scholarly journals Organ-Protective Effects of Red Wine Extract, Resveratrol, in Oxidative Stress-Mediated Reperfusion Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Fu-Chao Liu ◽  
Hsin-I Tsai ◽  
Huang-Ping Yu
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reperfusion Injury ◽  
Intracellular Signaling ◽  
Red Wine ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Sirtuin 1 ◽  
Oxygen Species ◽  
Protective Effects

Resveratrol, a polyphenol extracted from red wine, possesses potential antioxidative and anti-inflammatory effects, including the reduction of free radicals and proinflammatory mediators overproduction, the alteration of the expression of adhesion molecules, and the inhibition of neutrophil function. A growing body of evidence indicates that resveratrol plays an important role in reducing organ damage following ischemia- and hemorrhage-induced reperfusion injury. Such protective phenomenon is reported to be implicated in decreasing the formation and reaction of reactive oxygen species and pro-nflammatory cytokines, as well as the mediation of a variety of intracellular signaling pathways, including the nitric oxide synthase, nicotinamide adenine dinucleotide phosphate oxidase, deacetylase sirtuin 1, mitogen-activated protein kinase, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha, hemeoxygenase-1, and estrogen receptor-related pathways. Reperfusion injury is a complex pathophysiological process that involves multiple factors and pathways. The resveratrol is an effective reactive oxygen species scavenger that exhibits an antioxidative property. In this review, the organ-protective effects of resveratrol in oxidative stress-related reperfusion injury will be discussed.

scholarly journals NADPH Oxidase as a Therapeutic Target for Oxalate Induced Injury in Kidneys

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Sunil Joshi ◽  
Ammon B. Peck ◽  
Saeed R. Khan
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Tissue Injury ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Renal Tissue ◽  
Oxygen Species ◽  
Gene Expressions

A major role of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes is to catalyze the production of superoxides and other reactive oxygen species (ROS). These ROS, in turn, play a key role as messengers in cell signal transduction and cell cycling, but when they are produced in excess they can lead to oxidative stress (OS). Oxidative stress in the kidneys is now considered a major cause of renal injury and inflammation, giving rise to a variety of pathological disorders. In this review, we discuss the putative role of oxalate in producing oxidative stress via the production of reactive oxygen species by isoforms of NADPH oxidases expressed in different cellular locations of the kidneys. Most renal cells produce ROS, and recent data indicate a direct correlation between upregulated gene expressions of NADPH oxidase, ROS, and inflammation. Renal tissue expression of multiple NADPH oxidase isoforms most likely will impact the future use of different antioxidants and NADPH oxidase inhibitors to minimize OS and renal tissue injury in hyperoxaluria-induced kidney stone disease.

Oxidative Stress and Hypertension

2021 ◽  
Vol 128 (7) ◽  
pp. 993-1020
Author(s):  
Kathy K. Griendling ◽  
Livia L. Camargo ◽  
Francisco J. Rios ◽  
Rhéure Alves-Lopes ◽  
Augusto C. Montezano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Animal Models ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Antioxidant Systems ◽  
Inflammasome Activation ◽  
Oxygen Species ◽  
Organ Systems

A link between oxidative stress and hypertension has been firmly established in multiple animal models of hypertension but remains elusive in humans. While initial studies focused on inactivation of nitric oxide by superoxide, our understanding of relevant reactive oxygen species (superoxide, hydrogen peroxide, and peroxynitrite) and how they modify complex signaling pathways to promote hypertension has expanded significantly. In this review, we summarize recent advances in delineating the primary and secondary sources of reactive oxygen species (nicotinamide adenine dinucleotide phosphate oxidases, uncoupled endothelial nitric oxide synthase, endoplasmic reticulum, and mitochondria), the posttranslational oxidative modifications they induce on protein targets important for redox signaling, their interplay with endogenous antioxidant systems, and the role of inflammasome activation and endoplasmic reticular stress in the development of hypertension. We highlight how oxidative stress in different organ systems contributes to hypertension, describe new animal models that have clarified the importance of specific proteins, and discuss clinical studies that shed light on how these processes and pathways are altered in human hypertension. Finally, we focus on the promise of redox proteomics and systems biology to help us fully understand the relationship between ROS and hypertension and their potential for designing and evaluating novel antihypertensive therapies.

scholarly journals The impact of reactive oxygen species in the development of cardiometabolic disorders: a review

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Roland Akhigbe ◽  
Ayodeji Ajayi
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Acid Oxidation ◽  
Ros Generation ◽  
Metabolic Memory ◽  
Oxygen Species ◽  
Cardiometabolic Disorders ◽  
The Impact

AbstractOxidative stress, an alteration in the balance between reactive oxygen species (ROS) generation and antioxidant buffering capacity, has been implicated in the pathogenesis of cardiometabolic disorders (CMD). At physiological levels, ROS functions as signalling mediators, regulates various physiological functions such as the growth, proliferation, and migration endothelial cells (EC) and smooth muscle cells (SMC); formation and development of new blood vessels; EC and SMC regulated death; vascular tone; host defence; and genomic stability. However, at excessive levels, it causes a deviation in the redox state, mediates the development of CMD. Multiple mechanisms account for the rise in the production of free radicals in the heart. These include mitochondrial dysfunction and uncoupling, increased fatty acid oxidation, exaggerated activity of nicotinamide adenine dinucleotide phosphate oxidase (NOX), reduced antioxidant capacity, and cardiac metabolic memory. The purpose of this study is to discuss the link between oxidative stress and the aetiopathogenesis of CMD and highlight associated mechanisms. Oxidative stress plays a vital role in the development of obesity and dyslipidaemia, insulin resistance and diabetes, hypertension via various mechanisms associated with ROS-led inflammatory response and endothelial dysfunction.

scholarly journals Protective effect of kudzu root vinegar and adenosine against UVB-induced oxidative stress in human keratinocytes

2020 ◽  
Vol 3 (2) ◽  
pp. 184-192
Author(s):  
Ji Eun Park ◽  
◽  
Young Mi Kim
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hacat Cell ◽  
Reactive Oxygen ◽  
Human Keratinocytes ◽  
Mitogen Activated Protein Kinase ◽  
Hacat Cells ◽  
Oxygen Species ◽  
Protective Effects ◽  
Skin Damage

Ultraviolet (UV) irradiation generates reactive oxygen species (ROS) in cells, which induces sunburn cell formation, melanoma, photoaging, and skin cancer. This study examines the anti-photodamage effects of kudzu root vinegar and adenosine in UVB-exposed human keratinocytes (HaCaT cells). UVB significantly decreased HaCaT cell viability, whereas kudzu root vinegar and adenosine did not exhibit cytotoxic effects and increased the viability of HaCaT cells. To investigate the protective effects of kudzu root vinegar and adenosine on UVB-induced oxidative stress in HaCaT cells, ROS, matrix metalloproteinases (MMPs), and mitogen-activated protein kinase (MAPK) were analyzed. UVB-induced treatment reduced the activity of antioxidant enzymes; however, kudzu root vinegar and adenosine increased their activity. These results indicated that kudzu root vinegar and adenosine exert cytoprotective activity against UVB-induced oxidative stress in HaCaT cells. Moreover, they suppressed the UVB-induced downregulation of MMPs and inhibited the phosphorylation of MAPK induced by UVB-irradiation. Therefore, kudzu root vinegar and adenosine offer anti-oxidative effects, via lowering ROS production, suppressing JNK activation, and downregulating expression of MMPs. Our findings suggest that kudzu root vinegar and adenosine have potential application in preventing skin damage owing to UVB exposure. Keywords: reactive oxygen species (ROS), HaCaT cell, UVB, skin damage, anti-aging

Tetrahydrobiopterin compounds modulate intracellular signaling and reactive oxygen species levels in an in vitro model of ischemia-reperfusion injury

Pteridines ◽  
2013 ◽  
Vol 24 (3) ◽  
pp. 225-235
Author(s):  
Peter Santer ◽  
Thomas Ratschiller ◽  
Muhammad Imtiaz Ashraf ◽  
Ernst R. Werner ◽  
Gabriele Werner-Felmayer ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reperfusion Injury ◽  
Intracellular Signaling ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Solid Organ ◽  
Oxygen Species ◽  
Prolonged Incubation ◽  
Mitochondrial Ros

AbstractTetrahydrobiopterin (BH4) and 4-amino-tetrahydrobiopterin (ABH4) prevent acute rejection after solid organ transplantation. Moreover, BH4 also attenuates ischemia-reperfusion injury (IRI). The mechanisms underlying these protective effects are poorly defined. Activation of intracellular signaling proteins, including the mitogen-activated protein kinases (MAPKs) ERK, p38, and JNK, and the excessive production of mitochondrial reactive oxygen species (ROS) are observed mainly during early reperfusion. While the role of ROS in the initiation and progression of IRI is well understood, the contribution of individual signaling pathways is less clear. Here, we tested the potential effects of BH4 and ABH4 on MAPK activity and mitochondrial ROS levels. During hypoxia and reoxygenation (H/R), all three MAPKs were activated during early reoxygenation in cardiomyocytes and endothelial cells. p38 and JNK activation were further augmented by BH4 and ABH4, whereas ERK activation was not affected. Pretreatment with BH4 and ABH4 reduced the basal mitochondrial ROS levels as well as the H/R-induced increase in ROS. Prolonged incubation with ABH4, however, showed pro-apoptotic effects in cardiomyocytes. These data suggest that a protective effect of BH4 and ABH4 pretreatment may be attributed mainly to their antioxidant capacity. The effects on intracellular signaling are complex and warrant further investigations.

scholarly journals Reactive Oxygen Species: A Key Hallmark of Cardiovascular Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Nisha Panth ◽  
Keshav Raj Paudel ◽  
Kalpana Parajuli
Keyword(s):  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Intracellular Signaling ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Cardiovascular Complications ◽  
Oxygen Species

Cardiovascular diseases (CVDs) have been the prime cause of mortality worldwide for decades. However, the underlying mechanism of their pathogenesis is not fully clear yet. It has been already established that reactive oxygen species (ROS) play a vital role in the progression of CVDs. ROS are chemically unstable reactive free radicals containing oxygen, normally produced by xanthine oxidase, nicotinamide adenine dinucleotide phosphate oxidase, lipoxygenases, or mitochondria or due to the uncoupling of nitric oxide synthase in vascular cells. When the equilibrium between production of free radicals and antioxidant capacity of human physiology gets altered due to several pathophysiological conditions, oxidative stress is induced, which in turn leads to tissue injury. This review focuses on pathways behind the production of ROS, its involvement in various intracellular signaling cascades leading to several cardiovascular disorders (endothelial dysfunction, ischemia-reperfusion, and atherosclerosis), methods for its detection, and therapeutic strategies for treatment of CVDs targeting the sources of ROS. The information generated by this review aims to provide updated insights into the understanding of the mechanisms behind cardiovascular complications mediated by ROS.

Do reactive oxygen species play a role in myeloid leukemias?

Blood ◽  
2011 ◽  
Vol 117 (22) ◽  
pp. 5816-5826 ◽  
Author(s):  
Paul Spencer Hole ◽  
Richard Lawrence Darley ◽  
Alex Tonks
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Intracellular Signaling ◽  
Reactive Oxygen ◽  
Innate Immune ◽  
Current Evidence ◽  
Oxygen Species ◽  
Innate Immune Responses ◽  
Hematopoietic Malignancies ◽  
Myeloid Leukemias

Abstract Reactive oxygen species (ROS) are a heterogeneous group of molecules that are generated by mature myeloid cells during innate immune responses, and are also implicated in normal intracellular signaling. Excessive production of ROS (and/or a deficiency in antioxidant pathways) can lead to oxidative stress, a state that has been observed in several hematopoietic malignancies including acute and chronic myeloid leukemias (AML and CML). Currently it is unclear what the cause of oxidative stress might be and whether oxidative stress contributes to the development, progression, or maintenance of these diseases. This article reviews the current evidence suggesting a role for ROS both in normal hematopoiesis and in myeloid leukemogenesis, and discusses the usefulness of therapeutically targeting oxidative stress in myeloid malignancy.

scholarly journals Effect of Acupuncture on Oxidative Stress Induced by Cerebral Ischemia-Reperfusion Injury

Antioxidants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 248 ◽  
Author(s):  
Chao-Hsien Chen ◽  
Ching-Liang Hsieh
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Cochrane Library ◽  
Oxygen Species ◽  
Medical Subject Headings ◽  
The Cochrane Library

In this article, we review how acupuncture regulates oxidative stress to prevent ischemia–reperfusion injury. We electronically searched databases, including PubMed, Clinical Key and the Cochrane Library, from their inception to November 2019 by using the following medical subject headings and keywords: acupuncture, ischemia-reperfusion injury, oxidative stress, reactive oxygen species, and antioxidants. We concluded that acupuncture is effective in treating oxidation after ischemia-reperfusion injury. In addition to increasing the activity of antioxidant enzymes and downregulating the generation of reactive oxygen species (ROS), acupuncture also repairs the DNA, lipids, and proteins attacked by ROS and mediates downstream of the ROS pathway to apoptosis.

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