[18F]FPBMP: – a potential new positron emission tomography radioligand for imaging of translocator protein (18 kDa) in peripheral organs of rats

RSC Advances ◽  
2015 ◽  
Vol 5 (123) ◽  
pp. 101447-101454 ◽  
Author(s):  
Anjani K. Tiwari ◽  
Joji Yui ◽  
Yiding Zhang ◽  
Masayuki Fujinaga ◽  
Tomoteru Yamasaki ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Translocator Protein ◽  
Emission Tomography ◽  
Peripheral Tissues ◽  
Activated Microglia ◽  
Peripheral Organs ◽  
Positron Emission ◽  
Translocator Protein 18 Kda ◽  
Lung And Kidney

The five transmembrane translocator protein (18 kDa, TSPO) is abundantly expressed in the mitochondria of activated microglia (brain) and peripheral tissues, including those of the heart, lung and kidney.

Synthesis of two novel [18F]fluorobenzene-containing radiotracers via spirocyclic iodonium ylides and positron emission tomography imaging of translocator protein (18 kDa) in ischemic brain

2018 ◽  
Vol 16 (37) ◽  
pp. 8325-8335 ◽  
Author(s):  
Masayuki Fujinaga ◽  
Katsushi Kumata ◽  
Yiding Zhang ◽  
Akiko Hatori ◽  
Tomoteru Yamasaki ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Positron Emission Tomography Imaging ◽  
Translocator Protein ◽  
Emission Tomography ◽  
Ischemic Brain ◽  
Tomography Imaging ◽  
Positron Emission ◽  
Translocator Protein 18 Kda ◽  
Iodonium Ylides ◽  
The Brain

A new radiotracer for imaging TSPO: Ki, 0.70 nM and no radiolabeled metabolite in the brain.

scholarly journals [18F]FEDAC translocator protein positron emission tomography–computed tomography for early detection of mitochondrial dysfunction secondary to myocardial ischemia

2021 ◽  
Author(s):  
Rui Luo ◽  
Lei Wang ◽  
Fei Ye ◽  
Yan-Rong Wang ◽  
Wei Fang ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Positron Emission Tomography ◽  
Early Detection ◽  
Myocardial Ischemia ◽  
Mitochondrial Dysfunction ◽  
High Performance ◽  
Dynamic Imaging ◽  
Translocator Protein ◽  
Emission Tomography ◽  
Positron Emission

Abstract Background This study aimed to evaluate the biodistribution and kinetics of [18F]FEDAC targeting the translocator protein TSPO in the myocardium, and to explore its use for the identification of mitochondrial dysfunction. We also assessed the feasibility of [18F]FEDAC for the early detection of mitochondrial dysfunction associated with myocardial ischemia (MI). Methods The radiochemical purity and stability of [18F]FEDAC were analyzed by radio-high-performance liquid chromatography (radio-HPLC). Its biodistribution and kinetics were evaluated by dissection and dynamic imaging using micro-positron emission tomography–computed tomography (micro-PET–CT) in healthy mice. [18F]FEDAC was also applied in an MI rat model and in sham-operated controls. Mitochondrial changes were observed by immunohistochemical staining and electron microscopy. Results Radioactivity levels (%ID/g) in the myocardium in normal mice, determined by [18F]FEDAC, were 8.32 ± 0.80 at 5 min and 2.40 ± 0.10 at 60 min. PET showed significantly decreased uptake by injured cardiac tissue in MI rats, with maximal normal-to-ischemic uptake ratios of 10.47 ± 3.03 (1.5 min) and 3.92 ± 1.12 (27.5 min) (P = 0.025). Immunohistochemistry confirmed that TSPO expression was decreased in MI rats. Mitochondrial ultrastructure demonstrated significant swelling and permeability. Conclusion [18F]FEDAC uptake is reduced in the injured myocardium, consistent with mitochondrial dysfunction. These results may provide new evidence to aid the early detection of mitochondrial dysfunction associated with myocardial ischemic injury.

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