Increased Susceptibility to Plasma Lipid Peroxidation in Alzheimer Disease Patients
Increased Susceptibility to Plasma Lipid Peroxidation in Alzheimer Disease Patients
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DOI：
10.2174/1567205043332171
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发表时间：
2004-05-01
影响因子：
2.1
通讯作者：
Ferrarese, Carlo
中科院分区：
文献类型：
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作者：
Galbusera, Carmen;Facheris, Maurizio;Ferrarese, Carlo
氧化应激与A β-脂质相互作用有关，在阿尔茨海默病中起致病作用。我们研究了52例AD患者，42例健康对照和16例肌萎缩侧索硬化症，一种神经退行性疾病，其中氧化应激也发挥了致病作用的血浆脂质过氧化产物的修改。在铜催化的离体氧化应激之前和之后，通过硫代巴比妥酸反应物质（TBARS）测定血浆中的最终脂质过氧化产物。在基础条件下没有显著变化，但在铜诱导氧化后，AD患者的TBARS水平（19.0 μ M +/- 2.2）高于对照组（5.2 μ M +/- 0.8，p < 0.001）和ALS患者（7.6 μ M +/- 2.1，p < 0.01）。轻度和中度AD患者的刺激TBARS水平显著高于对照组（p < 0.0001），但在重度AD患者中并非如此，疾病严重程度与脂质过氧化之间存在显著负相关（p < 0.005，r（2）=0.21）。用维生素C和E治疗轻度和中度AD患者亚组（13例）3个月，使血浆脂质过氧化敏感性降低60%。因此，氧化应激，表达为离体脂质过氧化的易感性，似乎是一种早期现象，可能与AD的发病机制。
Oxidative stress, linked to Abeta-lipid interactions, plays a pathogenetic role in Alzheimer's disease. We investigated modifications of lipid peroxidation products in plasma of 52 AD patients, 42 healthy controls and 16 patients with amyotrophic lateral sclerosis, a neurodegenerative disease where oxidative stress also plays a pathogenetic role. Final lipid peroxidation products were measured in plasma by thiobarbituric acid reactive substances (TBARS) assay before and after ex vivo oxidative stress catalysed by copper. There were no significant changes at basal conditions, but after copper-induced oxidation TBARS levels were higher in AD patients (19.0 mu M +/- 2.2) versus both controls (5.2 mu M +/- 0.8, p < 0.001) and ALS patients (7.6 mu M +/- 2.1, p < 0.01). Stimulated TBARS levels were significantly higher in mild and moderate AD (p < 0.0001) with respect to controls, but not in severe AD patients, with a significant inverse correlation between disease severity and lipid peroxidation (p < 0.005, r(2)=0.21). Treatment of a subgroup (13) of mild and moderate AD patients with vitamin C and E for three months decreased plasma lipoperoxidation susceptibility by 60%. Thus, oxidative stress, expressed as ex vivo susceptibility to lipid peroxidation, appears to be an early phenomenon, probably related to AD pathogenetic mechanisms.