Poly(ADP-ribose) metabolism in ultraviolet irradiated human fibroblasts

Poly(ADP-ribose) metabolism in ultraviolet irradiated human fibroblasts

Exposure of human fibroblasts to 5 J/m2 of UV light resulted in a rapid increase of up to 1500% in the intracellular content of poly(ADP-ribose) and a rapid depletion of its metabolic precursor, NAD. When added just prior to UV treatment, the poly(ADP-ribose) polymerase inhibitor, 3-aminobenzamide,...

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Bibliographic Details
Published in:The Journal of biological chemistry Vol. 258; no. 1; pp. 103 - 107
Main Authors: Jacobson, E L, Antol, K M, Juarez-Salinas, H, Jacobson, M K
Format: Journal Article
Language:English
Published: United States Elsevier Inc 10-01-1983
American Society for Biochemistry and Molecular Biology
Subjects:
Cells, Cultured
Cytarabine - pharmacology
DNA Repair
DNA Replication - drug effects
DNA Replication - radiation effects
Fibroblasts - metabolism
Fibroblasts - radiation effects
Humans
Hydroxyurea - pharmacology
Infant, Newborn
Male
NAD - metabolism
NAD - radiation effects
Nucleoside Diphosphate Sugars - radiation effects
Poly Adenosine Diphosphate Ribose - metabolism
Poly Adenosine Diphosphate Ribose - radiation effects
Skin - drug effects
Skin - metabolism
Skin - radiation effects
Ultraviolet Rays
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Summary:Exposure of human fibroblasts to 5 J/m2 of UV light resulted in a rapid increase of up to 1500% in the intracellular content of poly(ADP-ribose) and a rapid depletion of its metabolic precursor, NAD. When added just prior to UV treatment, the poly(ADP-ribose) polymerase inhibitor, 3-aminobenzamide, totally blocked both the increase of poly(ADP-ribose) and decrease in NAD for up to 2.5 h. Addition of 3-aminobenzamide at the time of maximal accumulation of poly(ADP-ribose) resulted in a decrease to basal levels with a half-life of approximately 6 min. The rates of accumulation of poly(ADP-ribose) and depletion of NAD were increased in the presence of either 1-beta-arabinofuranosylcytosine or hydroxyurea. Since these agents are known to cause an additional accumulation of DNA strand breaks following UV irradiation, these data provide evidence for a mechanism in which the rate of poly(ADP-ribose) synthesis following DNA damage is regulated in intact cells by the number of DNA strand breaks. Under conditions in which the synthesis of poly(ADP-ribose) was blocked, DNA repair replication induced by UV light was neither stimulated nor inhibited.
ISSN:0021-9258
1083-351X
DOI:10.1016/S0021-9258(18)33226-5