Interactions Between Nitric Oxide and Lipid Oxidation Pathways: Implications for Vascular Disease
Abstract
Abstract—Nitric oxide (·NO) signaling pathways and lipid oxidation reactions are of central importance in both the maintenance of vascular homeostasis and the progression of vascular disease. Because both of these pathways involve free radical species that can also react together at extremely fast rates, convergent interactions between these pathways are expected. Biochemical and cell biology studies have defined multiple interactions of·NO with oxidizing lipids that could lead to either vascular protection or potentiation of inflammatory vascular injury. For example, low levels of·NO generated by endothelial nitric oxide synthase can terminate propagating lipid radicals and inhibit lipoxygenases, reactions that would be protective. Alternatively, if generated at elevated levels, for example, after inducible nitric oxide synthase expression in inflammation,·NO can be converted to prooxidant species, such as peroxynitrite (ONOO–) and nitrogen dioxide (·NO 2), that can potentiate inflammatory injury to vascular cells. Finally, both enzymatic and nonenzymatic lipid oxidation reactions can influence·NO bioactivity by directly scavenging·NO or altering the induction and catalytic activity of nitric oxide synthase enzymes. In this review, we summarize the biochemical interactions between·NO and lipid oxidation reactions and discuss the recognized and potential roles of these reactions in the vasculature.
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NO reacts rapidly with other free radicals such as O2 ̇̄ or lipid peroxyl radicals.
“NO reacts rapidly with other free radicals such as O2˙̄ or lipid peroxyl radicals (5, 48).”
From What Part of NO Don't You Understand? Some Answers to the Cardinal Questions in Nitric Oxide Biology (2010) · cites this paper as [48]
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- Authors
- O’Donnell, V. B., & Freeman, B. A.
- Affiliations
- University of Alabama at Birmingham (US)
- From the Wales Heart Research Institute (V.B.O’D.), University of Wales College of Medicine, Heath Park, Cardiff, Wales, UK; Departments of Anesthesiology, Biochemistry, and Molecular Genetics (B.A.F.), and the Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Ala.
- Venue
- Circulation Research
- Published
- 2001-01-19
- Volume
- 88
- Issue
- 1
- Pages
- 12-21
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2127710249
- Cited by
- 257
- References
- 158
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 1 · 2023: 6 · 2022: 7 · 2021: 8 · 2020: 8 · 2019: 6 · 2018: 6 · 2017: 3 · 2016: 7 · 2015: 6 · 2014: 6 · 2013: 12 · 2012: 11
- FWCI
- 2.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p60hl058418-05)
- National Heart, Lung, and Blood Institute (R01HL064937, P6-HL-58418, R01HL058115)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- nitric oxide, lipid peroxidation, nitric oxide synthase, endothelial nitric oxide synthase, inducible nitric oxide synthase, peroxynitrite, nitrogen dioxide, lipoxygenase inhibition, lipid radicals, vascular inflammation, vascular injury, nitric oxide scavenging, oxidative stress
- MeSH terms
- Animals, Humans, Lipids, Nitric Oxide, Vascular Diseases, Lipid Peroxidation, Lipid Metabolism
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