MECHANISM OF STIMULATORY, SECRETARY & TOXIC RESPONSE OF 2H3 CELL TO CARDIOTOXIN

Myo(2-)标记培养的大鼠嗜碱性粒细胞白血病细胞 在暴露于眼镜蛇心脏毒素后，24小时的肌醇 (Maja Maja Kaauthia)，大幅增加(5至7倍) 磷脂酰肌醇一磷酸(PIP)中的~3H-标记量 游泳池。增加的程度取决于浓度和 心脏毒素的暴露时间。再分配的动力学 不同的肌醇磷酸盐池内的标签表明 一个主要的作用是刺激磷脂酰肌醇激酶 将磷脂酰肌醇(PI)转化为PIP的活性。这 通过测定细胞膜中的酶活性来证实其作用。 准备工作。心脏毒素还导致了时间和浓度- 肌醇磷酸盐的依赖性增加(4-8%)，缓慢增加 在胞浆Ca2t中，组胺的分泌和乳酸的释放 2H3细胞的脱氢酶(LDH)活性。这个 组胺的释放，而不是乳酸脱氢酶的释放完全依赖于外界 钙。结果表明，心脏毒素刺激的释放 来自2H3细胞的组胺是通过钙依赖的 无细胞毒性的过程。这项研究和之前的研究表明 存在高活性的肌醇磷脂激酶和 RBL-2H3细胞膜上的磷酸单酯酶。

Cultured rat basophilic leukemia (RBL-2H3) cell labeled with myo(2- 3H)inositol for 24 hr showed, upon exposure to cobra cardiotoxin (Maja maja kaauthia), a substantial (5 to 7 fold) increase in the amount of 3H-label in the phosphatidyl inositol monophosphate (PIP) pool. The extent of increase was dependent on concentration and time of exposure to cardiotoxin. The kinetics of redistribution of label within the various inositol phosphate pools suggested that a major action was the stimulation of phosphatidylinositol kinase activity which converts phosphatidylinositol (PI) to PIP. This action was confirmed by assay of the enzyme activity in membrane preparations. Cardiotoxin also caused a time- and concentration- dependent increase in inositol phosphates (4-8%), a slow increase in cytosol Ca2t, secretion of histamine and release of lactate dehydrogenase (LDH) dehydrogenase (LDH) from the 2H3 cells. The release of histamine but not LDH was totally dependent on external calcium. The results suggest that cardiotoxin-stimulated release of histamine from 2H3 cells is through a Ca(2+)-dependent noncytotoxic process. This and previous studies indicate the presence of highly active inositol phospholipid kinases and phosphomonoesterases in membranes of RBL - 2H3 cells.