Brain redox imaging using nitroxide contrast agents and blood-brain barrier function in methamphetamine-treated mice

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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