Abstract
DNA damage inflicted by the alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine, or by UV254nm, stimulated the catabolism of protein-bound poly(ADP-ribose) in the chromatin of cultured hepatocytes. The stimulation was highest at the largest doses of DNA-damaging treatment. As a consequence, the half-life of ADP-ribosyl polymers may drop to less than 41 s. This rapid turnover contrasts with the slow catabolism of a constitutive fraction of polymers exhibiting a half-life of 7.7 h. Our data suggest that post-incisional stimulation of poly(ADP-ribose) biosynthesis in DNA-excision repair is coupled with an adaptation of poly(ADP-ribose) catabolism in mammalian cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Benzamides / pharmacology*
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Cells, Cultured
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Chromatin / drug effects
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Chromatin / metabolism
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Chromatin / radiation effects
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DNA Damage*
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Kinetics
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Liver / drug effects*
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Liver / metabolism
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Male
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Methylnitronitrosoguanidine / pharmacology*
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Nucleoside Diphosphate Sugars / metabolism*
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Poly Adenosine Diphosphate Ribose / metabolism*
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Poly Adenosine Diphosphate Ribose / radiation effects
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Radiation-Sensitizing Agents / pharmacology
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Rats
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Rats, Inbred Strains
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Ultraviolet Rays*
Substances
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Benzamides
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Chromatin
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Nucleoside Diphosphate Sugars
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Radiation-Sensitizing Agents
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Methylnitronitrosoguanidine
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Poly Adenosine Diphosphate Ribose
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3-aminobenzamide