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2-hydroxyestradiol induces oxidative DNA damage and apoptosis in human mammary epithelial cells

Cited 24 time in Web of Science Cited 25 time in Scopus
Authors
Hurh, Yeon-Jin; Chen, Zhi-Hua; Na, Hye-Kyung; Han, Soon- Young; Surh, YoungJoon
Issue Date
2004-12
Citation
Journal of Toxicology and Environmental Health - Part A, Vol.67 No.23-24, pp.1939-1953
Abstract
Catechol estrogens, the hydroxylated metabolites of 17beta-estradiol (E), have been considered to be implicated in estrogen-induced carcinogenesis. 2-Hydroxyestradiol (2-OHE2), a major oxidized metabolite of E-2 formed preferentially by cytochrome P-450 1A1, reacts with DNA to form stable adducts and exerts genotoxicity. 2-OHE2 can be oxidized to quinone, which is accompanied by generation of reactive oxygen species (ROS). in the present study, 2-OHE2 induced strand scission in Phichi1 74 phage DNA and oxidative base modifications in calf thymus DNA in the presence of cupric ion. In cultured human mammary epithelial (MCF-10A) cells, 2-OHE2 treatment produced ROS accumulation, 8-oxo-7,8-dihydroxy-2'-deoxyguanosine formation, cytotoxicity, and disruption of mitochondrial transmembrane potential, all of which were prevented by N-acetylcysteine. These findings, taken together, suggest that 2-OHE2-induced oxidative DNA damage and apoptosis in MCF-10A cells might be mediated by ROS generated via the redox cycling of this catechol estrogen.
ISSN
1528-7394
URI
https://hdl.handle.net/10371/172805
DOI
https://doi.org/10.1080/15287390490514598
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Graduate School of Convergence Science and Technology (융합과학기술대학원)Dept. of Molecular and Biopharmaceutical Sciences (분자의학 및 바이오제약학과)Journal Papers (저널논문_분자의학 및 바이오제약학과)
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