Stöber Barbara, Tanase Ursula, Herz Michael, Seidl Christof, Schwaiger Markus, Senekowitsch-Schmidtke Reingard
Department of Nuclear Medicine, Klinikum Rechts der Isar, Technische Universität München, Ismaninger Strasse 22, 81675, Munich, Germany.
Eur J Nucl Med Mol Imaging. 2006 Aug;33(8):932-9. doi: 10.1007/s00259-005-0047-5. Epub 2006 Apr 8.
Previous studies suggest that radiolabelled amino acids could be superior to FDG in differentiating tumour and inflammation. Therefore the aim of this study was to investigate the uptake of FET and MET in human tumour and inflammatory cells and to investigate their uptake kinetics.
For uptake studies, cells were incubated with 370 kBq FET or 3.7 kBq MET for 15 min. Kinetic studies were performed at variable concentrations of FET and MET. Competitive inhibition studies were done with BCH, MeAIB and L: -serine.
All inflammatory cells incorporated more MET than the tumour cells. The uptake of FET, in contrast, was significantly lower in all inflammatory cells than in the tumour cells. In tumour cells the uptake of MET was about five times the uptake of FET. The competitive inhibitors reduced uptake of both tracers to 20-40% in tumour cells and to 70% in inflammatory cells. Kinetic studies showed that MET and FET transport was saturable in all cells except macrophages and followed a Michaelis-Menten kinetic. Highest capacity (V (max)) and affinity (K (m)) for the uptake of MET was observed in granulocytes. Capacity and affinity for FET uptake were highest in the DHL-4 cells.
In contrast to MET, FET accumulated to a significantly greater extent in tumour cells than in inflammatory cells. The marked differences between tumour and inflammatory cells concerning FET and MET uptake suggest that FET and MET are substrates of different subtypes of the L system.
先前的研究表明，放射性标记的氨基酸在区分肿瘤和炎症方面可能优于氟代脱氧葡萄糖（FDG）。因此，本研究的目的是研究氟代乙基酪氨酸（FET）和甲基酪氨酸（MET）在人肿瘤细胞和炎症细胞中的摄取情况，并研究它们的摄取动力学。
在摄取研究中，将细胞与370 kBq的FET或3.7 kBq的MET孵育15分钟。在不同浓度的FET和MET下进行动力学研究。用BCH、甲基氨基异丁酸（MeAIB）和L-丝氨酸进行竞争性抑制研究。
所有炎症细胞摄取的MET均多于肿瘤细胞。相比之下，所有炎症细胞中FET的摄取明显低于肿瘤细胞。在肿瘤细胞中，MET的摄取量约为FET摄取量的五倍。竞争性抑制剂使两种示踪剂在肿瘤细胞中的摄取量降低至20%-40%，在炎症细胞中降低至70%。动力学研究表明，除巨噬细胞外，MET和FET的转运在所有细胞中均可饱和，并遵循米氏动力学。在粒细胞中观察到MET摄取的最大容量（V（max））和亲和力（K（m））最高。DHL-4细胞中FET摄取的容量和亲和力最高。
与MET不同，FET在肿瘤细胞中的积累程度明显高于炎症细胞。肿瘤细胞和炎症细胞在FET和MET摄取方面的显著差异表明，FET和MET是L系统不同亚型的底物。
