CoQ10 therapy attenuates amyloid β-peptide toxicity in brain mitochondria isolated from aged diabetic rats

被引:78
作者
Moreira, PI
Santos, MS
Sena, C
Nunes, E
Seiça, R
Oliveira, CR [1 ]
机构
[1] Univ Coimbra, Fac Med, Ctr Neurosci & Cell Biol, Inst Biochem, P-3004517 Coimbra, Portugal
[2] Univ Coimbra, Fac Med, Ctr Neurosci & Cell Biol, Inst Physiol, P-3004517 Coimbra, Portugal
[3] Univ Coimbra, Fac Sci & Technol, Ctr Neurosci & Cell Biol, Dept Zool, P-3004517 Coimbra, Portugal
关键词
amyloid beta-peptide; brain; coenzyme Q10; diabetes; mitochondria; neuroprotection;
D O I
10.1016/j.expneurol.2005.07.012
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Using brain mitochondria isolated from 20-month-old diabetic Goto-Kakizaki rats, we evaluated the efficacy of CoQ 10 treatment against mitochondrial dysfunction induced by A beta(1-40). For that purpose, several mitochondrial parameters were evaluated: respiratory indexes (RCR and ADP/O ratio), transmembrane potential (Delta Psi m), repolarization lag phase, repolarization and ATP levels and the capacity of mitochondria to produce hydrogen peroxide. We observed that 4 mu M A beta(1-40) induced a significant decrease in the RCR and ATP content and a significant increase in hydrogen peroxide production. CoQ 10 treatment attenuated the decrease in oxidative phosphorylation efficiency and avoided the increase in hydrogen peroxide production induced by the neurotoxic peptide. These results indicate that CoQ 10 treatment counteracts brain mitochondrial alterations induced by A beta(1-40) suggesting that CoQ 10 therapy can help to avoid a drastic energy deficiency that characterizes diabetes and Alzheimer's disease pathophysiology. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:112 / 119
页数:8
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