Nitric Oxide and Peroxynitrite in Health and Disease

Pacher, Pál; Beckman, Joseph S.; Liaudet, Lucas

doi:10.1152/physrev.00029.2006

Cited by 6,390Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative Mechanisms

Nitric Oxide and Peroxynitrite in Health and Disease

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Pacher, Pál, Beckman, Joseph S., Liaudet, Lucas·2007·Physiological Reviews

DOI 10.1152/physrev.00029.2006PMC PMC2248324

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Abstract

The discovery that mammalian cells have the ability to synthesize the free radical nitric oxide (NO) has stimulated an extraordinary impetus for scientific research in all the fields of biology and medicine. Since its early description as an endothelial-derived relaxing factor, NO has emerged as a fundamental signaling device regulating virtually every critical cellular function, as well as a potent mediator of cellular damage in a wide range of conditions. Recent evidence indicates that most of the cytotoxicity attributed to NO is rather due to peroxynitrite, produced from the diffusion-controlled reaction between NO and another free radical, the superoxide anion. Peroxynitrite interacts with lipids, DNA, and proteins via direct oxidative reactions or via indirect, radical-mediated mechanisms. These reactions trigger cellular responses ranging from subtle modulations of cell signaling to overwhelming oxidative injury, committing cells to necrosis or apoptosis. In vivo, peroxynitrite generation represents a crucial pathogenic mechanism in conditions such as stroke, myocardial infarction, chronic heart failure, diabetes, circulatory shock, chronic inflammatory diseases, cancer, and neurodegenerative disorders. Hence, novel pharmacological strategies aimed at removing peroxynitrite might represent powerful therapeutic tools in the future. Evidence supporting these novel roles of NO and peroxynitrite is presented in detail in this review.

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The melanin-to-DNA chemiexcitation process is initiated by nitric oxide and superoxide, radicals triggered by ultraviolet light or inflammation.
“That process was initiated by nitric oxide and superoxide, radicals triggered by ultraviolet light or inflammation.”
From Chemiexcitation: Mammalian Photochemistry in the Dark† (2023) · cites this paper as [34]
The Biological Chemistry and Local Inflammation sections describe nitric oxide and superoxide production in inflammatory settings and a pathway leading to DNA damage (pages unavailable). They do not describe melanin-to-DNA chemiexcitation or establish that ultraviolet light triggers the radicals in that process. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Glutamate induces •NO in neurons and is released during ischemia-reperfusion such as stroke or sleep apnea, which are accompanied by ONOO-.
“The endogenous excitotoxin glutamate also induces •NO in neurons (216) and is released during ischemia-reperfusion such as in stroke or sleep apnea, which are accompanied by ONOO– (34).”
From Chemiexcitation: Mammalian Photochemistry in the Dark† (2023) · cites this paper as [34]
The section on stroke and reperfusion injury says cerebral ischemia causes extracellular glutamate to accumulate. The section on peroxynitrite in stroke describes peroxynitrite formation during ischemia and reperfusion. The passages support the stroke example, but do not establish the claim about sleep apnea. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Pacher et al. review indicated that peroxynitrite and 3-NT formation are relevant as diagnostic biomarkers for several pathologic conditions.
“Already in 2008, Pacher et al. published an outstanding and detailed review about the role of peroxynitrite and 3-NT formation in human health and disease, indicating their relevance as diagnostic biomarker for several pathologic conditions [188].”
From Protein oxidation - Formation mechanisms, detection and relevance as biomarkers in human diseases (2021) · cites this paper as [188]
In Biological Chemistry (page unavailable), the review calls nitrotyrosine an important biological marker and reports its detection in many disease-affected tissues. The neurodegenerative-disorders section (page unavailable) says elevated free nitrotyrosine in cerebrospinal fluid has been proposed as a marker of neurodegeneration. These passages support relevance as disease-associated markers, but do not establish peroxynitrite and 3-NT formation as diagnostic biomarkers for several specific conditions. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Nitric oxide and superoxide combine instantly to form peroxynitrite.
“These radicals combine instantly to form the powerful oxidant peroxynitrite (ONOO−)”
From Chemiexcitation: Mammalian Photochemistry in the Dark† (2023) · cites this paper as [34]
Overexpression of eNOS is detrimental.
“Notably, overexpression of eNOS is also detrimental”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [708]

NO and related nitrogen oxides are critical endogenous regulators of cell and tissue function.
“Nitric oxide (NO; nitrogen monoxide) and related nitrogen oxides are now known to be critical endogenous regulators of cell and tissue function (1, 2).”
From What Part of NO Don't You Understand? Some Answers to the Cardinal Questions in Nitric Oxide Biology (2010) · cites this paper as [2]
The fate of NO is dramatically changed in the presence of other free radicals such as superoxide.
“Biologically, this means that the fate of NO is dramatically changed in the presence of other free radicals such as superoxide (O2˙̄) (2, 20–22).”
From What Part of NO Don't You Understand? Some Answers to the Cardinal Questions in Nitric Oxide Biology (2010) · cites this paper as [2]
The best studied reaction of NO with other free radicals is the very rapid reaction of NO with superoxide to form peroxynitrite.
“The best studied of these reactions is the very rapid reaction of NO with superoxide to form peroxynitrite (2, 21, 22, 24).”
From What Part of NO Don't You Understand? Some Answers to the Cardinal Questions in Nitric Oxide Biology (2010) · cites this paper as [2]
Nitric oxide •NO is a ubiquitous cellular signaling molecule, found in a variety of cell types, including vascular endothelium, platelets, macrophages, and neuronal cells.
“Nitric oxide •NO is a ubiquitous cellular signaling molecule, found in a variety of cell types, including vascular endothelium, platelets, macrophages, and neuronal cells [23].”
From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [23]
The presence of free radicals such as superoxide changes the fate of NO: once reacted, it forms peroxynitrite and can no longer bind to ferrous heme.
“The presence of free radicals such as superoxide (O2.−) [82-85] changes the fate of NO: once reacted, it forms peroxynitrite [82, 84, 85] and can no longer bind to ferrous heme [86].”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [82]
NO derived from the integration of NOS3 and NOS1 activities plays key roles in regulating systemic blood pressure and acutely regulating organ blood flow, whereas NOS2-derived NO species are most recognized for their impact on pathogen killing and inflammatory processes.
“Overall, NO derived from the integration of NOS3 and NOS1 activities play key roles in regulating systemic blood pressure and acutely regulating organ blood flow, whereas NOS2-derived NO species are most well recognized for their impact on pathogen killing and inflammatory processes [82].”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [82]

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Authors: Pacher, P., Beckman, J. S., & Liaudet, L.
Affiliations: National Institutes of Health (US)
ORCID: Pacher, Pál
Beckman, Joseph S.
Liaudet, Lucas
Venue: Physiological Reviews
Publisher: American Physiological Society
Published: 2007-01
Volume: 87
Issue: 1
Pages: 315-424
ISSN: 0031-9333 (ISSN-L)
1522-1210
DOI: 10.1152/physrev.00029.2006
PMC: PMC2248324
OpenAlex: W2122386753
Cited by: 6,390
References: 1,513
Citations by year: 2026: 266 · 2025: 278 · 2024: 275 · 2023: 315 · 2022: 382 · 2021: 412 · 2020: 377 · 2019: 359 · 2018: 358 · 2017: 375 · 2016: 344 · 2015: 329 · 2014: 390 · 2013: 351 · 2012: 391
FWCI: 29.04
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Physiological Reviews (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
IRIS (submittedVersion)
SERVAL (Université de Lausanne) (submittedVersion, other-oa)
Funders: National Institutes of Health
National Institute on Alcohol Abuse and Alcoholism (Z01AA000375)
National Institute of Environmental Health Sciences (ES-00040, P01ES000040, ES-00240)
National Center for Complementary and Integrative Health (AT-02034, P01AT002034)
Topics: Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Keywords: nitric oxide, peroxynitrite, superoxide, oxidative stress, nitric oxide signaling, apoptosis, necrosis, stroke, myocardial infarction, chronic heart failure, diabetes mellitus, shock, chronic inflammatory diseases, cancer, neurodegenerative diseases, peroxynitrite scavengers
MeSH terms: Animals, Disease, Health, Humans, Nitric Oxide, Peroxynitrous Acid

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Nitric Oxide and Peroxynitrite in Health and Disease

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