Casademont Jordi, Rodriguez-Santiago Benjamín, Miró Oscar, Beato Anna, López Sònia, Nunes Virginia, Cardellach Francesc
Muscle Research Unit, Internal Medicine Department, Hospital Clínic, IDIBAPS, University of Barcelona, Barcelona, Spain.
Aging Clin Exp Res. 2005 Feb;17(1):1-7. doi: 10.1007/BF03337713.
The potential influence of impaired oxidative metabolism in the modulation of manifestations in sporadic Alzheimer's disease (AD) has attracted much attention in the last 50 years. Unfortunately, many clinical and experimental results aiming at proving this hypothesis are still controversial. The aim was to study the enzymatic activities of respiratory chain (RC) complexes I through V in three brain areas of a group of patients with definite AD, and to compare the results with a group of normal brains. We simultaneously assessed the lipid peroxidation of the samples as a measure of free radical damage.
The specific activity of the individual complexes of the RC was measured spectrophotometrically, and the loss of cis-parinaric acid fluorescence was used to determine the chemical process of lipid peroxidation.
We were not able to detect differences in any of the analyzed RC enzymatic activities, or in the level of lipid peroxidation between patients with AD and controls. Instead, differences were found in the number of mitochondria and in the intrinsic enzymatic activities of complexes III and IV in various brain areas.
Spectrophotometric enzymatic analyses of respiratory complexes in brain homogenates do not support the primary contribution of mitochondrial RC dysfunction in the pathogenesis of AD.
在过去50年里,氧化代谢受损在散发性阿尔茨海默病(AD)临床表现调节中的潜在影响备受关注。不幸的是,许多旨在证明这一假说的临床和实验结果仍存在争议。本研究旨在检测一组确诊为AD的患者三个脑区中呼吸链(RC)复合体I至V的酶活性,并与一组正常大脑进行比较。同时,我们评估了样本的脂质过氧化情况,以此作为自由基损伤的指标。
采用分光光度法测定RC各复合体的比活性,通过顺式-紫黄质酸荧光损失来确定脂质过氧化的化学过程。
我们未能检测到AD患者与对照组在任何分析的RC酶活性或脂质过氧化水平上的差异。相反,在不同脑区的线粒体数量以及复合体III和IV的固有酶活性方面发现了差异。
对脑匀浆中呼吸复合体进行分光光度酶分析并不支持线粒体RC功能障碍在AD发病机制中的主要作用。