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分娩前肥大细胞缺陷的W/W小鼠胚胎中组氨酸脱羧酶活性未增加。

Absence of increase of histidine decarboxylase activity in mast cell-deficient W/W mouse embryos before parturition.

作者信息

Watanabe T, Kitamura Y, Maeyama K, Go S, Yamatodani A, Wada H

出版信息

Proc Natl Acad Sci U S A. 1981 Jul;78(7):4209-12. doi: 10.1073/pnas.78.7.4209.

Abstract

The histidine decarboxylase (L-histidine carboxylase, EC 4.1.1.22) activity of whole W/W mouse embryos, which are devoid of mast cells, remained very low and did not show the rapid increase before birth (17-20 days of gestation) seen in wild-type +/+ embryos. During the same period, the histamine content also remained very low and no mast cells were detected in the W/W embryos, in the contrast to the large increase in both histamine content and number of mast cells in wild-type embryos. These findings imply that the histamine in embryos is largely derived from mast cells. In +/+ mice, histidine decarboxylase activity decreased rapidly soon after birth without concomitant decrease in histamine content or number of mast cells, suggesting that the enzyme activity in mast cells is regulated by some unknown mechanism.

摘要

完全缺乏肥大细胞的W/W小鼠全胚胎的组氨酸脱羧酶(L-组氨酸羧化酶,EC 4.1.1.22)活性一直很低,且未表现出野生型+/+胚胎在出生前(妊娠17 - 20天)出现的快速增加。在同一时期,W/W胚胎中的组胺含量也一直很低,且未检测到肥大细胞,这与野生型胚胎中组胺含量和肥大细胞数量的大幅增加形成对比。这些发现表明胚胎中的组胺很大程度上来源于肥大细胞。在+/+小鼠中,出生后不久组氨酸脱羧酶活性迅速下降,但组胺含量或肥大细胞数量并未随之减少,这表明肥大细胞中的酶活性受某种未知机制调控。

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