Abstract | BACKGROUND: A growing body of evidence from animal studies supports the hypothesis that oxidative stress-mediated mechanisms play a central role in early atherogenesis. In contrast, clinical trials with antioxidant vitamins have not produced consistent results in humans with established atherosclerosis. METHODS AND RESULTS: CONCLUSIONS: These results demonstrate that in LDLR KO, vitamin E supplementation reduces progression of established atherosclerosis by suppressing oxidative and inflammatory reactions and increasing nitric oxide levels.
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Authors | Tillmann Cyrus, Yuemang Yao, Joshua Rokach, Lina X Tang, Domenico Praticò |
Journal | Circulation
(Circulation)
Vol. 107
Issue 4
Pg. 521-3
(Feb 04 2003)
ISSN: 1524-4539 [Electronic] United States |
PMID | 12566360
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- 8,12-iso-isoprostane F2alpha-VI
- Biomarkers
- Dietary Fats
- Receptors, LDL
- Triglycerides
- Vitamin E
- Nitric Oxide
- Cholesterol
- Dinoprost
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Topics |
- Animals
- Aorta
(drug effects, pathology)
- Arteriosclerosis
(drug therapy, pathology)
- Biomarkers
(blood)
- Cholesterol
(blood)
- Dietary Fats
(adverse effects)
- Dietary Supplements
- Dinoprost
(analogs & derivatives, blood)
- Disease Progression
- Immunohistochemistry
- Lipid Peroxidation
(drug effects)
- Mice
- Mice, Knockout
- Nitric Oxide
(metabolism)
- Receptors, LDL
(deficiency, genetics)
- Treatment Outcome
- Triglycerides
(blood)
- Vitamin E
(blood, therapeutic use)
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