Key result
Alpha-fluoromethylhistidine inhibits late-pregnancy histidine decarboxylase increases in fetal mice and maternal kidneys.
Why the study?
The origin and regulation of increased histidine decarboxylase activity in maternal mouse kidneys during late pregnancy were unclear, particularly regarding mast cell involvement.
The study demonstrates that the pregnancy-associated increase in kidney histidine decarboxylase activity is of non-mast cell origin and is mediated through estrogen receptors.
Estrogen-mediated non-mast cell histidine decarboxylase induction in pregnancy models; leaves open human relevance and clinical translation.
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.
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Maeyama et al. (1985) studied Pregnancy. alpha-fluoromethylhistidine (alpha-FMH) was evaluated on Histidine decarboxylase (HDC) activity. Administration of alpha-fluoromethylhistidine almost completely inhibited the increase of histidine decarboxylase activity during late pregnancy in fetal mice and maternal kidneys.
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