophy of the kidney developed after WBH.

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While fractionated X-irradiation induced a high incidence lymphomas in BALB/cHeA mice (77% in females and 86% in males), it induced the disease at an extremely low incidence in STS/A mice (8% in females and 9% in males). The latent period of lymphoma development was short in BALB/cHeA mice, but relatively long in STS/A mice. No significant difference of incidence of the disease between sexes in either strain was observed. F₁ hybrid mice showed an intermediate incidence of radiation-induced lymphomas. This suggests that neither resistance of STS/A mice nor susceptibility of BALB/cHeA mice to radiogenic lymphomas is dominant.

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