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慢性疲劳综合征中的抗氧化状态与脂蛋白过氧化

Antioxidant status and lipoprotein peroxidation in chronic fatigue syndrome.

作者信息

Manuel y Keenoy B, Moorkens G, Vertommen J, De Leeuw I

机构信息

University Hospital, University of Antwerp, Belgium.

出版信息

Life Sci. 2001 Mar 16;68(17):2037-49. doi: 10.1016/s0024-3205(01)01001-3.

DOI:10.1016/s0024-3205(01)01001-3
PMID:11388705
Abstract

The aetiology and pathogenesis of the Chronic Fatigue Syndrome (CFS) are still largely unresolved. Accompanying metabolic disorders such as selective n-6 fatty acid depletion suggest that oxidative stress and more specifically lipid peroxidation might play a role in its pathogenesis. In order to investigate this hypothesis, oxidant-antioxidant status and its impact on lipoprotein peroxidation in vitro was examined in 61 patients with unexplained fatigue lasting more than 1 month. They were subdivided into 2 groups: group CFS+ (33 subjects) fulfilled the 1988 Center of Disease Control criteria for CFS and group CFS- did not but was similar as regards age, sex distribution and clinical characteristics. Antioxidant status was similar in the 2 groups except for lower serum transferrin in the CFS + (mean (95 % CI) 2.41 (2.28-2.54) versus 2.73 (2.54-2.92) g/L in the CFS-, p = 0.009) and higher lipoprotein peroxidation in vitro: 6630 (5949-7312) versus 5581 (4852-6310) nmol MDA/mg LDL and VLDL cholesterol x minutes, p = 0.035). CFS intensified the influence of LDL cholesterol (p = 0.012) and of transferrin (p = 0.045) on peroxidation in vitro, suggesting additional pro-oxidant effects. These results indicate that patients with CFS have increased susceptibility of LDL and VLDL to copper-induced peroxidation and that this is related both to their lower levels of serum transferrin and to other unidentified pro-oxidising effects of CFS.

摘要

慢性疲劳综合征(CFS)的病因和发病机制在很大程度上仍未明确。伴随的代谢紊乱,如选择性n-6脂肪酸耗竭,提示氧化应激,更具体地说是脂质过氧化可能在其发病机制中起作用。为了研究这一假设,对61例持续不明原因疲劳超过1个月的患者进行了体外氧化-抗氧化状态及其对脂蛋白过氧化影响的检测。他们被分为两组:CFS+组(33名受试者)符合1988年疾病控制中心的CFS标准,CFS-组不符合,但在年龄、性别分布和临床特征方面相似。两组的抗氧化状态相似,但CFS+组血清转铁蛋白较低(均值(95%可信区间)为2.41(2.28 - 2.54)g/L,而CFS-组为2.73(2.54 - 2.92)g/L,p = 0.009),且体外脂蛋白过氧化较高:6630(5949 - 7312)对5581(4852 - 6310)nmol丙二醛/毫克低密度脂蛋白和极低密度脂蛋白胆固醇×分钟,p = 0.035)。CFS增强了低密度脂蛋白胆固醇(p = 0.012)和转铁蛋白(p = 0.045)对体外过氧化的影响,提示存在额外的促氧化作用。这些结果表明,CFS患者的低密度脂蛋白和极低密度脂蛋白对铜诱导的过氧化敏感性增加,这与他们较低的血清转铁蛋白水平以及CFS的其他未明确的促氧化作用有关。

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