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阿尔茨海默病患者的铜、铜蓝蛋白和超氧化物歧化酶。一项病例对照研究。

Copper, ceruloplasmin and superoxide dismutase in patients with Alzheimer's disease . a case-control study.

作者信息

Snaedal J, Kristinsson J, Gunnarsdóttir S, Baldvinsson M, Jóhannesson T

机构信息

Geriatric Department, Reykjavik Hospital, University of Iceland, Reykjavik, Iceland.

出版信息

Dement Geriatr Cogn Disord. 1998 Sep-Oct;9(5):239-42. doi: 10.1159/000017067.

Abstract

The copper-containing enzyme superoxide dismutase (SOD) is a key enzyme in suppressing the amounts of superoxide anion radicals. Ceruloplasmin, the copper-transporting protein in plasma, also possesses an important redox capacity. In this study the levels of copper and ceruloplasmin as well as SOD-activity and ceruloplasmin oxidative activity were analyzed in order to throw some light on possible defects in copper mechanisms in patients diagnosed with Alzheimer's disease (AD). The study included 44 patients with AD and their healthy age- and gender-matched controls. No difference of significance was seen when comparing the copper or ceruloplasmin concentration in plasma of AD patients to that of their paired controls. The SOD activity in red blood cells was significantly lower in the patients than in their controls (p = 0.019). The ceruloplasmin oxidative activity in plasma of Alzheimer's patients was greatly reduced as compared to that of age- and gender-matched controls and the difference was highly significant (p = 0.0005). Ceruloplasmin activity and SOD activity were not found to be intrinsically correlated. It was postulated that reduced oxidative activity of ceruloplasmin in plasma might be either a cause or a consequence of AD and that reduced SOD activity might further add to the oxidative disturbances in AD due to defective ceruloplasmin activity.

摘要

含铜酶超氧化物歧化酶(SOD)是抑制超氧阴离子自由基数量的关键酶。血浆中的铜转运蛋白铜蓝蛋白也具有重要的氧化还原能力。在本研究中,分析了铜和铜蓝蛋白的水平以及SOD活性和铜蓝蛋白氧化活性,以便了解被诊断为阿尔茨海默病(AD)的患者铜机制中可能存在的缺陷。该研究纳入了44名AD患者及其年龄和性别匹配的健康对照者。将AD患者血浆中的铜或铜蓝蛋白浓度与其配对对照者的浓度进行比较时,未发现显著差异。患者红细胞中的SOD活性显著低于其对照者(p = 0.019)。与年龄和性别匹配的对照者相比,阿尔茨海默病患者血浆中的铜蓝蛋白氧化活性大大降低,差异非常显著(p = 0.0005)。未发现铜蓝蛋白活性与SOD活性存在内在相关性。据推测,血浆中铜蓝蛋白氧化活性降低可能是AD的原因或结果,而SOD活性降低可能会因铜蓝蛋白活性缺陷而进一步加剧AD中的氧化紊乱。

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