Dubick M A, Keen C L, DiSilvestro R A, Eskelson C D, Ireton J, Hunter G C
U.S. Army Institute of Surgical Research,Mechanical Trauma Research Branch, Fort Sam Houston, Texas 78234-6315, USA.
Proc Soc Exp Biol Med. 1999 Jan;220(1):39-45. doi: 10.1046/j.1525-1373.1999.d01-6.x.
The present study further investigates evidence for lipid peroxidation in atherosclerotic aortic tissue by determining the activity of antioxidant enzymes and concentrations of lipid peroxide fluorochromes in abdominal aortas from 15 patients with abdominal aortic aneurysms (AAA), an additional 7 patients with ruptured abdominal aneurysms, and 12 patients with atherosclerotic occlusive disease (AOD). Aortas from nonatherosclerotic organ donors served as nondiseased controls. Cu, Zn-superoxide dismutase (Cu,Zn-SOD) activities in AAA and AOD tissues were 16% and 25% of control activity, respectively. Mn-SOD activity in diseased aortae were about 65% of controls. CuZn-SOD protein in AAA and AOD was 56% and 100% of controls, respectively, resulting in significantly lower CuZn-SOD specific activity in these tissues. Ruptured AAA tissue also had low SOD activity and protein. Glutathione peroxidase (GPx) activity in AAA and AOD aortas was 70% and 65% of controls, respectively, and glutathione reductase (GR) activity in AAA and AOD aortas was 80% and 65% of control activities, respectively. These results were associated with significantly higher lipid peroxide fluorochromes, expressed as U/g aorta, in both groups of atherosclerotic aortas than in controls. AOD aortas had 33% higher fluorescence than AAA aortas, but the highest levels were seen in ruptured AAA. These data further support the involvement of free radicals and lipid peroxidation in atherosclerotic aortic disease, but do not indicate that these mechanisms are specifically involved in aneurysm formation versus development of occlusive disease.
本研究通过测定抗氧化酶活性以及脂质过氧化物荧光染料的浓度，进一步探究动脉粥样硬化主动脉组织中脂质过氧化的证据。研究对象包括15例腹主动脉瘤（AAA）患者、另外7例破裂腹主动脉瘤患者以及12例动脉粥样硬化闭塞性疾病（AOD）患者的腹主动脉，同时选取非动脉粥样硬化器官供体的主动脉作为无疾病对照。AAA和AOD组织中的铜锌超氧化物歧化酶（Cu,Zn-SOD）活性分别为对照活性的16%和25%。病变主动脉中的锰超氧化物歧化酶（Mn-SOD）活性约为对照的65%。AAA和AOD中的铜锌超氧化物歧化酶蛋白分别为对照的56%和100%，导致这些组织中铜锌超氧化物歧化酶的比活性显著降低。破裂的AAA组织也具有较低的超氧化物歧化酶活性和蛋白水平。AAA和AOD主动脉中的谷胱甘肽过氧化物酶（GPx）活性分别为对照的70%和65%，AAA和AOD主动脉中的谷胱甘肽还原酶（GR）活性分别为对照活性的80%和65%。这些结果与两组动脉粥样硬化主动脉中以每克主动脉单位（U/g aorta）表示的脂质过氧化物荧光染料水平显著高于对照相关。AOD主动脉的荧光比AAA主动脉高33%，但在破裂的AAA中荧光水平最高。这些数据进一步支持自由基和脂质过氧化参与动脉粥样硬化主动脉疾病，但并未表明这些机制具体参与动脉瘤形成与闭塞性疾病发展的差异。
