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Title: THE HARMFUL GENETIC EFFECTS OF RADIATION

Journal Article · · Journal of the National Medical Association (U.S.)
OSTI ID:4634618

Evidence relating to the injurious mutagenic effects of ionizing radiation on biological systems is considered from the point of view of animal experimentation and its pertinence to the increasing radiation burden of human populations. Most evidence for harmful genetic effects from at least the higher doses of radiation comes mainly from studies on Drosophila and the mouse. As in Drosophila, mutations in the mouse appear in linear relation to the dose. One difference in the mouse is that the same radiation dose delivered over a longer period produces fewer mutations than higher intensities. This suggests that some repair may occur during chronic doses at the lower rates. It is pointed out that such data may only be converted into estimates of total radiation damage per roentgen from the total number of genes and the demonstration that the mutations observed, whether lethals or selected visibles, show sensitivities which are average for all genes. The average induced rate for the mouse has been calculated to be 21.3 x 10/sup -8/ per gene per r, and for certain specific loci in Drosophila the value is approximates 1.5 X 10/sup 8/, suggesting that the mammal is about 16 times more sensitive than the insect. From similar data it was calculated that the dose which would double the natural mutation rate for both flies and mice is about 40 r. This is a convenient figure, and may be used for men on the basis of tahulated spontameous mutation rates. It is suggested that minor increases in the mutation frequency from low level radiation are imaginary hazards, and that a slight increase in selection would remove many of the harmful mutants as they appear. There is some reason to believe that minor genetic changes are corrected at the cellular level. Thus position is discussed in terms of recent changes in gene theory relating to microbial genetics. This reveals evidence for a mechanism of repair of radiation damage at the level of the smallest genetic units. It is possible, or even probable, that such a mechanlsm operates in premeiotic stages between genes in heterozygous condition in higher organisms. Critical tests have not yet been made, but they might show reduced expression of lethals or semilethals in subsequent generations after radiation, as compared with the results at higher doses. They might appear as so- called conversion which might be interpreted as crossing over by partial replication. It is concluded that the genetic hazards of radiation are overemphasized and that minor deleterious mutations are selected out early or are repaired before they appear. (BBB)

Research Organization:
Amherst Coll., Amherst, Mass.
NSA Number:
NSA-17-038806
OSTI ID:
4634618
Journal Information:
Journal of the National Medical Association (U.S.), Vol. Vol: 54; Other Information: Orig. Receipt Date: 31-DEC-63
Country of Publication:
Country unknown/Code not available
Language:
English

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