The accumulation of 67Ga in inflammatory lesions increased with time after injection of turpentine iol and reached a plateau 5 days later. At that time the uptake in the lesions was larger than any other tissue, after ten days the lesion uptake decreased. In experiments using rats which had been kept for 5 days after subcutaneous injection of turpentine oil, the accumulation of 67Ga in inflammatory lesions increased with time until six days after administration of 67Ga-citrate. It is clear from this study that 67Ga is avidly accumulated in areas where the subcutanous tissue is infiltrated with neutrophils and macrophages, that it is not accumulated at the sites in which neutrophils are crowded, that nuclear material, mitochondria, lysosomes and microsomes do not play a major role in 67Ga accumulation in the lesion and that the main binding acid mucopolysaccharide in the lesion is acid mucopolysaccharide which is none of the following: keratan sulfate, heparan sulfate, heparin, or chondroitin sulfate A, B or C. It is presumed that the main 67Ga binding acid mucopolysaccharide is keratan polysulfate (or other oversulfated acid mucopolysaccharides).

67Ga accumulation in inflammatory lesion and its mechanism: Comparison with malignant tumor

The present study was undertaken to determine the structure of67Ga-binding acid mucopolysaccharide in tumor tissues. It was determined from measuring neutral saccharide in the structure that the principal67Ga-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 main67Ga-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 main67Ga-binding acid mucopolysaccharide in tumor is keratan polysulfate and that this acid mucopolysaccharide plays the most important role in tumor accumuation of67Ga.

I. Ando

Papers

On the67Ga-binding acid mucopolysaccharide in malignant tumor