17 beta-Oestradiol attenuates nucleotide excision repair |
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| Authors: | Evans Mark D Butler John M Nicoll Karen Cooke Marcus S Lunec Joseph |
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| Affiliation: | Oxidative Stress Group, Department of Clinical Biochemistry, P.O. Box 65, Robert Kilpatrick Clinical Sciences Building, University of Leicester, Leicester Royal Infirmary, University Hospitals of Leicester NHS Trust, Leicester LE2 7LX, UK. mde2@le.ac.uk |
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| Abstract: | Epidemiological studies strongly suggest associations between chronic exposure to endogenous oestrogens and the development of breast and gynaecological tumours. Two mechanisms by which 17 beta-oestradiol (E2) may enhance tumorigenesis are: (i) enhancement of cell proliferation and (ii) the production of reactive, genotoxic metabolites. Here we suggest an additional mechanism, inhibition of DNA repair. The removal of UV-induced thymine dimers from human keratinocytes, reflective of nucleotide excision repair, was significantly attenuated by treatment of cells with E2. In contrast, treatment with 17 alpha-oestradiol had no effect. Mechanisms are proposed for this effect of E2, which may contribute to its carcinogenic potential. |
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