| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2008: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Research Abstract |
Urea toxin is suggested to be induced the glutamatergic neuronal damage mediated by the activity of N-methyl-D-aspartate (NMDA) receptor. In this study, we aimed to demonstrate brain redox alterations in chronic kidney disease mouse noninvasively, using overhauser-enhanced magnetic resonance imaging (OMRI).
The reduction rate of 3-methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine-l-oxyl (methoxycarbonyl-PROXYL), a redox-sensitive contrast agent, was used as an index of the redox status in vivo. No changes were seen in the 8-OHdG (8-Hydroxydeoxyguanosine) or the memory disturbance at 2 or 4 weeks after CKD onset, but after 4 weeks of CKD, the methoxycarbonyl-PROXYL reduction rate, calculated from continuous images, had increased significantly. At 8 weeks after CKD onset, we observed an increase in the number of 8-OHdG-immunopositive cells and the disturbance in the memory. Thus, the noninvasive imaging of the brain redox alterations was associated with the initial stages of CKD cause brain injury.
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