Repair of cyclobutyl pyrimidine dimers in human skin: Variability among normal humans in nucleotide excision and in photorepair

Betsy M. Sutherland, Haim Hacham, Paula Bennett, John C. Sutherland, Michael Moran, R. W. Gange

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background/Aims: Photoreactivation (PR) of cyclobutyl pyrimidine dimers (CPD) in human skin remains controversial. Recently Whitmore et al. (1) reported negative results of experiments using two photorepair light (PRL) sources on UV-irradiated skin of volunteers. However, their PRL sources induced substantial levels of dimers in skin, suggesting that the additional dimers formed could have obscured PR. We met a similar problem of dimer induction by a PRL source. We designed and validated a PRL source of sufficient intensity to catalyse PR, but that did not induce CPD, and used it to measure photorepair in human skin. Methods and Results: Using a solar simulator filtered with three types of UV-filters, we found significant dimer formation in skin, quantified by number average length analysis using electrophoretic gels of isolated skin DNA. To prevent scattered UV from reaching the skin, we interposed shields between the filters and skin, and showed that the UV-filtered/shielded solar simulator system did not induce damage in isolated DNA or in human skin. We exposed skin of seven healthy human volunteers to 302 nm radiation, then to the improved PRL source (control skin areas were kept in the dark for measurement of excision repair). Conclusions: Using a high intensity PRL source that did not induce dimers in skin, we found that three of seven subjects carried out rapid photorepair of dimers; two carried out moderate or slow dimer photorepair, and three did not show detectable photorepair. Excision repair was similarly variable in these volunteers. Subjects with slower excision repair showed rapid photorepair, whereas those with rapid excision generally showed little or no photoreactivation.

Original languageEnglish (US)
Pages (from-to)109-116
Number of pages8
JournalPhotodermatology Photoimmunology and Photomedicine
Volume18
Issue number3
DOIs
StatePublished - Jun 1 2002

Fingerprint

Pyrimidine Dimers
Nucleotides
Skin
Light
DNA Repair
Volunteers
DNA
Solar System
Healthy Volunteers

Keywords

  • Human skin
  • Photolyase
  • Photoreactivation
  • Pyrimidine dimer
  • UV

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Radiology Nuclear Medicine and imaging
  • Dermatology

Cite this

Repair of cyclobutyl pyrimidine dimers in human skin : Variability among normal humans in nucleotide excision and in photorepair. / Sutherland, Betsy M.; Hacham, Haim; Bennett, Paula; Sutherland, John C.; Moran, Michael; Gange, R. W.

In: Photodermatology Photoimmunology and Photomedicine, Vol. 18, No. 3, 01.06.2002, p. 109-116.

Research output: Contribution to journalArticle

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abstract = "Background/Aims: Photoreactivation (PR) of cyclobutyl pyrimidine dimers (CPD) in human skin remains controversial. Recently Whitmore et al. (1) reported negative results of experiments using two photorepair light (PRL) sources on UV-irradiated skin of volunteers. However, their PRL sources induced substantial levels of dimers in skin, suggesting that the additional dimers formed could have obscured PR. We met a similar problem of dimer induction by a PRL source. We designed and validated a PRL source of sufficient intensity to catalyse PR, but that did not induce CPD, and used it to measure photorepair in human skin. Methods and Results: Using a solar simulator filtered with three types of UV-filters, we found significant dimer formation in skin, quantified by number average length analysis using electrophoretic gels of isolated skin DNA. To prevent scattered UV from reaching the skin, we interposed shields between the filters and skin, and showed that the UV-filtered/shielded solar simulator system did not induce damage in isolated DNA or in human skin. We exposed skin of seven healthy human volunteers to 302 nm radiation, then to the improved PRL source (control skin areas were kept in the dark for measurement of excision repair). Conclusions: Using a high intensity PRL source that did not induce dimers in skin, we found that three of seven subjects carried out rapid photorepair of dimers; two carried out moderate or slow dimer photorepair, and three did not show detectable photorepair. Excision repair was similarly variable in these volunteers. Subjects with slower excision repair showed rapid photorepair, whereas those with rapid excision generally showed little or no photoreactivation.",
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