Maeyama K, Ohno A, Taguchi Y, Watanabe T, Wada H
Jpn J Pharmacol. 1985 Oct;39(2):145-51. doi: 10.1254/jjp.39.145.
The increase of histidine decarboxylase (HDC) activity during late pregnancy in the whole bodies of fetal mice and the kidneys of their mothers were almost completely inhibited by i.p. administration of 25 mg/kg of alpha-fluoromethylhistidine (alpha-FMH), a suicide inhibitor of HDC, starting on day 13 of pregnancy. The increase of HDC in fetal mice was previously shown to be in mast cells [T. Watanabe et al., Proc. Natl. Acad. Sci. U.S.A. 78, 4209-4212 (1981)]. The increase of HDC in maternal kidneys was examined by using estrogen and W/WV mice, which were devoid of mast cells and infertile. Treatment of castrated mice with 17-beta-estradiol increased the HDC activity of the kidney, and this increase was antagonized by concomitant treatment with clomiphene, an antiestrogen, confirming that the increase is mediated through an estrogen receptor. HDC activity in the kidney of W/WV mice was also increased by estradiol treatment, indicating that HDC activity was associated with non-mast cells.
从妊娠第13天开始，通过腹腔注射25 mg/kg的α-氟甲基组氨酸（α-FMH，组氨酸脱羧酶（HDC）的自杀性抑制剂），几乎完全抑制了妊娠后期胎鼠全身及其母鼠肾脏中HDC活性的增加。先前已证明胎鼠中HDC的增加存在于肥大细胞中[T. Watanabe等人，《美国国家科学院院刊》78, 4209 - 4212 (1981)]。通过使用雌激素和W/WV小鼠（缺乏肥大细胞且不育）来研究母鼠肾脏中HDC的增加情况。用17-β-雌二醇处理去势小鼠可增加肾脏的HDC活性，而同时用抗雌激素药物氯米芬处理可拮抗这种增加，证实这种增加是通过雌激素受体介导的。用雌二醇处理W/WV小鼠的肾脏，其HDC活性也会增加，表明HDC活性与非肥大细胞有关。
