| Autor: |
de Lima-Bessa KM; Department of Microbiology, Institute of Biomedical Sciences, University of São Paulo, Avenue Prof Lineu Prestes, São Paulo, SP, Brazil., Armelini MG, Chiganças V, Jacysyn JF, Amarante-Mendes GP, Sarasin A, Menck CF |
| Jazyk: |
angličtina |
| Zdroj: |
DNA repair [DNA Repair (Amst)] 2008 Feb 01; Vol. 7 (2), pp. 303-12. Date of Electronic Publication: 2007 Dec 21. |
| DOI: |
10.1016/j.dnarep.2007.11.003 |
| Abstrakt: |
Ultraviolet (UV) light generates two major DNA lesions: cyclobutane pyrimidine dimers (CPDs) and pyrimidine-(6-4)-pyrimidone photoproducts (6-4PPs), but the specific participation of these two lesions in the deleterious effects of UV is a longstanding question. In order to discriminate the precise role of unrepaired CPDs and 6-4PPs in UV-induced responses triggering cell death, human fibroblasts were transduced by recombinant adenoviruses carrying the CPD-photolyase or 6-4PP-photolyase cDNAs. Both photolyases were able to prevent UV-induced apoptosis in cells deficient for nucleotide excision repair (NER) to a similar extent, while in NER-proficient cells UV-induced apoptosis was prevented only by CPD-photolyase, with no effects observed when 6-4PPs were removed by the specific photolyase. These results strongly suggest that both CPDs and 6-4PPs contribute to UV-induced apoptosis in NER-deficient cells, while in NER-proficient cells, CPDs are the only lesions responsible for UV-killing, probably due to the rapid repair of 6-4PPs by NER. As a consequence, the difference in skin photosensitivity, including carcinogenesis, of most of the xeroderma pigmentosum patients and of normal people is probably not only a quantitative aspect, but depends on the type of DNA damage induced by sunlight and its rate of repair. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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