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1 the formation of mitogens, including 16alpha-hydroxyestrone.
2 s of daidzein, genistein, and 2- and 16alpha-hydroxyestrone.
3 f nonestrogenic to estrogenic metabolites (2-hydroxyestrone 1/16 alpha-hydroxyestrone) than did those
4 inistration of the CYP1B1 metabolite 16alpha-hydroxyestrone (1.5 mg . kg(-1) . d(-1) IP) caused the d
5 e urinary 2-hydroxyestrone (2-OH) to 16alpha-hydroxyestrone (16alpha-OH) ratio (P < 0.05), and equol-
6 f urinary 2-hydroxyestrone (2OHE(1)):16alpha-hydroxyestrone (16alpha-OHE(1)) was higher in Singapore
7 olites, such as 4-hydroxyestrone and 16alpha-hydroxyestrone (16alpha-OHE), and can also promote local
9 the biologically active metabolite, 16alpha-hydroxyestrone (16alphaOHE1), may be associated with a l
10 vone concentration (P < 0.05), the urinary 2-hydroxyestrone (2-OH) to 16alpha-hydroxyestrone (16alpha
11 xyadenosine adducts induced by quinones of 2-hydroxyestrone, 2-hydroxyestradiol, or 2-hydroxyestriol
12 ol, 17-epiestriol, 16-ketoestradiol, 16alpha-hydroxyestrone, 2-methoxyestrone, 4-methoxyestrone, 2-hy
13 to determine whether the ratio of urinary 2-hydroxyestrone (2OHE(1)):16alpha-hydroxyestrone (16alpha
14 biologically inactive estrogen metabolite, 2-hydroxyestrone (2OHE1), to the biologically active metab
15 thod also allows for the identification of 2-hydroxyestrone-3-methyl ether in urine obtained from bot
17 trone, 2-methoxyestrone, 4-methoxyestrone, 2-hydroxyestrone-3-methyl ether, 2-methoxyestradiol, 4-met
18 -hydroxy and 2- and 4-methoxy derivatives; 2-hydroxyestrone-3-methyl ether; 17beta-estradiol and its
19 oxy and its 2-, 4-methoxy derivatives, and 2-hydroxyestrone-3-methyl ether; 17beta-estradiol and its
20 , 4-, and 16alpha-hydroxy derivatives, and 2-hydroxyestrone-3-methyl ether; estradiol and its 2-, 4-m
21 r, 2-methoxyestradiol, 4-methoxyestradiol, 2-hydroxyestrone, 4-hydroxyestrone, and 2-hydroxyestradiol
24 ampal neuronal cells as an in vitro model, 4-hydroxyestrone, an estrone metabolite with little estrog
25 ens into carcinogenic metabolites, such as 4-hydroxyestrone and 16alpha-hydroxyestrone (16alpha-OHE),
26 l (E2) and 2 urinary estrogen metabolites (2-hydroxyestrone and 16alpha-hydroxyestrone) with radiogra
27 However, UGT2B16 efficiently conjugated 4-hydroxyestrone and 4-tert-butylphenol, substrates that a
29 rogens (2- or 4-hydroxyestradiol and 2- or 4-hydroxyestrone) are chemically reactive estrogen metabol
30 the cycle mean daily urinary excretion of 2-hydroxyestrone (averaged over the entire cycle) from 11.
32 95% CI 1.49-5.68) compared with women with 2-hydroxyestrone concentrations in the middle tertile), af
33 However, the mean daily excretion of 16alpha-hydroxyestrone did not change (7.0 +/- 1.14 nmol/12-h du
34 increased by 90-115%, and the rate of 6beta-hydroxyestrone formation (a minor metabolite formed in l
35 have a ratio of 16alpha-hydroxyestrone to 2-hydroxyestrone in the highest tertile (>0.86; OR 1.86, 9
36 having baseline urinary concentrations of 2-hydroxyestrone in the lowest tertile (OR 2.9, 95% CI 1.4
38 proteins, catalyzed the glucuronidation of 4-hydroxyestrone, indicating that the carboxyl terminus of
41 olites (e.g., 4-hydroxyestradiol and 16alpha-hydroxyestrone) may be of unique importance for stimulat
42 Lower urinary 2-hydroxyestrogen/16-alpha-hydroxyestrone (OR per 1-ln decrease = 2.04; 95% CI, 1.1
45 nic metabolites (2-hydroxyestrone 1/16 alpha-hydroxyestrone) than did those who obtained calcium prim
48 were more likely to have a ratio of 16alpha-hydroxyestrone to 2-hydroxyestrone in the highest tertil
49 The ratio of 2-hydroxyestrone to 16alpha-hydroxyestrone was higher during the isoflavone-rich soy
50 lower baseline serum estradiol and urinary 2-hydroxyestrone with developing knee OA in middle-aged wo
51 en metabolites (2-hydroxyestrone and 16alpha-hydroxyestrone) with radiographically defined prevalent