Brain redox imaging using nitroxide contrast agents and blood-brain barrier function in methamphetamine-treated mice
Hirotada G Fujii 1 and Miho C Emoto 1
Center for Medical Education, Sapporo
Medical University, Sapporo, Hokkaido, Japan
Methamphetamine (METH)-induced neurotoxicity is known to
be caused in part by oxidative stress. The purpose of
this study was to examine the effect of oxidative stress
in METH-treated mice using a redox-sensitive nitroxide,
3-methoxycarbonyl-PROXYL (MCP), and to visualize brain
redox status by noninvasive EPR imaging. Rates of
reduction of MCP in the mouse brain were significantly
accelerated after treatment with METH, which was
remarkably suppressed by a dopamine synthesis inhibitor.
The present results suggest that METH induced oxidative
conditions in the mouse brain which resulted in
oxidative damage. Using a blood-brain barrier
(BBB)-impermeable gadolinium contrast agent, MRI of
METH-treated mice displayed dysfunction of the BBB.
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