在 homozygous homocystinuria 中氧化应激和血小板激活
G Davì1, G Di Minno, A Coppola
1Center of Excellence on Aging, Department of Biomedical Sciences, University of Chieti G. D'Annunzio, Chieti, Italy. gdavi@unich.it
Circulation
|September 6, 2001
概括
严重的高homocysteinemia (CbetaSD) 增加氧化损伤,导致增强的血小板激活. 维生素E补充剂在患者中减少了这种损伤和激活的标志物.
科学领域:
- 生物化学 生物化学
- 心血管医学 心血管医学
- 代谢障碍 代谢障碍 代谢障碍
背景情况:
- 严重的高homocysteinemia,由cystathionineβ-合成酶缺乏症 (CbetaSD) 引起,与过早的动脉血性血管疾病有关.
- 同类氨酸通过氧化应激机制与血管损伤有关.
研究的目的:
- 调查CbetaSD患者体内8-异质前列腺素F ((2α) 的形成是否在体内升高.
- 为了确定这种升高是否与体内血小板激活相关,通过血小板素代谢物分泌量来测量.
- 评估维生素E补充剂对这些标记物的影响.
主要方法:
- 从13名同卵性CbetaSD患者和健康对照组收集了尿液和血液样本.
- 测量了尿液中的8-iso-PGF ((2α) 和11-dehydro-TXB ((2) 的分泌量.
- 评估了血中的同类半氨酸和维生素E水平.
- 服用维生素E (600毫克/天2周) 和重新测量标记物.
主要成果:
- 与对照组相比,CbetaSD患者的尿液8-iso-PGF(2alpha) 和11-dehydro-TXB(2) 排泄量显著增加.
- 这两种标志物与血类固醇和彼此相关.
- 维生素E补充剂显著增加了血维生素E水平,并减少了8-iso-PGF ((2alpha) 和11-dehydro-TXB ((2) 的分泌.
- 在尿液中的8-iso-PGF和血维生素E水平之间观察到强烈的反相关性.
结论:
- 增强的阿拉基酸过氧化到F(2) - 异素可能会将高血糖蛋白和血小板激活与CbetaSD联系起来.
- 这些发现支持对CbetaSD患者维生素E补充剂的进一步调查.
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