Abstract
MANY biological systems are able to repair ultraviolet damage. One of the more extensively studied repair systems in both prokaryotic and eukaryotic organisms involves the excision of ultraviolet-induced, cyclobutane pyrimidine dimers from irradiated DNA1,2. A number of lines of evidence, reviewed elsewhere, indicate that similar repair systems may also act on alterations to DNA that result from the action of other agents3–5. Although the most readily detectable damage to DNAarising from exposure to ionizing radiation is single-strand breaks, there are indications that an excision repair system also operates on such exposed DNAs. For example, there is a small host-cell reactivating effect on irradiated bacteriophage6, and, as shown by Alper7,8, bacteria that are deficient in the ability to reactivate ultraviolet-irradiated bacteriophage (and therefore presumably lacking a functioning excision system) are also more sensitive to X-irradiation. Alper described two types of ionizing radiation damage to microorganisms: (1) N-type—arising from irradiation carried out anoxically—for which there could be extensive repair, and (2) O-type—arising from radiation effects mediated by oxygen–for which there was little repair. Hariharan and Cerutti9,10 have described a radiation product of thymine in γ-irradiated Micrococcus radiodurans and have shown that such a product appears selectively in the acid-soluble fraction of the cells during post-irradiation incubation. The appearance of such a product is analogous to the appearance of pyrimidine dimers in the acid-soluble fraction of cells during excision repair after ultraviolet irradiation.
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SETLOW, R., CARRIER, W. Endonuclease Activity toward DNA irradiated in vitro by Gamma Rays. Nature New Biology 241, 170–172 (1973). https://doi.org/10.1038/newbio241170a0
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DOI: https://doi.org/10.1038/newbio241170a0
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