摘要: The natural hormone 17β-estradiol (E2) induces tumors in various organs of rats, mice, and hamsters. In humans, slightly elevated circulating estrogen levels caused either by increased endogenous production or therapeutic doses medications increase breast uterine cancer risk. Several epigenetic mechanisms tumor induction this have been proposed based on its lack mutagenic activity bacterial mammalian cell test systems. More recent evidence supports a dual role carcinogenesis as stimulating proliferation procarcinogen inducing genetic damage. Tumors may be initiated metabolic conversion E2 to 4-hydroxyestradiol catalyzed specific 4-hydroxylase (CYP1B1) further activation catechol reactive semiquinone/quinone intermediates. types direct indirect free radical-mediated DNA damage are induced E2, 4-hydroxyestradiol, corresponding quinone cell-free systems, cells i...
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