Abstract
Purpose : To obtain evidence that the p53 gene is indispensable for reduction of high teratogenic risk of radiation at a high dose-rate to zero risk by lowering the dose-rate. Materials and methods : Wild-type p53 (+/+), heterozygous p53 (+/-) and null p53 (-/-) mice were exposed to γ-rays at high or low dose-rates during days 9.5-10.5 of gestation. The incidence of malformations and prenatal deaths was studied. Frequencies of cells dying by apoptosis were measured during or after protracted irradiation. Results : After irradiation with 2 Gy, the frequency of apoptotic cells increased to 20% for p53 (+/+) mice and did not increase at all for p53 (-/-) mice. For p53 (+/+) mice, 2 Gy γ-rays induced 70% malformations when given at 1.06 Gy/min, but no malformations above the control when given at 1.2m Gy/min. In contrast, after irradiation of p53 (-/-) foetuses with 2 Gy at 1.2m Gy/min, the incidence of malformations increased 12% above control levels. Conclusion : Foetal irradiation with 2 Gy at 1.2m Gy/min was not teratogenic for p53 (+/+) mice but teratogenic for p53 (-/-) mice. This indicates that the p53 gene is indispensable for a threshold effect in the risk of radiation at low doses or dose-rates.
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