Effects of alpha-fluoromethylhistidine on increase in histidine decarboxylase activity of maternal mouse kidney observed during late pregnancy and evidence for its non-mast cell origin by using estrogen and W/WV mice.

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.