Satoh Takashi, Itoh Shinji, Seki Toshio, Itoh Shungo, Nomura Norikazu, Yoshizawa Itsuo
Hokkaido College of Pharmacy, 7-1 Katsuraoka-cho, Otaru, Hokkaido, Japan.
J Steroid Biochem Mol Biol. 2002 Oct;82(2-3):209-16. doi: 10.1016/s0960-0760(02)00154-1.
To examine the influence on aromatase and sulfatase pathways in estrogen pool by drugs reported to cause gynecomastia as the side effect, 29 ethical drugs were incubated with human placental microsomes as an enzyme source. The percent inhibition of drugs on aromatase pathway was obtained by sum of the velocity constants of two products, estrone (E1) and estradiol (E2) from testosterone (T) as the substrate, and that on sulfatase pathway was obtained as the velocity constant of production of E1 from estrone sulfate (E1S). Although several drugs including ketoconazole showed a significant inhibition effect on aromatase pathway at their non-clinical over-dose concentration (100 microM), no influence on the inhibition was observed in any drugs at their approximately therapeutic concentration (1 microM). However, several drugs including spironolactone gave the product ratio (E2/E1) having higher value than that of the control, the result means spironolactone inhibits the conversion of E2 to E1. No inhibitory effect of the drugs tested on estrogen production from E1S (sulfatase pathway) was confirmed. The results suggest the possibility that the tested drugs known to cause gynecomastia have no inhibitory effect essentially on aromatase and sulfatase pathways.
为了研究据报道有导致男性乳房发育副作用的药物对雌激素池中的芳香化酶和硫酸酯酶途径的影响,将29种处方药与人胎盘微粒体作为酶源一起孵育。药物对芳香化酶途径的抑制百分比通过以睾酮(T)为底物的两种产物雌酮(E1)和雌二醇(E2)的速度常数之和获得,对硫酸酯酶途径的抑制百分比通过硫酸雌酮(E1S)产生E1的速度常数获得。尽管包括酮康唑在内的几种药物在其非临床过量浓度(100微摩尔)时对芳香化酶途径显示出显著抑制作用,但在其大约治疗浓度(1微摩尔)时,未观察到任何药物对抑制作用有影响。然而,包括螺内酯在内的几种药物的产物比率(E2/E1)高于对照组,结果表明螺内酯抑制E2向E1的转化。未证实受试药物对E1S产生雌激素(硫酸酯酶途径)有抑制作用。结果提示,已知会导致男性乳房发育的受试药物基本上对芳香化酶和硫酸酯酶途径没有抑制作用。