4-Hydroxyestradiol, an metabolite of estradiol, forms adducts with adenine (N3) and guanine (N7) by depurinating sites in DNA of cultured human breast epithelial cells. This effect may play an important role in malignant transformation of these cells.
Catechol estrogens, especially 4-hydroxylated metabolites of 17beta-estradiol (E(2)), are responsible for estrogen-induced carcinogenesis. 4-Hydroxyestradiol (4-OHE(2)), a major metabolite of E(2) formed preferentially by cytochrome P-450 1B1, is oxidized to E(2)-3,4-quinone, which can react with DNA to yield the depurinating adducts
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 20(7), 1502-1515 (2011-05-26)
Current models of breast cancer risk prediction do not directly reflect mammary estrogen metabolism or genetic variability in exposure to carcinogenic estrogen metabolites. We developed a model that simulates the kinetic effect of genetic variants of the enzymes CYP1A1, CYP1B1
Keratinocyte growth factor (KGF) is expressed by uterine endometrial epithelial cells during the estrous cycle and during pregnancy in pigs, whereas KGF receptor is expressed in conceptus trophectoderm and endometrial epithelia. In particular, KGF expression in the endometrium is highest
The Science of the total environment, 407(7), 2209-2215 (2009-01-28)
Oxidative compounds have been demonstrated to decrease the fertilization capability and viability of offspring of treated spermatozoa. As estrogen and its hydroxylated metabolites readily undergo redox cycling, this study was undertaken to determine if estrogens and other oxidants could damage
Catecholestrogens [4-hydroxyestradiol (4-OHE(2))] have been implicated in human carcinogenesis, although the mechanism remains unestablished. In this study pUC 18 plasmid DNA was modified with 4-OHE(2) and nitric oxide (NO). The modification induced in native DNA exhibited hyperchromicity, single strand breaks
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