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首页> 外文期刊>Free radical research >Brain imaging in methamphetamine-treated mice using a nitroxide contrast agent for EPR imaging of the redox status and a gadolinium contrast agent for MRI observation of blood-brain barrier function
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Brain imaging in methamphetamine-treated mice using a nitroxide contrast agent for EPR imaging of the redox status and a gadolinium contrast agent for MRI observation of blood-brain barrier function

机译：在使用甲基苯丙胺治疗的小鼠中进行脑成像，使用一氧化氮造影剂对氧化还原状态进行EPR成像，将g造影剂用于MRI观察血脑屏障功能

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Methamphetamine (METH)-induced neurotoxicity is associated with mitochondrial dysfunction and enhanced oxidative stress. The aims of the present study conducted in the mouse brain repetitively treated with METH were to (1) examine the redox status using the redox-sensitive imaging probe 3-methoxycarbonyl-2,2,5,5-tetramethylpiperidine-1-oxyl (MCP) and (2) non-invasively visualize the brain redox status with electron paramagnetic resonance (EPR) imaging. The rate of reduction of MCP was measured from a series of temporal EPR images of mouse heads, and this rate was used to construct a two-dimensional map of rate constants called a "redox map." The obtained redox map clearly illustrated the change in redox balance in the METH-treated mouse brain that is a known result of oxidative damage. Biochemical assays also showed that the level of thiobarbituric acid-reactive substance, an index of lipid peroxidation, was increased in mouse brains by METH. The enhanced reduction in MCP observed in mouse brains was remarkably suppressed by treatment with the dopamine synthase inhibitor, alpha-methyl-p-tyrosine, suggesting that enhancement of the reduction reaction of MCP resulted from enzymatic reduction in the mitochondrial respiratory chain. Furthermore, magnetic resonance imaging (MRI) of METH-treated mice using a blood-brain barrier (BBB)-impermeable paramagnetic contrast agent revealed BBB dysfunction after treatment with METH for 7 days. MRI also indicated that the impaired BBB recovered after withdrawal of METH. EPR imaging and MRI are useful tools not only for following changes in the redox status and BBB dysfunction in mouse brains repeatedly administered METH, but also for tracing the drug effect after withdrawal of METH.
机译：甲基苯丙胺（METH）诱导的神经毒性与线粒体功能障碍和氧化应激增强有关。本研究的目的是反复用METH进行治疗的小鼠大脑是（1）使用对氧化还原敏感的成像探针3-甲氧羰基-2,2,5,5-四甲基哌啶-1-氧基（MCP）检查氧化还原状态）和（2）通过电子顺磁共振（EPR）成像无创地观察大脑的氧化还原状态。从一系列的小鼠头部的时间EPR图像中测量MCP的降低速率，并将该速率用于构建速率常数的二维图，称为“氧化还原图”。所获得的氧化还原图清楚地说明了经过METH处理的小鼠大脑中氧化还原平衡的变化，这是氧化损伤的已知结果。生化分析还表明，甲基苯丙氨酸甲酯可增加小鼠大脑中硫代巴比妥酸反应性物质的水平（脂质过氧化的指标）。用多巴胺合酶抑制剂α-甲基-对-酪氨酸处理可显着抑制小鼠大脑中MCP的增强，这表明MCP还原反应的增强是由线粒体呼吸链的酶促还原引起的。此外，使用不可透过血脑屏障（BBB）的顺磁造影剂对METH治疗的小鼠进行的磁共振成像（MRI）显示，在用METH治疗7天后，BBB功能障碍。 MRI也显示受损的BBB在停用METH后得以恢复。 EPR成像和MRI不仅是跟踪重复施用METH的小鼠大脑中氧化还原状态和BBB功能障碍变化的有用工具，而且对于追踪METH停药后的药物作用，都是有用的工具。

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