Superoxide, peroxynitrite and oxidative/nitrative stress in inflammation

2006 ◽  
Vol 34 (5) ◽  
pp. 965-970 ◽  
Author(s):  
D. Salvemini ◽  
T.M. Doyle ◽  
S. Cuzzocrea
Keyword(s):  
Reactive Oxygen Species ◽  
Chronic Inflammation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Comprehensive Review ◽  
Limited Space ◽  
Review Articles ◽  
Nitrative Stress ◽  
Acute And Chronic Inflammation ◽  
Considerable Body

A considerable body of evidence suggests that formation of potent reactive oxygen species and resulting oxidative/nitrative stress play a major role in acute and chronic inflammation and pain. Much of the knowledge in this field has been gathered by the use of pharmacological and genetic approaches. In this mini review, we will evaluate recent advances made towards understanding the roles of reactive oxygen species in inflammation, focusing in particular on superoxide and peroxynitrite. Given the limited space to cover this broad topic, here we will refer the reader to comprehensive review articles whenever possible.

scholarly journals Novel Antioxidant Properties of Doxycycline

2018 ◽  
Vol 19 (12) ◽  
pp. 4078 ◽  
Author(s):  
Dahn Clemens ◽  
Michael Duryee ◽  
Cleofes Sarmiento ◽  
Andrew Chiou ◽  
Jacob McGowan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Chronic Inflammation ◽  
Antioxidant Properties ◽  
Antibacterial Properties ◽  
Reactive Oxygen ◽  
Protein Adducts ◽  
Oxygen Species ◽  
Free System

Doxycycline (DOX), a derivative of tetracycline, is a broad-spectrum antibiotic that exhibits a number of therapeutic activities in addition to its antibacterial properties. For example, DOX has been used in the management of a number of diseases characterized by chronic inflammation. One potential mechanism by which DOX inhibits the progression of these diseases is by reducing oxidative stress, thereby inhibiting subsequent lipid peroxidation and inflammatory responses. Herein, we tested the hypothesis that DOX directly scavenges reactive oxygen species (ROS) and inhibits the formation of redox-mediated malondialdehyde-acetaldehyde (MAA) protein adducts. Using a cell-free system, we demonstrated that DOX scavenged reactive oxygen species (ROS) produced during the formation of MAA-adducts and inhibits the formation of MAA-protein adducts. To determine whether DOX scavenges specific ROS, we examined the ability of DOX to directly scavenge superoxide and hydrogen peroxide. Using electron paramagnetic resonance (EPR) spectroscopy, we found that DOX directly scavenged superoxide, but not hydrogen peroxide. Additionally, we found that DOX inhibits MAA-induced activation of Nrf2, a redox-sensitive transcription factor. Together, these findings demonstrate the under-recognized direct antioxidant property of DOX that may help to explain its therapeutic potential in the treatment of conditions characterized by chronic inflammation and increased oxidative stress.

scholarly journals Reactive oxygen species: rapid fire in inflammation

2017 ◽  
Vol 39 (4) ◽  
pp. 30-33 ◽  
Author(s):  
Sonia Ingram ◽  
Marina Diotallevi
Keyword(s):  
Reactive Oxygen Species ◽  
Inflammatory Response ◽  
Chronic Inflammation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Crucial Element

Everyone has encountered it at some point: inflammation. That horrible feeling when you've hurt yourself and the skin and tissue around the injury swells, goes red, feels hot and painful. It is even worse if it gets infected, then you really know about it! You can feel sick, weak and feverish as your body tries to fight off the infection and heal itself. Inflammation is really important for keeping us healthy. Sometimes, however, the body's inflammatory response can be a bit overzealous, not shutting down when it's supposed to, which can lead to various problems and even a state of disease. To fully understand and be able to effectively treat these diseases, we need a better understanding of how and why this chronic inflammation occurs. Could a crucial element in our lives, oxygen, be key to furthering our understanding?

Crosstalk between Oxidative Stress, Chronic Inflammation and Disease Progression in Essential Thrombocythemia

2019 ◽  
Vol 70 (10) ◽  
pp. 3486-3489
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Disease Progression ◽  
Chronic Inflammation ◽  
Essential Thrombocythemia ◽  
Reactive Oxygen ◽  
Low Grade ◽  
Oxygen Species ◽  
Inflammation Markers ◽  
Leukemic Transformation

Essential thrombocythemia (ET) is a Philadelphia-negative chronic myeloproliferative neoplasm characterized by acquired somatic mutations: JAK2, CALR or MPL. It is associated with low-grade chronic inflammation, oxidative stress, overproduction of reactive oxygen species (ROS) and antioxidant deficiency. In ET, chronic inflammation and oxidative stress contribute to the genomic instability, the clonal evolution to myelofibrosis and the leukemic transformation. We evaluated ROS levels and the total antioxidant capacity (TAC) in 62 ET patients and investigated the relationship between ROS, TAC, chronic inflammation, leukocytosis, JAK2V617F mutation, and disease progression to myelofibrosis or leukemic transformation. We observed increased levels of ROS and inflammation markers and a decreased TAC in ET patients vs. controls. The acute myeloid leukaemia transformation associated increased levels of oxidative stress and inflammation markers and increased leukocyte counts, while myelofibrosis progression associated an increase in ROS and serum ferritin. Keywords: essential thrombocythemia, reactive oxygen species, inflammation, JAK2V617F

The Pathogenesis of Vitiligo

2013 ◽  
Vol 17 (3) ◽  
pp. 153-172 ◽  
Author(s):  
Neel Malhotra ◽  
Marlene Dytoc
Keyword(s):  
Reactive Oxygen Species ◽  
Genetic Predisposition ◽  
Reactive Oxygen ◽  
Review Article ◽  
Oxygen Species ◽  
Comprehensive Review ◽  
Pigmentary Disorder ◽  
The World ◽  
The Way

Background: Vitiligo is a commonly encountered pigmentary disorder. Numerous studies and investigations from all over the world have attempted to determine the mechanisms behind this disease; however, the pathogenesis of vitiligo remains elusive. Objective: In this comprehensive review article, we present the findings behind the five overarching theories of what causes this disfiguring and psychologically debilitating disease. Method: We begin our discussion with the role of genetic predisposition and move onward to the neural theory first proposed in the 1950s. Next we discuss the autoimmune hypothesis, followed by the reactive oxygen species model, and conclude by describing the findings of the more recent melanocytorrhagy hypothesis. Conclusion: Although the exact pathogenesis of vitiligo is uncertain, each of these theories likely plays a role. Understanding each theory would pave the way for therapeutic advances for this disease.

scholarly journals Prodrug strategies for targeted therapy triggered by reactive oxygen species

MedChemComm ◽  
2019 ◽  
Vol 10 (9) ◽  
pp. 1531-1549 ◽  
Author(s):  
Jorge Peiró Cadahía ◽  
Viola Previtali ◽  
Nikolaj S. Troelsen ◽  
Mads H. Clausen
Keyword(s):  
Reactive Oxygen Species ◽  
Targeted Therapy ◽  
State Of The Art ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Future Perspectives ◽  
Comprehensive Review

A comprehensive review of ROS-activated produg strategies for targeted therapy, including state-of-the-art and future perspectives.

Mitochondria as a source of reactive oxygen species

2009 ◽  
pp. c3 ◽  
Author(s):  
Helena M. Cochemé ◽  
Michael P. Murphy
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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