Abstract
Data on hereditary effects of radiation in man remain very limited, and hence estimation of genetic hazards is based largely on results from animals. In males, extensive work on gene mutations and chromosome aberrations has shown that not only reduction of dose rate but also fractionation of the dose can reduce the mutational yield, and such effects may be due to changes in the cell population structure with prolonged or repeated treatment. In female mice the dose–response relationship for gene mutation is curved, probably due to the effects of DNA repair. Mouse primary oocytes, which receive the major part of the lifetime dose, are very insensitive to mutation by radiation, but it is not yet known whether all species are equally insensitive.
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