Zimmermann C, Winnefeld K, Streck S, Roskos M, Haberl R L
Department of Neurology, Krankenhaus Munich-Harlaching, LMU Munich, Munich, Germany.
Eur Neurol. 2004;51(3):157-61. doi: 10.1159/000077662. Epub 2004 Apr 1.
Antioxidant enzymes like copper/zinc superoxide dismutase (SOD), catalase and gluthatione peroxidase (GSHPx) are part of intracellular protection mechanisms to overcome oxidative stress and are known to be activated in vascular diseases and acute stroke. We investigated the differences of antioxidant capacity in acute stroke and stroke risk patients to elucidate whether the differences are a result of chronic low availability in arteriosclerosis and stroke risk or due to changes during acute infarction.
Antioxidant enzymes were examined in 11 patients within the first hours and days after acute ischemic stroke and compared to risk- and age-matched patients with a history of stroke in the past 12 months (n = 17). Antioxidant profile was determined by measurement of glutathione (GSH), malondialdehyde (MDA), SOD, GSHPx and minerals known to be involved in antioxidant enzyme activation like selenium, iron, copper and zinc.
In comparison to stroke risk patients, patients with acute ischemic stroke had significant changes of the GSH system during the first hours and days after the event: GSH was significantly elevated in the first hours (p < 0.01) and GSHPx was elevated 1 day after the acute stroke (p < 0.05). Selenium, a cofactor of GSHPx, was decreased (p < 0.01). GSHPx levels were negatively correlated with National Institutes of Health Stroke Scale (NIHSS) scores on admission (r = -0.84, p < 0.001) and NIHSS scores after 7 days (r = -0.63, p < 0.05). MDA levels showed a trend for elevation in the first 6 h after the acute stroke (p = 0.07). No significant differences of SOD, iron, copper nor zinc levels could be identified.
Differences of antioxidant capacity were found for the GSH system with elevation of GSH and GSHPx after acute stroke, but not for other markers. The findings support the hypothesis that changes of antioxidant capacity are part of acute adaptive mechanisms during acute stroke.
铜/锌超氧化物歧化酶（SOD）、过氧化氢酶和谷胱甘肽过氧化物酶（GSHPx）等抗氧化酶是细胞内抵御氧化应激保护机制的一部分，已知在血管疾病和急性卒中中会被激活。我们研究了急性卒中和卒中风险患者抗氧化能力的差异，以阐明这些差异是动脉硬化和卒中风险导致的慢性低水平状态的结果，还是急性梗死期间变化的结果。
在11例急性缺血性卒中发病后的最初数小时和数天内检测抗氧化酶，并与12个月内有卒中病史、年龄和风险匹配的患者（n = 17）进行比较。通过测量谷胱甘肽（GSH）、丙二醛（MDA）、SOD、GSHPx以及已知参与抗氧化酶激活的矿物质如硒、铁、铜和锌来确定抗氧化谱。
与卒中风险患者相比，急性缺血性卒中患者在发病后的最初数小时和数天内GSH系统有显著变化：发病后最初数小时GSH显著升高（p < 0.01），急性卒中后1天GSHPx升高（p < 0.05）。GSHPx的辅因子硒降低（p < 0.01）。GSHPx水平与入院时美国国立卫生研究院卒中量表（NIHSS）评分呈负相关（r = -0.84，p < 0.001），与7天后NIHSS评分也呈负相关（r = -0.63，p < 0.05）。急性卒中后最初6小时MDA水平有升高趋势（p = 0.07）。未发现SOD、铁、铜和锌水平有显著差异。
急性卒中后GSH系统抗氧化能力存在差异，表现为GSH和GSHPx升高，但其他指标无差异。这些发现支持了抗氧化能力变化是急性卒中期间急性适应性机制一部分的假说。
