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

先前培养的大鼠嗜碱性白血病（RBL-2 H3）细胞 用肌-（2- 3 H）肌醇标记24小时， 释放（3 H）肌醇磷酸和相互下降， (3H)暴露于眼镜蛇心脏毒素后肌醇磷脂 (Naja眼镜蛇）。 最显著的影响是选择性的 磷脂酰肌醇中3 H标记量增加 单磷酸盐（PIP）池。 增加的程度取决于 浓度和暴露时间的影响 的 各种肌醇脂质内标记物再分布的动力学 和肌醇磷酸池表明，一个主要的行动是 刺激磷脂酰肌醇激酶活性， 磷脂酰肌醇（PI）至PIP。 这一行动得到了 测定膜制备物中的酶活性。 毒素还引起了时间和浓度依赖性的 组胺分泌和乳酸脱氢酶释放 (LDH)从2 H3细胞。 释放组胺而非LDH 完全依赖于外部钙。 结果提示 心脏毒素刺激2 H3细胞释放组胺， 通过CA（2+）依赖性非细胞毒性过程。

Cultured rat basophilic leukemia (RBL-2H3) cells previously labeled with myo-(2-3H)inositol for 24 hr showed an appreciable release of (3H) inositiol phosphates and a reciprocal decline in (3H) inositol phospholipids upon exposure to cobra cardiotoxin (Naja naja kaauthia). The most significant effect was a selective increase in the amount of 3H-label in the phosphotidyl 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 lipid and 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 secretion of histamine and release of lactate 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.