V79 cells have been exposed to X-rays or 238Pu alpha-particles or to X-rays following priming alpha-particle doses of 0.5, 2 or 2.5 Gy. The survival curve for exposure to alpha-particles was exponential with a D0 of 0.89 Gy. Following exposure to priming alpha-particle doses the resulting X-ray survival curves had the same slope as the single dose X-ray curve, but a reduced shoulder. For alpha-particle priming doses of 0.5 and 2 Gy this reduction was the same as for the same X-ray doses. 2.5 Gy alpha-particles reduced the subsequent X-ray curve Dq to almost zero. alpha-particles do cause damage capable of interacting with X-ray damage.
Summary.-Misonidazole (MISO) potentiates the action of cyclophosphamide (CY) and melphalan in the WHFIB culture-adapted fibrosarcoma, whether assayed by cell survival or tumour-growth delay. In the case of CY, MISO also inhibited recovery from potentially lethal drug damage. The optimum effect was seen when MISO was given 1 h before CY, though it was also effective when given 6 h before or 1 h after the drug. Other radiosensitizers also potentiated the action of CY. There was only a small effect of MISO on the LD50 of CY and no effect on CY toxicity as assayed by changes in blood counts or damage to bladder epithelium. However, mice bearing multiple lung tumours were less able to cope with the combined treatment than those bearing s.c. tumours.
V79 Chinese hamster cells have been irradiated with X-rays and neutrons given simultaneously. The oxygen enhancement ratio and r.b.e. were measured as a function of the proportion of the dose due to the neutrons, which varied from 0 to 100 per cent. These were compared with the values calculated assuming the two types of radiation act independently, following an approach suggested by Curtis. The o.e.r. was less than the predicted value when the neutrons contributed less than about 40 per cent of the total dose. The r.b.e. also did not vary as predicted on the basis of independent action. The 'oxygen gain factor' reached half its maximum value when the proportion of the dose due to neutrons was only about 27 per cent. The results imply that there may be interaction between the damage caused by X-rays and neutrons and that beams having only 20 to 30 per cent of their dose due to high l.e.t. radiation, could be of therapeutic benefit.
The ability of acutely hypoxic tumour cells to recover from sublethal damage following irradiation in vivo and in vitro has been measured using a single tumour system. The methods of assay were tumour growth delay, local tumour control and tumour cell survival in vitro following treatment in vivo or in vitro. Tumours in vivo or cells in vitro rendered acutely hypoxic during irradiation were irradiated with either single doses or two doses 24 hours apart. Cells left in situ had a greater capacity for recovery than those treated either in vivo or in vitro and then assayed in vitro. It is suggested that tumours may not show a systematically reduced capacity for recovery relative to normal tissues, unless chronically hypoxic tumour cells have a reduced capacity for recovery and determine the response. However, the results imply that deductions as to the ability of tumour cells to recover from sublethal damage (whether chronically hypoxic or not), which rely on in vitro assays, may underestimate the extent of recovery.
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