血管性痴呆和阿尔茨海默病中的脂质过氧化与抗氧化酶活性

Lipid peroxidation and antioxidant enzyme activities in vascular and Alzheimer dementias.

作者信息

Casado Angela, Encarnación López-Fernández M, Concepción Casado M, de La Torre Rosario

机构信息

Departamento de Fisiopatología Celular y Molecular, Centro de Investigaciones Biológicas (CSIC), Ramiro de Maeztu, 9, Madrid 28040, Spain.

出版信息

Neurochem Res. 2008 Mar;33(3):450-8. doi: 10.1007/s11064-007-9453-3. Epub 2007 Aug 25.

Abstract

It has been reported that oxidative stress may play a role in the pathogenesis of dementia of the Alzheimer type (AD) and the cerebral ischemia which causes vascular dementia (VD). We measured malondialdehyde (MDA) levels and superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) activities in blood samples from patients with AD and VD and in healthy non-demented controls (CTR) which similar ages to the patients, in order to evaluate the degree of oxidative stress in patients with AD and VD. A sample of 150 subjects consisting of 50 patients with AD; 50 patients with VD and 50 CTR, aged from 65 to 85 years on, was analyzed. Most of the changes observed were in SOD activity and MDA levels. Catalase activity were least affected. Significant differences were observed in SOD and GR activity between males and females in CRT and in patients with AD, but not in VD. We have found a decrease in antioxidant enzymes activities (SOD, CAT, GPx and GR) in patients with AD and VD and significant differences were observed between CRT and AD patients for ages from 65 to 74, 75 to 84 and from 85 years to 94 years in SOD activity and MDA levels (P < 0.001). MDA levels increase with age in VD, AD and CTR. No significant variation with respect to sex were detected, but significant variations in MDA levels were detected between CRT and patients with VD and AD (P < 0.001). We conclude that oxidative stress plays an important role in the brain damage for both AD and VD, being observed higher levels of oxidative stress for AD that for VD.

摘要

据报道,氧化应激可能在阿尔茨海默病(AD)型痴呆以及导致血管性痴呆(VD)的脑缺血发病机制中发挥作用。我们测量了AD和VD患者以及年龄与患者相似的健康非痴呆对照者(CTR)血样中的丙二醛(MDA)水平以及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)和谷胱甘肽还原酶(GR)的活性,以评估AD和VD患者的氧化应激程度。对150名受试者进行了分析,其中包括50名AD患者、50名VD患者和50名CTR,年龄在65岁至85岁以上。观察到的大多数变化在于SOD活性和MDA水平。过氧化氢酶活性受影响最小。在CTR以及AD患者中,男性和女性的SOD和GR活性存在显著差异,但在VD患者中未观察到。我们发现AD和VD患者的抗氧化酶活性(SOD、CAT、GPx和GR)降低,并且在65至74岁、75至84岁以及85至94岁年龄段的CTR和AD患者之间,SOD活性和MDA水平存在显著差异(P < 0.001)。在VD、AD和CTR中,MDA水平随年龄增加。未检测到性别方面的显著差异,但在CTR与VD和AD患者之间检测到MDA水平存在显著差异(P < 0.001)。我们得出结论,氧化应激在AD和VD的脑损伤中均起重要作用,并且观察到AD的氧化应激水平高于VD。

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