Antioxidant enzyme activity in human abdominal aortic aneurysmal and occlusive disease

Citation
Ma. Dubick et al., Antioxidant enzyme activity in human abdominal aortic aneurysmal and occlusive disease, P SOC EXP M, 220(1), 1999, pp. 39-45
Citations number
45
Categorie Soggetti
Medical Research General Topics
Journal title
PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE
ISSN journal
00379727 → ACNP
Volume
220
Issue
1
Year of publication
1999
Pages
39 - 45
Database
ISI
SICI code
0037-9727(199901)220:1<39:AEAIHA>2.0.ZU;2-R
Abstract
The present study further investigates evidence for lipid peroxidation in a therosclerotic aortic tissue by determining the activity of antioxidant enz ymes and concentrations of lipid peroxide fluorochromes in abdominal aortas from 15 patients with abdominal aortic aneurysms (AAA), an additional 7 pa tients with ruptured abdominal aneurysms, and 12 patients with atherosclero tic occlusive disease (AOD). Aortas from nonatherosclerotic organ donors se rved as nondiseased controls. Cu,Zn-superoxide dismutase (Cu,Zn-SOD) activi ties in AAA and AOD tissues were 16% and 25% of control activity, respectiv ely. Mn-SOD activity in diseased aortae were about 65% of controls. CuZn-SO D protein in AAA and AOD was 56% and 100% of controls, respectively, result ing in significantly lower CuZn-SOD specific activity in these tissues. Rup tured AAA tissue also had low SOD activity and protein. Glutathione peroxid ase (GPx) activity in AAA and AOD aortas was 70% and 65% of controls, respe ctively, and glutathione reductase (GR) activity in AAA and AOD aortas was 80% and 65% of control activities, respectively. These results were associa ted with significantly higher lipid peroxide fluorochromes, expressed as U/ g aorta, in both groups of atherosclerotic aortas than in controls. AOD aor tas had 33% higher fluorescence than AAA aortas, but the highest levels wer e seen in ruptured AAA. These data further support the involvement of free radicals and lipid peroxidation in atherosclerotic aortic disease, but do n ot indicate that these mechanisms are specifically involved in aneurysm for mation versus development of occlusive disease.