Basic and Clinical Studies on Imaging for Tumor and Inflammatory Lesion by Ga-67 and In-111

本研究旨在探讨Ga-67在恶性肿瘤和炎性病变中的蓄积机制。通过测定结构中的中性糖，确定肿瘤中与Ga-67结合的酸性粘多糖主要是硫酸角蛋白和/或多硫酸角蛋白。另一方面，粘多糖处理的结果表明，肿瘤中主要的结合Ga-67的酸性粘多糖不是硫酸角蛋白、硫酸肝素、肝素，也不是硫酸软骨素A、B或C。根据目前的结果，推测肿瘤中主要的结合Ga-67的酸性粘多糖是多硫酸角蛋白，这种酸性粘多糖在肿瘤聚集中起着最重要的作用。注射松节油后，炎性病变对Ga-67的摄取率随时间增加，5天后达到平台期。在这个时候，病变的发生率比任何其他组织都大。放射自显影观察表明，与中性粒细胞和巨噬细胞渗入的皮下组织相对应，Ga-67大量积聚，核素主要集中在这些细胞周围。生化研究表明，Ga-67与酸性粘多糖(多硫酸角蛋白等)结合。在损伤处。另一方面，炎性病变的毛细血管通透性明显高于正常组织。根据目前的结果，炎性病变对Ga-67摄取的机制如下：炎性病变中Ga-67的蓄积主要是由于Ga-67通过通透性增加的毛细血管渗入中性粒细胞和巨噬细胞的皮下组织。在炎性病变中，Ga-67优先与酸性粘多糖(多硫酸角蛋白等)结合。它们构成了细胞间物质。

This study was undertaken to investigate the mechanism of accumulation of Ga-67 in the malignant tumor and the inflammatory lesion. It was determined from measuring neutral saccharide in the structure that the principal Ga-67-binding acid mucopolysaccharide in the tumor was keratan sulfate and/or keratan polysulfate. On the other hand, it was clarified from the results of mucopolysaccharase treatment that the main Ga-67-binding acid mucopolysaccharide in tumor was not keratan sulfate, heparan sulfate, heparin, nor chondroitin sulfate A,B,or C. Based on the present results, it was deduced that the main Ga-67-binding acid mucopolysaccharide in tumor is keratan polysulfate and that this acid mucopolysaccharide plays the most important role in tumor accumulation of Ga-67.The uptake rate of Ga-67 in the inflammatory lesion was increased with time after injection of turpentine oil and reached a plateau five days later, and at this time the rate for the lesion was larger than those for any other tissues. From the observation by autoradiography, it was revealed that Ga-67 was avidly accumulated corresponding to the subcutaneous tissue infiltrated with neutrophils and macrophages, and this nuclide was concentrated intercellularly around these cells. And it became clear from biochemical study that Ga-67 was bound to the acid mucopolysaccharide (keratan polysulfate, etc.) in the lesion. On the other hand, capillary permeability in this lesion was much greater than that of normal tissues.based on the present results, mechanisms of Ga-67 uptake into inflammatory lesion are concluded as follows:accumulation of Ga-67 in the inflammatory lesion is primarily due to leakage of Ga-67 into the subcutaneous tissue infiltrated with neutrophils and macrophages through capillaries with increased permeability. In the inflammatory lesion, Ga-67 is preferentially bound to the acid mucopolysaccharides(keratan polysulfate, etc.) which compose intercellular substances.