Bihler I, Charles P, Sawh P C
Cell Calcium. 1982 Aug;3(3):243-62. doi: 10.1016/0143-4160(82)90004-5.
The tissue/medium distribution of the nonmetabolized glucose analog [14C]-3-O-methyl-D-glucose was measured in pigeon erythrocytes and related to changes in 45Ca uptake and efflux, total calcium content and ATP levels. Sugar transport was not affected by changes in external Ca2+. However, both sugar and 45Ca influx were increased by the Ca-ionophore A23187. In the absence of external Ca2+, the ionophore caused a delayed increase in sugar transport and net loss of calcium, probably through releasing Ca2+ from internal storage sites into the cytoplasm. Increasing internal Na+ through Na+ pump inhibition or using the sodium ionophore monensin did not alter influx of sugar or 45Ca, indicating Na+-Ca2+ exchange was absent in these cells. The results are consistent with A23187 causing increased Ca2+ influx or release from mitochondrial storage and the resulting rise in cytoplasmic Ca2+ stimulating hexose transport. Experiments with low Mg++ and high K+ media and measurements of ATP levels exclude alternative explanations for the action of A23187. We conclude that sugar transport regulation in avian erythrocytes is Ca2+-dependent and resembles that in muscle in its basic mechanism. It differs in the response to some modulating agents, largely because of a different pattern of Ca2+ fluxes in these cells.
在鸽红细胞中测定了非代谢性葡萄糖类似物[¹⁴C]-3-O-甲基-D-葡萄糖的组织/介质分布，并将其与⁴⁵Ca摄取和流出、总钙含量及ATP水平的变化相关联。糖转运不受细胞外Ca²⁺变化的影响。然而，Ca离子载体A23187可增加糖和⁴⁵Ca的流入。在无细胞外Ca²⁺的情况下，该离子载体导致糖转运延迟增加和钙的净丢失，这可能是通过将Ca²⁺从内部储存位点释放到细胞质中实现的。通过抑制Na⁺泵增加细胞内Na⁺或使用钠离子载体莫能菌素，均未改变糖或⁴⁵Ca的流入，表明这些细胞中不存在Na⁺-Ca²⁺交换。结果表明，A23187导致Ca²⁺流入增加或从线粒体储存中释放，进而导致细胞质Ca²⁺升高，刺激己糖转运。在低Mg²⁺和高K⁺培养基中进行的实验以及ATP水平的测量排除了对A23187作用的其他解释。我们得出结论，禽类红细胞中的糖转运调节是Ca²⁺依赖性的，其基本机制与肌肉中的相似。它在对某些调节因子的反应上有所不同，主要是因为这些细胞中Ca²⁺通量的模式不同。
