Linked Life Data

12017477

Source:http://linkedlifedata.com/resource/pubmed/id/12017477

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2002-5-17
pubmed:abstractText
Oxidative DNA damage has been implicated in some of the biological properties of UVA but so far not in the acute photosensitivity or cellular sensitivity. In contrast to pyrimidine dimers, oxidative DNA damage is predominantly processed by base excision repair (BER). In order to further clarify the role of oxidative DNA damage and its repair in the acute cellular response to UV light, we studied UVA1 and UVB sensitivities in three different cell model systems with modified BER. 8-Oxoguanine-DNA-glycosylase 1-/- (OGG1-/-) mouse embryonal fibroblasts and human fibroblasts in which BER was inhibited by incubation with methoxyamine were hypersensitive to UVA1, in particular to low doses. This hypersensitivity could be partially corrected by reexpression of OGG1 in OGG1-/- cells. The Chinese hamster ovary (CHO) cells with upregulated AP-endonuclease 1 exhibited reduced UVA1 sensitivity. UVB sensitivity was not altered in any of the cell models. These results indicate that DNA damage, in particular oxidative DNA damage, contributes to cellular UVA1 sensitivity and underline a pivotal role of its repair in the cellular responses to UVA1.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0031-8655
pubmed:author
pubmed:issnType
Print
pubmed:volume
75
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
507-12
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Modulation of base excision repair alters cellular sensitivity to UVA1 but not to UVB1.
pubmed:affiliation
Department of Dermatology, Boston University School of Medicine, MA 02118, USA.
pubmed:publicationType
Journal Article, Comparative Study