DNA repair in human cells, as assayed by the photolysis of 5-bromodeoxyuridine incorporated during repair, takes one of two limiting forms, depending on the nature of the original insult to the DNA. Damage from ionizing radiation is repaired by the insertion of three or four nucleotides during a brief period (∼60 min) after the insult, but in the case of ultraviolet radiation there is extensive excision of bases (∼100) during a protracted period (18 to 20 hr). Similarly, chemicals that damage DNA fall into two categories, those that result in the ionizing or “short” type of DNA repair (ethyl methanesulfonate, methyl methanesulfonate, propane sultone) and those that result in the ultraviolet or “long” type of repair (N-acetoxy-2-acetylaminofluorene, 2-methoxy-6-chloro-9-[3-(ethyl-2-chloroethyl)aminopropylamino] acridine dihydrochloride). In addition, some chemicals (4-nitroquinoline 1-oxide) cause damage that apparently is repaired by both mechanisms. When agents that induce long repair in normal cells are used to treat cells from patients with the genetic disease xeroderma pigmentosum (characterized by extreme sensitivity to ultraviolet radiation), defective repair is seen. Thus it is possible that long repair involves the action of an endonuclease (thought to be lacking in xeroderma cells) on a distortion or intercalation in the DNA. Short repair may involve the simple excision and replacement of a few bases at the site of a single-strand break.


Research sponsored jointly by National Cancer Institute Grant Y01-CP-40013 and by the United States Atomic Energy Commission under contract with the Union Carbide Corporation.

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