The metabolism of [ 3
H]estrone sulfate ([ 3
H]E 1
S) was studied in normal breast tissue from 10 premenopausal women without oral contraceptives (OC), in 12 OC users and in 9 untreated postmenopausal women. [ 3
H]E 1
S was converted into estrone ([ 3
H]E
... (More)
The metabolism of [ 3
H]estrone sulfate ([ 3
H]E 1
S) was studied in normal breast tissue from 10 premenopausal women without oral contraceptives (OC), in 12 OC users and in 9 untreated postmenopausal women. [ 3
H]E 1
S was converted into estrone ([ 3
H]E 1
) and estradiol-17β ([ 3
H]E 2
) by tissue samples from all three groups of women, with only minor formation of other unconjugated compounds. The rate of [ 3
H]E 2
formation was significantly higher in premenopausal women without OC than in postmenopausal women. Among premenopausal women, OC users had a significantly lower rate of total hydrolysis and of [ 3
H]E 1
formation than non-users. The rate of total hydrolysis of [ 3
H]E 1
S in normal breast tissue from all three groups of women was similar to that in muscle, but the rate of [ 3
H]E 2
formation was ten times higher. Both total hydrolysis rate and rate of [ 3
H]E 2
formation were significantly lower in normal breast tissue than in breast carcinoma and in normal and neoplastic endometrium. The specific ability of normal breast tissue to convert E 1
S into the terminal biologically active estrogen E 2
may be important for estrogenic stimulation of the breast in subjects with low circulating E 2
levels. The lower rate of E 1
formation in OC users may reflect an inhibitory effect of the progestagen compound in such preparations.
@article{b57f130b-54af-4b72-ad7c-84f235bcbd78,
abstract = {{<p><br>
The metabolism of [<br>
<sup>3</sup><br>
H]estrone sulfate ([<br>
<sup>3</sup><br>
H]E<br>
<sub>1</sub><br>
S) was studied in normal breast tissue from 10 premenopausal women without oral contraceptives (OC), in 12 OC users and in 9 untreated postmenopausal women. [<br>
<sup>3</sup><br>
H]E<br>
<sub>1</sub><br>
S was converted into estrone ([<br>
<sup>3</sup><br>
H]E<br>
<sub>1</sub><br>
) and estradiol-17β ([<br>
<sup>3</sup><br>
H]E<br>
<sub>2</sub><br>
) by tissue samples from all three groups of women, with only minor formation of other unconjugated compounds. The rate of [<br>
<sup>3</sup><br>
H]E<br>
<sub>2</sub><br>
formation was significantly higher in premenopausal women without OC than in postmenopausal women. Among premenopausal women, OC users had a significantly lower rate of total hydrolysis and of [<br>
<sup>3</sup><br>
H]E<br>
<sub>1</sub><br>
formation than non-users. The rate of total hydrolysis of [<br>
<sup>3</sup><br>
H]E<br>
<sub>1</sub><br>
S in normal breast tissue from all three groups of women was similar to that in muscle, but the rate of [<br>
<sup>3</sup><br>
H]E<br>
<sub>2</sub><br>
formation was ten times higher. Both total hydrolysis rate and rate of [<br>
<sup>3</sup><br>
H]E<br>
<sub>2</sub><br>
formation were significantly lower in normal breast tissue than in breast carcinoma and in normal and neoplastic endometrium. The specific ability of normal breast tissue to convert E<br>
<sub>1</sub><br>
S into the terminal biologically active estrogen E<br>
<sub>2</sub><br>
may be important for estrogenic stimulation of the breast in subjects with low circulating E<br>
<sub>2</sub><br>
levels. The lower rate of E<br>
<sub>1</sub><br>
formation in OC users may reflect an inhibitory effect of the progestagen compound in such preparations.</p>}},
author = {{Söderqvist, Gunnar and Olsson, Håkan and Wilking, Nils and von Schoultz, Bo and Carlström, Kjell}},
issn = {{0960-0760}},
language = {{eng}},
month = {{01}},
number = {{2-3}},
pages = {{221--224}},
publisher = {{Elsevier}},
series = {{Journal of Steroid Biochemistry and Molecular Biology}},
title = {{Metabolism of estrone sulfate by normal breast tissue : Influence of menopausal status and oral contraceptives}},
url = {{http://dx.doi.org/10.1016/0960-0760(94)90148-1}},
doi = {{10.1016/0960-0760(94)90148-1}},
volume = {{48}},
year = {{1994}},
}
; Wilking, Nils
LU
; von Schoultz, Bo
and Carlström, Kjell
(1994)
In Journal of Steroid Biochemistry and Molecular Biology
48(2-3).
p.221-224