Open AccessSteroid 16α‐Hydroxylase from Human Fetal Liver; Inhibition by Steroids
Author(s) -
Sano Yumiko,
Shibusawa Haru,
Yoshida Nobutaka,
Sekiba Kaoru,
Okinaga Shoichi,
Arai Kiyoshi
Publication year - 1980
Publication title -
acta obstetricia et gynecologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.401
H-Index - 102
eISSN - 1600-0412
pISSN - 0001-6349
DOI - 10.3109/00016348009155404
Subject(s) - medicine , fetus , steroid , pregnancy , endocrinology , hormone , biology , genetics
The 16α‐hydroxylase system in fetal liver which used dehydroepiandrosterone (DHA) or pregnenolone as substrate, was apparently inhibited by various endogenous and synthetic steroids: DHA, pregnenolone, their sulfates, androstenediol, androstenetriol, estrone, estradiol‐17β, ethynylestradiol and chlormadinone‐acetate. The inhibition constants (Ki) towards DHA were as follows; pregnenolone 22 μM, DHA‐sulfate 13 μM, pregnenolone‐sulfate 21 μM, androstenediol 16 μM, androstenetriol 53 μM, estrone 32 μM, estradiol‐17β 75 μM, ethynylestradiol 22 μM and chlormadinone‐acetate 27 μM. The Ki values towards pregnenolone were DHA 6.3 μM, DHA‐sulfate 8.3 μM, pregnenolone‐sulfate 3.9 μM, androstenediol 8.7 μM, androstenetriol 14.7 μM, estradiol‐17β 15.4 μM and ethynylestradiol 16.0 μM, respectively. The reaction products, 16αOH‐DHA and 16αOH‐pregnenolone, showed little inhibitory effect upon the 16α‐hydroxylase.