Transport of calcium ions by Ehrlich ascites-tumour cells.
Transport of calcium ions by Ehrlich ascites-tumour cells.
复制标题
艾利希腹水肿瘤细胞对钙离子的转运。
作者：
Y. Landry;A. Lehninger
同位素和原子吸收测量表明，当艾氏腹水肿瘤细胞与琥珀酸盐、磷酸盐和鱼藤酮有氧孵育时，会积累 Ca2+。 Ca2+ 不会刺激精心制备的艾利希细胞的耗氧量，但当细胞置于低渗透介质中时会刺激耗氧量。谷氨酸和苹果酸都不支持“完整”艾利希细胞摄取 Ca2+，内源性 NAD 相关呼吸也不支持。 Ca2+ 的吸收完全依赖于线粒体能量耦合机制。这是一个意想不到的发现，琥珀酸支持的最大 Ca2+ 吸收需要鱼藤酮，鱼藤酮可以阻止内源性 NAD 连接底物的氧化。磷酸盐充当 Ca2+ 进入的共阴离子。 Ca2+ 的吸收也得到细胞外 ATP 的支持；没有其他核苷 5'-二磷酸或三磷酸具有活性。 Ca2+ 的积累显然发生在线粒体中，因为寡霉素和苍术苷抑制 ATP 支持的 Ca2+ 吸收。糖酵解不支持 Ca2+ 的吸收。从破坏的细胞释放的游离线粒体和能够吸收台盼蓝的通透性受损的细胞都不对观察到的能量耦合 Ca2+ 吸收总量的任何大部分负责。报告的观察结果还表明，电子流过能量守恒位点 1 会促进艾利希细胞释放 Ca2+，并且细胞外 ATP 会增加细胞膜的通透性，从而使 ATP 和 Ca2+ 更容易进入细胞。
Ehrlich ascites-tumour cells accumulate Ca2+ when incubated aerobically with succinate, phosphate and rotenone, as revealed by isotopic and atomic-absorption measurements. Ca2+ does not stimulate oxygen consumption by carefully prepared Ehrlich cells, but des so when the cells are placed in a hypo-osmotic medium. Neither glutamate nor malate support Ca2+ uptake in 'intact' Ehrlich cells, nor does the endogenous NAD-linked respiration. Ca2+ uptake is completely dependent on mitochondrial energy-coupling mechansims. It was an unexpected finding that maximal Ca2+ uptake supported by succinate requires rotenone, which blocks oxidation of enogenous NAD-linked substrates. Phosphate functions as co-anion for entry of Ca2+. Ca2+ uptake is also supported by extra-cellular ATP; no other nucleoside 5'-di- or tri-phosphate was active. The accumulation of Ca2+ apparently takes place in the mitochondria, since oligomycin and atractyloside inhibit ATP-supported Ca2+ uptake. Glycolysis does not support Ca2+ uptake. Neither free mitochondria released from disrupted cells nor permeability-damaged cells capable of absorbing Trypan Blue were responsible for any large fraction of the total observed energy-coupled Ca2+ uptake. The observations reported also indicate that electron flow through energy-conserving site 1 promotes Ca2+ release from Ehrlich cells and that extra-cellular ATP increase permeability of the cell membrane, allowing both ATP and Ca2+ to enter the cells more readily.