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The survival of depurinated Form I SV40 DNA was studied in normal human fibroblasts and in D-complementation Xeroderma pigmentosum (XP) fibroblasts. Survival was measured with an infective center assay. Heat-acid and methyl methanesulfonate (MMS) were used as depurinating agents. After 3 hrs of depurination by heat--acid treatment, infectivity in normal cells was less than 15% of the controls compared to more than 50% for the XP D cell strains. Similar results were obtained with MMS-treated DNA. These results are contrary to expectation since apurinic endonuclease activity, which is presumed to be involved in the repair of apurinic sites, is much lower in XP D cell strains than in normal cell strains. Our results indicate that another mechanism for the repair of apurinic sites could exist.
R D Kudrna, and
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E E Penhoet
September 1991,
Mutation research,
R D Kudrna, and
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E E Penhoet
April 1976,
Proceedings of the National Academy of Sciences of the United States of America,
R D Kudrna, and
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May 1985,
Nihon Hifuka Gakkai zasshi. The Japanese journal of dermatology,
R D Kudrna, and
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May 1993,
Carcinogenesis,
R D Kudrna, and
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E E Penhoet
January 1974,
Mutation research,
R D Kudrna, and
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E E Penhoet
January 1979,
Mutation research,
R D Kudrna, and
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E E Penhoet
December 1991,
Human genetics,
R D Kudrna, and
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E E Penhoet
September 1989,
Mutation research,
R D Kudrna, and
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E E Penhoet
April 1976,
Mutation research,
R D Kudrna, and
J Smith, and
S Linn, and
E E Penhoet
January 1992,
Mutation research,
