镉离子（Cd2+）对伴刀豆球蛋白A刺激的淋巴细胞中钙离子通量及增殖的影响。

Effects of Cd2+ upon Ca2+ fluxes and proliferation in concanavalin A-stimulated lymphocytes.

作者信息

Scott I G, Wolff C H, Akerman K E, Andersson L C

出版信息

Exp Cell Res. 1985 Jan;156(1):191-7. doi: 10.1016/0014-4827(85)90273-3.

Abstract

The mitogenic response of human peripheral blood lymphocytes to the lectin concanavalin A (conA) is inhibited by micromolar concentrations of CdCl2. This inhibition is partially relieved by an increase in the external Ca2+ concentration (from 0.6 to 2.2 mM). The initial rate of conA-induced 45Ca2+ influx is unaltered by CdCl2, although the level of 45Ca2+ accumulation increases. The basal rate of 45Ca2+ entry is not measurably disturbed by CdCl2 (100 microM). The steady-state efflux of 45Ca2+ and the calmodulin-activated (Ca2+ + Mg2+)-ATPase activity of erythrocyte ghosts are inhibited by CdCl2 (10 microM). Thus, the mechanism behind the Cd2+-induced suppression of the mitogenic response to conA is not due to alteration of mitogen-stimulated Ca2+ influx. We suggest that Cd2+ competes with Ca2+ for intracellular Ca2+-binding molecules, such as calmodulin, essential for the induction of cell proliferation.

摘要

微摩尔浓度的氯化镉（CdCl₂）可抑制人外周血淋巴细胞对凝集素刀豆球蛋白A（ConA）的促有丝分裂反应。外部钙离子浓度升高（从0.6 mM增至2.2 mM）可部分缓解这种抑制作用。尽管⁴⁵Ca²⁺积累水平增加，但CdCl₂不会改变ConA诱导的⁴⁵Ca²⁺内流的初始速率。CdCl₂（100 μM）对⁴⁵Ca²⁺进入的基础速率没有明显干扰。CdCl₂（10 μM）可抑制⁴⁵Ca²⁺的稳态外流以及红细胞膜的钙调蛋白激活的（Ca²⁺ + Mg²⁺）-ATP酶活性。因此，Cd²⁺诱导的对ConA促有丝分裂反应抑制的机制并非由于有丝分裂原刺激的Ca²⁺内流改变。我们认为，Cd²⁺与Ca²⁺竞争细胞内Ca²⁺结合分子，如对诱导细胞增殖至关重要的钙调蛋白。