| Literature DB >> 26082015 |
Toshimitsu Okamura1, Maki Okada1, Tatsuya Kikuchi1, Hidekatsu Wakizaka1, Ming-Rong Zhang1.
Abstract
A disturbance in redox balance has been implicated in the pathogenesis of a number of diseases. This study sought to examine the feasibility of imaging brain redox status using a (11)C-labeled dihydroquinoline derivative ([(11)C]DHQ1) for positron emission tomography (PET). The lipophilic PET tracer [(11)C]DHQ1 was rapidly oxidized to its hydrophilic form in mouse brain homogenate. The redox modulators diphenyleneiodonium and apocynin significantly reduced the initial velocity of [(11)C]DHQ1 oxidation, and apocynin also caused concentration-dependent inhibition of the initial velocity. Moreover, [(11)C]DHQ1 readily entered the brain by diffusion after administration and underwent oxidation into the hydrophilic cationic form, which then slowly decreased. By contrast, apocynin treatment inhibited the in vivo oxidation of [(11)C]DHQ1 to the hydrophilic cationic form, leading to a rapid decrease of radioactivity in the brain. Thus, the difference in the [(11)C]DHQ1 kinetics reflects the alteration in redox status caused by apocynin. In conclusion, [(11)C]DHQ1 is a potential PET tracer for imaging of redox status in the living brain.Entities:
Mesh：
Substances：
Year: 2015 PMID： 26082015 PMCID： PMC4671112 DOI： 10.1038/jcbfm.2015.132
Source DB: PubMed Journal: J Cereb Blood Flow Metab ISSN： 0271-678X Impact factor: 6.200