The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
Ascorbate Prevents the Interaction of Superoxide and Nitric Oxide Only at Very High Physiological Concentrations
Abstract
The bioactivity of nitric oxide (.NO) depends, in part, on its interaction with superoxide. Usually, superoxide dismutase (SOD) preserves .NO bioactivity by limiting the availability of superoxide. Ascorbic acid also effectively scavenges superoxide, but the extent to which this interaction is necessary for intact .NO bioactivity is not known. Therefore, the present study examined the effect of ascorbic acid on .NO bioactivity with isolated rabbit arterial segments. A steady flux of superoxide (1.15 to 2.3 micromol . L-1 . min-1) produced either by pyrogallol autoxidation or a hypoxanthine/xanthine oxidase system inhibited endothelium-derived .NO-mediated arterial relaxation elicited by acetylcholine. This effect of superoxide was completely blocked by SOD (300 IU/mL) and the manganese SOD mimic EUK-8 (300 micromol/L) and partially inhibited by ascorbic acid (10 mmol/L). Lower concentrations of ascorbic acid were ineffective despite scavenging >90% of superoxide. We increased the endogenous flux of superoxide (3.2+/-0.3-fold) by inhibiting vascular copper-zinc SOD with diethyldithiocarbamate. This increased endogenous flux of superoxide produced an impairment of .NO-mediated arterial relaxation that was reversed by EUK-8 (300 micromol/L) but not ascorbic acid (10 mmol/L) despite equivalent scavenging of the endogenous superoxide flux. We used 3-nitrotyrosine formation (from peroxynitrite) as an indicator of .NO interaction with superoxide and found that SOD and EUK-8 compete more effectively with .NO for superoxide than does ascorbic acid. These data indicate that preservation of .NO bioactivity by superoxide scavengers depends not only on superoxide scavenging activity, but also on the rate of superoxide scavenging. Normal extracellular concentrations of ascorbic acid (30 to 150 micromol/L) are not likely to prevent the interaction of .NO with superoxide under physiological conditions.
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“However, in competition with NO, a concentration of vitamin C about 10 mM is needed to block the interaction of NO with the superoxide by effective scavenging of the latter [167].”
From Vitamin C-Sources, Physiological Role, Kinetics, Deficiency, Use, Toxicity, and Determination (2021) · cites this paper as [167]
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Marklund, S. L., & MARKLUND, G. (1974) · European Journal of Biochemistry · doi:10.1111/j.1432-1033.1974.tb03714.x · Cited by 10,382
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
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
The reaction of NO with superoxide
Huie, R. E., & Padmaja, S. (1993) · Free Radical Research Communications · doi:10.3109/10715769309145868 · Cited by 2,121
Pryor, W. A. (1976) · Cited by 1,876
Hypercholesterolemia increases endothelial superoxide anion production.
Ohara, Y., Peterson, T. E., & Harrison, D. G. (1993) · Journal of Clinical Investigation · doi:10.1172/jci116491 · Cited by 1,765
Peroxynitrite-mediated tyrosine nitration catalyzed by superoxide dismutase
Ischiropoulos, H., Zhu, L., Chen, J., Tsai, M., Martin, J. C., Smith, C. D. L., & Beckman, J. S. (1992) · Archives of Biochemistry and Biophysics · doi:10.1016/0003-9861(92)90431-u · Cited by 1,499
Superoxide anions and hyperoxia inactivate endothelium-derived relaxing factor
Rubanyi, G. M., & Vanhoutte, P. M. (1986) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1986.250.5.h822 · Cited by 1,193
Superoxide Radical: An Endogenous Toxicant
Fridovich, I. (1983) · The Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pa.23.040183.001323 · Cited by 1,168
How to Characterize a Biological Antioxidant
Halliwell, B. B. (1990) · Free Radical Research Communications · doi:10.3109/10715769009148569 · Cited by 941
Cited by
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Role of Oxidative Modifications in Atherosclerosis
Stocker, R., & Keaney, J. F. (2004) · Physiological Reviews · doi:10.1152/physrev.00047.2003 · Cited by 2,651
Heitzer, T., Schlinzig, T., Krohn, K., Meinertz, T., & Münzel, T. (2001) · Circulation · doi:10.1161/hc4601.099485 · Cited by 1,961
“Diabetes mellitus, n (%) 57 (21) 20 (22) 37 (20)”
Vitamin C as an Antioxidant: Evaluation of Its Role in Disease Prevention
Padayatty, S. J., Katz, A., Wang, Y., Eck, P., Kwon, O., Lee, J.-H., Chen, S., Corpe, C., Dutta, A., Dutta, S. K., et al. (2003) · Journal of the American College of Nutrition · doi:10.1080/07315724.2003.10719272 · Cited by 1,949
“Thus vitamin C may have favorable effects on vascular dilatation, possibly through its antioxidant effects on NO [133,134], but these findings are not consistent [135].”
BackgroundCreager, M. A., Lüscher, T. F., of, P. W. T. A., Cosentino, F., & Beckman, J. A. (2003) · Circulation · doi:10.1161/01.cir.0000091257.27563.32 · Cited by 1,675
Vitamin C: The known and the unknown and Goldilocks
Padayatty, S., & Levine, M. (2016) · Oral Diseases · doi:10.1111/odi.12446 · Cited by 753
“…using vitamin C Similarly, in vivo infusion of mM concentrations of ascorbate have been used to demonstrate many effects including vasodilatation (Levine et al., 1996a, Motoyama et al., 1997, Beckman et al., 2001, Vita et al., 1998, Jackson et al., 1998, Duffy et al., 2001, Kaufmann et al., 2000).”
Metadata
- Authors
- Jackson, T. S., Xu, A., Vita, J. A., & Keaney, J. F.
- Affiliations
- Boston University (US)
- Venue
- Circulation Research
- Published
- 1998-11-02
- Volume
- 83
- Issue
- 9
- Pages
- 916-922
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2155603952
- Cited by
- 400
- References
- 48
- Citations by year
- 2025: 9 · 2024: 6 · 2023: 4 · 2022: 4 · 2021: 18 · 2020: 15 · 2019: 13 · 2018: 9 · 2017: 7 · 2016: 14 · 2015: 12 · 2014: 17 · 2013: 17 · 2012: 21
- FWCI
- 11.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health (5r01hl059346-02, HL59346, HL55854, 1r01hl053398-01a1)
- National Heart, Lung, and Blood Institute (HL59346, HL 53398, P01HL055854, HL-55854)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- vitamin C, superoxide, nitric oxide, superoxide dismutase, peroxynitrite, nitrotyrosine, endothelium-derived nitric oxide, acetylcholine-induced relaxation, diethyldithiocarbamate
- MeSH terms
- Animals, Ascorbic Acid, Endothelium, Vascular, Female, Male, Nitric Oxide, Pyrogallol, Rabbits, Superoxides, Vasodilation
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