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Title: Use of metabolic inhibitors to compare the excision repair of pyrimidine dimers and nondimer DNA damages in human skin fibroblasts exposed to 254-nm and sunlamp-produced > 310-nm ultraviolet radiation

Abstract

Normal human skin fibroblasts were exposed to either 0-5 J/m/sup 2/ of 254-nm ultraviolet (UV) radiation or 0-50 kJ/m/sup 2/ of the Mylar-filtered UV (>310 nm) produced by a fluorescent sunlamp. These cells were then incubated for 0-20 min in medium containing 10 mM hydroxyurea (HU) and 0.1 mM 1-..beta..-D-arabinofuranosyl cytosine (ara C), and the yield of DNA strand breaks was measured by means of the alkaline elution technique. For cells irradiated with 254-nm UV, which results primarily in the formation of cyclobutane pyrimidine dimers, a rapid increase in DNA strand breaks was detected following incubation with these metabolic inhibitors. In contrast, only a low level of strand breaks formed in cells incubated with HU and ara C after irradiation with approximately equitoxic fluences of sunlamp UV >310 nm, which mainly causes the induction of nondimer DNA lesions. Hence, these results are consistent with the conclusion that the pathways involved in the repair of nondimer DNA damages induced by UV wavelengths >310 nm differ from the repair of pyrimidine dimers.

Authors:
; ;
Publication Date:
Research Org.:
Univ. of Texas Health Science Center, Dallas
OSTI Identifier:
5433251
Resource Type:
Journal Article
Journal Name:
Environ. Mutagen.; (United States)
Additional Journal Information:
Journal Volume: 8:3
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; FIBROBLASTS; DNA REPAIR; FURANS; RADIOSENSITIVITY EFFECTS; HYDROXYUREA; PYRIMIDINE DIMERS; RADIOINDUCTION; STRAND BREAKS; EXTREME ULTRAVIOLET RADIATION; FAR ULTRAVIOLET RADIATION; SKIN; AMIDES; ANIMAL CELLS; BIOLOGICAL RECOVERY; BIOLOGICAL REPAIR; BODY; CONNECTIVE TISSUE CELLS; ELECTROMAGNETIC RADIATION; HETEROCYCLIC COMPOUNDS; HYDROXY COMPOUNDS; ORGANIC COMPOUNDS; ORGANIC NITROGEN COMPOUNDS; ORGANIC OXYGEN COMPOUNDS; ORGANS; RADIATIONS; RECOVERY; REPAIR; SOMATIC CELLS; ULTRAVIOLET RADIATION; 560121* - Radiation Effects on Cells- External Source- (-1987)

Citation Formats

Rosenstein, B S, Chao, C C.K., and Ducore, J M. Use of metabolic inhibitors to compare the excision repair of pyrimidine dimers and nondimer DNA damages in human skin fibroblasts exposed to 254-nm and sunlamp-produced > 310-nm ultraviolet radiation. United States: N. p., 1986. Web. doi:10.1002/em.2860080303.
Rosenstein, B S, Chao, C C.K., & Ducore, J M. Use of metabolic inhibitors to compare the excision repair of pyrimidine dimers and nondimer DNA damages in human skin fibroblasts exposed to 254-nm and sunlamp-produced > 310-nm ultraviolet radiation. United States. https://doi.org/10.1002/em.2860080303
Rosenstein, B S, Chao, C C.K., and Ducore, J M. 1986. "Use of metabolic inhibitors to compare the excision repair of pyrimidine dimers and nondimer DNA damages in human skin fibroblasts exposed to 254-nm and sunlamp-produced > 310-nm ultraviolet radiation". United States. https://doi.org/10.1002/em.2860080303.
@article{osti_5433251,
title = {Use of metabolic inhibitors to compare the excision repair of pyrimidine dimers and nondimer DNA damages in human skin fibroblasts exposed to 254-nm and sunlamp-produced > 310-nm ultraviolet radiation},
author = {Rosenstein, B S and Chao, C C.K. and Ducore, J M},
abstractNote = {Normal human skin fibroblasts were exposed to either 0-5 J/m/sup 2/ of 254-nm ultraviolet (UV) radiation or 0-50 kJ/m/sup 2/ of the Mylar-filtered UV (>310 nm) produced by a fluorescent sunlamp. These cells were then incubated for 0-20 min in medium containing 10 mM hydroxyurea (HU) and 0.1 mM 1-..beta..-D-arabinofuranosyl cytosine (ara C), and the yield of DNA strand breaks was measured by means of the alkaline elution technique. For cells irradiated with 254-nm UV, which results primarily in the formation of cyclobutane pyrimidine dimers, a rapid increase in DNA strand breaks was detected following incubation with these metabolic inhibitors. In contrast, only a low level of strand breaks formed in cells incubated with HU and ara C after irradiation with approximately equitoxic fluences of sunlamp UV >310 nm, which mainly causes the induction of nondimer DNA lesions. Hence, these results are consistent with the conclusion that the pathways involved in the repair of nondimer DNA damages induced by UV wavelengths >310 nm differ from the repair of pyrimidine dimers.},
doi = {10.1002/em.2860080303},
url = {https://www.osti.gov/biblio/5433251}, journal = {Environ. Mutagen.; (United States)},
number = ,
volume = 8:3,
place = {United States},
year = {Wed Jan 01 00:00:00 EST 1986},
month = {Wed Jan 01 00:00:00 EST 1986}
}