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2
Atherosclerosis as disease of redox-sensitive genes.动脉粥样硬化作为氧化还原敏感基因的疾病。
Trans Am Clin Climatol Assoc. 1998;109:129-45; discussion 145-6.
3
Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase.对氧磷酶可抑制高密度脂蛋白氧化并维持其功能。对氧磷酶可能具有过氧化作用。
J Clin Invest. 1998 Apr 15;101(8):1581-90. doi: 10.1172/JCI1649.
4
L-2-Oxothiazolidine-4-carboxylic acid reverses endothelial dysfunction in patients with coronary artery disease.L-2-氧代噻唑烷-4-羧酸可逆转冠心病患者的内皮功能障碍。
J Clin Invest. 1998 Mar 15;101(6):1408-14. doi: 10.1172/JCI1155.
5
Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease.C反应蛋白的血浆浓度与外周血管疾病发生风险
Circulation. 1998 Feb 10;97(5):425-8. doi: 10.1161/01.cir.97.5.425.
6
Protein oxidation in aging, disease, and oxidative stress.衰老、疾病及氧化应激中的蛋白质氧化
J Biol Chem. 1997 Aug 15;272(33):20313-6. doi: 10.1074/jbc.272.33.20313.
7
Lewis A. Conner Memorial Lecture. Oxidative modification of LDL and atherogenesis.刘易斯·A·康纳纪念讲座。低密度脂蛋白的氧化修饰与动脉粥样硬化形成。
Circulation. 1997 Feb 18;95(4):1062-71. doi: 10.1161/01.cir.95.4.1062.
8
Mitochondrial DNA damage is more extensive and persists longer than nuclear DNA damage in human cells following oxidative stress.在氧化应激后,人类细胞中的线粒体DNA损伤比核DNA损伤更广泛,且持续时间更长。
Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):514-9. doi: 10.1073/pnas.94.2.514.
9
Combined effects of lipid peroxidation and antioxidant status on carotid atherosclerosis in a population aged 59-71 y: The EVA Study. Etude sur le Vieillisement Artériel.脂质过氧化和抗氧化状态对59 - 71岁人群颈动脉粥样硬化的联合影响:EVA研究。动脉老化研究。
Am J Clin Nutr. 1997 Jan;65(1):121-7. doi: 10.1093/ajcn/65.1.121.
10
Risk factors for lung cancer and for intervention effects in CARET, the Beta-Carotene and Retinol Efficacy Trial.CARET(β-胡萝卜素与视黄醇功效试验)中肺癌的危险因素及干预效果
J Natl Cancer Inst. 1996 Nov 6;88(21):1550-9. doi: 10.1093/jnci/88.21.1550.

氧化应激在动脉粥样硬化中的作用:希望与炒作。

The role of oxidative stress in atherosclerosis: the hope and the hype.

作者信息

Runge M S

机构信息

University of Texas Medical Branch, Galveston 77555, USA.

出版信息

Trans Am Clin Climatol Assoc. 1999;110:119-29; discussion 129-30.

PMID:10344012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2194301/
Abstract

Numerous lines of investigation support the importance of oxidative stress in the development of atherosclerosis. Results from studies in isolated cells and in animal models of atherosclerosis are compelling, as are those from a select number of clinical trials. Unfortunately, the results of prospective, randomized clinical studies have been disappointing and may reflect our current inability to accurately assess oxidative risk and the response to antioxidant therapy. Only when it is possible to accurately and easily measure oxidative stress will it be possible to accurately determine the efficacy of different antioxidant approaches.

摘要

众多研究方向都支持氧化应激在动脉粥样硬化发展过程中的重要性。在分离细胞和动脉粥样硬化动物模型中的研究结果令人信服,一些临床试验的结果也是如此。不幸的是,前瞻性随机临床研究的结果并不理想,这可能反映出我们目前无法准确评估氧化风险以及对抗氧化治疗的反应。只有当能够准确且轻松地测量氧化应激时,才有可能准确确定不同抗氧化方法的疗效。