Scheffel U, Wagner H N, Tsan M F
J Nucl Med. 1986 Mar;27(3):395-8.
A significant fraction of intravenously injected 67Ga localizes in the liver. The mechanism of 67Ga uptake by the liver is not clear. Hepatocyte membranes contain galactose-specific receptors which selectively remove asialo-glycoproteins from the circulation by way of endocytosis. In this investigation, we examined whether endocytic uptake of asialo-transferrin would involve 67Ga transport into hepatocytes. We demonstrated that asialo-transferrin bound 67Ga as effectively as apotransferrin. Human asialo-transferrin markedly enhanced 67Ga uptake by isolated, perfused rat livers. Human asialo-orosomucoid, but not orosomucoid competitively inhibited hepatic uptake of the 67Ga asialo-transferrin complex, indicating that hepatic 67Ga uptake in the presence of asialo-transferrin occurred by way of galactose-specific receptors. Our results point to a novel pathway for metal ion transport into hepatocytes by way of galactose receptor mediated endocytosis.
静脉注射的67Ga有很大一部分定位于肝脏。肝脏摄取67Ga的机制尚不清楚。肝细胞膜含有半乳糖特异性受体，可通过内吞作用从循环中选择性清除去唾液酸糖蛋白。在本研究中，我们研究了去唾液酸转铁蛋白的内吞摄取是否会涉及67Ga转运到肝细胞中。我们证明，去唾液酸转铁蛋白结合67Ga的能力与脱铁转铁蛋白一样有效。人去唾液酸转铁蛋白显著增强了离体灌注大鼠肝脏对67Ga的摄取。人去唾液酸血清类黏蛋白而非血清类黏蛋白竞争性抑制肝脏对67Ga去唾液酸转铁蛋白复合物的摄取，表明在去唾液酸转铁蛋白存在的情况下，肝脏对67Ga的摄取是通过半乳糖特异性受体进行的。我们的结果指出了一种通过半乳糖受体介导的内吞作用将金属离子转运到肝细胞中的新途径。
