The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Hypercholesterolemia increases endothelial superoxide anion production.
Open accessAbstract
Indirect evidence suggests accelerated degradation of endothelium-derived nitric oxide (ENDO) by superoxide anion (O2-) in hypercholesterolemic vessels (HV). To directly measure O2- production by normal vessels (NV) and HV, we used an assay for O2- based on the chemiluminescence (CL) of lucigenin (L). HV (1 mo cholesterol-fed rabbits) produced threefold more O2- than NV (1.47 +/- 0.20 nM/mg tissue/min, n = 7 vs. 0.52 +/- 0.05 nmol/mg tissue/min, n = 8, P < 0.001). Endothelial removal increased O2- production in NV (0.73 +/- 0.08, n = 6, P < 0.05), while decreasing it in HV (0.76 +/- 0.15, n = 5, P < 0.05). There was no difference between denuded HV and denuded NV. Oxypurinol, a noncompetitive inhibitor of xanthine oxidase, normalized O2- production in HV, but had no effect in NV. In separate isometric tension studies treatment with oxypurinol improved acetylcholine induced relaxations in HV, while having no effect on responses in normal vessels. Oxypurinol did not alter relaxations to nitroprusside. Thus, the endothelium is a source of O2- in hypercholesterolemia probably via xanthine oxidase activation. Increased endothelial O2- production in HV may inactivate endothelium-derived nitric oxide and provide a source for other oxygen radicals, contributing to the early atherosclerotic process.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Its mechanism of action is based on the reaction with the FAD moiety of the NOX dehydrogenase domain (699).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [699]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Furchgott, R. F., & Zawadzki, J. V. (1980) · Nature · doi:10.1038/288373a0 · Cited by 12,064
Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor
Palmer, R. M. J., Ferrige, A. G., & Moncada, S. (1987) · Nature · doi:10.1038/327524a0 · Cited by 10,704
Beckman, J. S., Beckman, T. W., Chen, J., Marshall, P. A., & Freeman, B. A. (1990) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.87.4.1620 · Cited by 7,029
Babior, B. M., Kipnes, R. S., & Curnutte, J. T. (1973) · Journal of Clinical Investigation · doi:10.1172/jci107236 · Cited by 2,931
Superoxide anion is involved in the breakdown of endothelium-derived vascular relaxing factor
Gryglewski, R. J., Palmer, R. M. J., & Moncada, S. (1986) · Nature · doi:10.1038/320454a0 · Cited by 2,400
Abnormal Endothelium-Dependent Vascular Relaxation in Patients with Essential Hypertension
Panza, J. A., Quyyumi, A. A., Brush, J. E., & Epstein, S. E. (1990) · New England Journal of Medicine · doi:10.1056/nejm199007053230105 · Cited by 2,366
Quantitative Aspects of the Production of Superoxide Anion Radical by Milk Xanthine Oxidase
Fridovich, I. (1970) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)62884-4 · Cited by 1,035
Myers, P. R., Minor, R. L., Guerra, R., Bates, J. N., & Harrison, D. G. (1990) · Nature · doi:10.1038/345161a0 · Cited by 973
Self-citationAllen, R. C., STJERNHOLM, R. L., & Steele, R. H. (1972) · Biochemical and Biophysical Research Communications · doi:10.1016/0006-291x(72)90545-1 · Cited by 955
Endothelium-dependent vasodilation is attenuated in patients with heart failure.
Kubo, S. H., Rector, T. S., Bank, A. J., Williams, R. E., & Heifetz, S. M. (1991) · Circulation · doi:10.1161/01.cir.84.4.1589 · Cited by 775
Cited by
Sorted by citations
Free Radicals in the Physiological Control of Cell Function
Dröge, W. (2002) · Physiological Reviews · doi:10.1152/physrev.00018.2001 · Cited by 9,855
Increased oxidative stress in obesity and its impact on metabolic syndrome
Furukawa, S., Fujita, T., Shimabukuro, M., Iwaki, M., Yamada, Y., Nakajima, Y., Nakayama, O., Makishima, M., Matsuda, M., & Shimomura, I. (2004) · Journal of Clinical Investigation · doi:10.1172/jci21625 · Cited by 5,508
Corretti, M. C., Anderson, T. J., Benjamin, E. J., Celermajer, D. S., Charbonneau, F., Creager, M. A., Deanfield, J. E., Drexler, H., Gerhard‐Herman, M. D., Herrington, D. M., et al. (2002) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(01)01746-6 · Cited by 4,606
Endothelial dysfunction in cardiovascular diseases: the role of oxidant stress
Cai, H., & Harrison, D. G. (2000) · Circulation Research · doi:10.1161/01.res.87.10.840 · Cited by 3,839
Self-citationNAD(P)H Oxidase: Role in Cardiovascular Biology and Disease
Griendling, K. K., Sorescu, D., & Ushio-Fukai, M. (2000) · Circulation Research · doi:10.1161/01.res.86.5.494 · Cited by 2,886
Metadata
- Authors
- Ohara, Y., Peterson, T. E., & Harrison, D. G.
- Affiliations
- Emory University (US)
- ORCID
- Harrison, D G
- Venue
- Journal of Clinical Investigation
- Published
- 1993-06-01
- Volume
- 91
- Issue
- 6
- Pages
- 2546-2551
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC443316
- OpenAlex
- W2135633069
- Cited by
- 1,765
- References
- 41
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 10 · 2023: 9 · 2022: 15 · 2021: 21 · 2020: 29 · 2019: 29 · 2018: 18 · 2017: 30 · 2016: 26 · 2015: 28 · 2014: 43 · 2013: 43 · 2012: 47
- FWCI
- 26.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health (5r01hl032717-09)
- National Heart, Lung, and Blood Institute (R01HL039006, HL-32717, HL-39006)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Keywords
- hypercholesterolemia, superoxide, endothelium, nitric oxide degradation, xanthine oxidase, oxypurinol, chemiluminescence, lucigenin, atherosclerosis, endothelial dysfunction, acetylcholine-induced relaxation, cholesterol-fed rabbits
- MeSH terms
- Acridines, Animals, Aorta, Cholesterol, Cholesterol, Dietary, Endothelium, Vascular, Hypercholesterolemia, Luminescent Measurements, Male, Oxypurinol, Rabbits, Superoxides, Xanthine Oxidase
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
