scholarly journals The Role of Nrf2 and PPARγ in the Improvement of Oxidative Stress in Hypertension and Cardiovascular Diseases

2020 ◽  
pp. S541-S553
Author(s):  
I DOVINOVA ◽  
M KVANDOVA ◽  
P BALIS ◽  
L GRESOVA ◽  
M MAJZUNOVA ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Nuclear Receptor ◽  
Redox Regulation ◽  
Reactive Oxygen ◽  
Peroxisome Proliferator ◽  
Oxygen Species ◽  
Response Element ◽  
Stress Oxidative

Reactive oxygen species are an important element of redox regulation in cells and tissues. During physiological processes, molecules undergo chemical changes caused by reduction and oxidation reactions. Free radicals are involved in interactions with other molecules, leading to oxidative stress. Oxidative stress works two ways depending on the levels of oxidizing agents and products. Excessive action of oxidizing agents damages biomolecules, while a moderate physiological level of oxidative stress (oxidative eustress) is necessary to control life processes through redox signaling required for normal cellular operation. High levels of reactive oxygen species (ROS) mediate pathological changes. Oxidative stress helps to regulate cellular phenotypes in physiological and pathological conditions. Nrf2 (nuclear factor erythroid 2-related factor 2, NFE2L2) transcription factor functions as a target nuclear receptor against oxidative stress and is a key factor in redox regulation in hypertension and cardiovascular disease. Nrf2 mediates transcriptional regulation of a variety of target genes. The Keap1-Nrf2-ARE system regulates many detoxification and antioxidant enzymes in cells after the exposure to reactive oxygen species and electrophiles. Activation of Nrf2/ARE signaling is differentially regulated during acute and chronic stress. Keap1 normally maintains Nrf2 in the cytosol and stimulates its degradation through ubiquitination. During acute oxidative stress, oxidized molecules modify the interaction of Nrf2 and Keap1, when Nrf2 is released from the cytoplasm into the nucleus where it binds to the antioxidant response element (ARE). This triggers the expression of antioxidant and detoxification genes. The consequence of long-term chronic oxidative stress is activation of glycogen synthase kinase 3β (GSK-3β) inhibiting Nrf2 activity and function. PPARγ (peroxisome proliferator-activated receptor gamma) is a nuclear receptor playing an important role in the management of cardiovascular diseases, hypertension and metabolic syndrome. PPARγ targeting of genes with peroxisome proliferator response element (PPRE) has led to the identification of several genes involved in lipid metabolism or oxidative stress. PPARγ stimulation is triggered by endogenous and exogenous ligands – agonists and it is involved in the activation of several cellular signaling pathways involved in oxidative stress response, such as the PI3K/Akt/NOS pathway. Nrf2 and PPARγ are linked together with their several activators and Nrf2/ARE and PPARγ/PPRE pathways can control several types of diseases.

scholarly journals Redox Regulation and Oxidative Stress: The Particular Case of the Stallion Spermatozoa

Antioxidants ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 567 ◽  
Author(s):  
Fernando J. Peña ◽  
Cristian O’Flaherty ◽  
José M. Ortiz Rodríguez ◽  
Francisco E. Martín Cano ◽  
Gemma L. Gaitskell-Phillips ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Redox Regulation ◽  
Redox Homeostasis ◽  
Reactive Oxygen ◽  
Mitochondrial Activity ◽  
Oxygen Species ◽  
Redox Biology ◽  
Major Interest ◽  
And Oxidative Stress

Redox regulation and oxidative stress have become areas of major interest in spermatology. Alteration of redox homeostasis is recognized as a significant cause of male factor infertility and is behind the damage that spermatozoa experience after freezing and thawing or conservation in a liquid state. While for a long time, oxidative stress was just considered an overproduction of reactive oxygen species, nowadays it is considered as a consequence of redox deregulation. Many essential aspects of spermatozoa functionality are redox regulated, with reversible oxidation of thiols in cysteine residues of key proteins acting as an “on–off” switch controlling sperm function. However, if deregulation occurs, these residues may experience irreversible oxidation and oxidative stress, leading to malfunction and ultimately death of the spermatozoa. Stallion spermatozoa are “professional producers” of reactive oxygen species due to their intense mitochondrial activity, and thus sophisticated systems to control redox homeostasis are also characteristic of the spermatozoa in the horse. As a result, and combined with the fact that embryos can easily be collected in this species, horses are a good model for the study of redox biology in the spermatozoa and its impact on the embryo.

scholarly journals Identification of a Functional Peroxisome Proliferator-Activated Receptor Response Element in the Rat Catalase Promoter

2002 ◽  
Vol 16 (12) ◽  
pp. 2793-2801 ◽  
Author(s):  
Geoffrey D. Girnun ◽  
Frederick E. Domann ◽  
Steven A. Moore ◽  
Mike E. C. Robbins
Keyword(s):  
Reactive Oxygen Species ◽  
Transcription Factors ◽  
Inflammatory Response ◽  
Reactive Oxygen ◽  
Peroxisome Proliferator ◽  
Oxygen Species ◽  
Response Element ◽  
Peroxisome Proliferator Activated Receptor ◽  
Promoter Deletion Analysis

Abstract Peroxisomal proliferator-activated receptor (PPAR)γ has been shown to decrease the inflammatory response via transrepression of proinflammatory transcription factors. However, the identity of PPARγ responsive genes that decrease the inflammatory response has remained elusive. Because generation of the reactive oxygen species hydrogen peroxide (H2O2) plays a role in the inflammatory process and activation of proinflammatory transcription factors, we wanted to determine whether the antioxidant enzyme catalase might be a PPARγ target gene. We identified a putative PPAR response element (PPRE) containing the canonical direct repeat 1 motif, AGGTGA-A-AGTTGA, in the rat catalase promoter. In vitro translated PPARγ and retinoic X receptor-α proteins were able to bind to the catalase PPRE. Promoter deletion analysis revealed that the PPRE was functional, and a heterologous promoter construct containing a multimerized catalase PPRE demonstrated that the PPRE was necessary and sufficient for PPARγ-mediated activation. Treatment of microvascular endothelial cells with PPARγ ligands led to increases in catalase mRNA and activity. These results demonstrate that PPARγ can alter catalase expression; this occurs via a PPRE in the rat catalase promoter. Thus, in addition to transrepression of proinflammatory transcription factors, PPARγ may also be modulating catalase expression, and hence down-regulating the inflammatory response via scavenging of reactive oxygen species.

scholarly journals Reactive Oxygen Species and Abiotic Stress in Plants

2020 ◽  
Vol 21 (20) ◽  
pp. 7433 ◽  
Author(s):  
Tsanko Gechev ◽  
Veselin Petrov
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Abiotic Stress ◽  
Abiotic Stresses ◽  
Gene Networks ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Special Issue ◽  
Stress Oxidative ◽  
Acid Toxicity

Abiotic stresses cause plant growth inhibition, damage, and in the most severe cases, cell death, resulting in major crop yield losses worldwide. Many abiotic stresses lead also to oxidative stress. Recent genetic and genomics studies have revealed highly complex and integrated gene networks which are responsible for stress adaptation. Here we summarize the main findings of the papers published in the Special Issue “ROS and Abiotic Stress in Plants”, providing a global picture of the link between reactive oxygen species and various abiotic stresses such as acid toxicity, drought, heat, heavy metals, osmotic stress, oxidative stress, and salinity.

scholarly journals The Combination of Black Soybean Tempeh and Purple Sweet Potato Affect Reactive Oxygen Species and Malondialdehyde Level in Streptozotocin-Induced Diabetic Rats

2020 ◽  
Vol 25 (2) ◽  
pp. 76
Author(s):  
Eka Pratama Putri ◽  
Sri Rahayu Lestari ◽  
Abdul Gofur
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
The Body ◽  
Oxygen Species ◽  
Sweet Potatoes ◽  
Purple Sweet Potato ◽  
Stress Oxidative

Hyperglycemia conditions increase free radicals in the body that cause oxidative stress. Oxidative stress increase lipid peroxidation activity and reactive oxygen species (ROS). An antioxidant can prevent a free radical movement. The materials that contain potent antioxidants are black soybeans tempeh (BST) and purple sweet potatoes (PSP). The antioxidants in the BST are isoflavones with their derivates, and PSP is anthocyanins. This study aimed to determine the effect of BST and PSP extract on reactive oxygen species (ROS) and malondialdehyde (MDA) levels. In this study, rats were given a high-fat diet, 10% sucrose drink, and injected with multiple low-dose streptozotocin to induce T2DM. The animal's experiment divided into six groups: healthy rats, DM rats, DM rats + glibenclamide, DM rats + combination of BST and PSP in 3:1, 1:1, and 1:3 respectively. ROS levels were determined using the ELISA method and MDA levels were determined using spectrophotometer according to Thiobarbituric Acid (TBA) method. Our result suggests that the combination of BST and PSP significantly reduces ROS and MDA levels.

scholarly journals Extracellular Reactive Oxygen Species (ROS) Production in Fresh Donkey Sperm Exposed to Reductive Stress, Oxidative Stress and NETosis

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1367
Author(s):  
Iván Yánez-Ortiz ◽  
Jaime Catalán ◽  
Yentel Mateo-Otero ◽  
Marta Dordas-Perpinyà ◽  
Sabrina Gacem ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Selection Process ◽  
Reactive Oxygen ◽  
Polymorphonuclear Neutrophils ◽  
Ros Production ◽  
Oxygen Species ◽  
Oxidative Stresses ◽  
Stress Oxidative

Jenny shows a large endometrial reaction after semen influx to the uterus with a large amount of polymorphonuclear neutrophils (PMN) migrating into the uterine lumen. PMN act as a sperm selection mechanism through phagocytosis and NETosis (DNA extrudes and, together with proteins, trap spermatozoa). While a reduced percentage of spermatozoa are phagocytosed by PMN, most are found to be attached to neutrophil extracellular traps (NETs). This selection process together with sperm metabolism produces a large amount of reactive oxygen species (ROS) that influence the reproductive success. The present study aimed to determine the extracellular ROS production in both sperm and PMN. With this purpose, (1) donkey sperm were exposed to reductive and oxidative stresses, through adding different concentrations of reduced glutathione (GSH) and hydrogen peroxide (H2O2), respectively; and (2) PMN were subjected to NETosis in the presence of the whole semen, sperm, seminal plasma (SP) or other activators such as formyl-methionyl-leucyl-phenylalanine (FMLP). Extracellular ROS production (measured as H2O2 levels) was determined with the Amplex® Red Hydrogen Peroxide/Peroxidase Assay Kit. Donkey sperm showed more resilience to oxidative stress than to the reductive one, and GSH treatments led to greater H2O2 extracellular production. Moreover, not only did SP appear to be the main inducer of NETosis in PMN, but it was also able to maintain the extracellular H2O2 levels produced by sperm and NETosis.

A Comprehensive Review of Oxidative Stress as the Underlying Mechanism in Atherosclerosis and the Inefficiency of Antioxidants to Revert this Process

2019 ◽  
Vol 24 (40) ◽  
pp. 4705-4710 ◽  
Author(s):  
Kevin G. Cabezas ◽  
Carmen R. Gómez-Fernandez ◽  
Roberto Vazquez-Padron
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Plaque Formation ◽  
Oxygen Species ◽  
Reductase Inhibitors ◽  
Hmg Coa Reductase Inhibitors ◽  
Coa Reductase

Background: Cardiovascular diseases account for the highest mortality rate in the United States. The major underlying mechanism driving the onset and maintenance of cardiovascular diseases is atherosclerosis. Atherosclerosis is a chronic disease affecting large and medium-size arteries; it proceeds through four main stages along different decades of life, beginning at birth. Atherosclerosis is a consequence of oxidative stress, where homeostasis between endogenous antioxidants and reactive oxygen species is disrupted. Failure of intrinsic antioxidants and prophylactic antioxidant supplements to prevent atherosclerosis formation is an ongoing area of research in the race to avert, manage and cure atherosclerosis. Methods: The purpose of this work was to elucidate the actions of reactive oxygen species and oxidative stress on the formation of atherosclerosis as well as the different stages of atherosclerosis and the different mechanisms to prevent it. Through an extensive review of scientific literature, this paper correlates cell damage caused by oxidative stress to atheromatous plaque formation, as well as an in-depth analysis of high-density lipoproteins and enzymatic and non-enzymatic antioxidant role on atherosclerosis prevention. The antioxidant mechanism is overwhelmed by atherosclerotic processes and fails to be the ideal treatment of atherosclerosis. There is no scientific data that correlates prophylactic and non-prophylactic antioxidant treatment to a decrease in mortality or comorbidities pertaining to atherosclerosis. This is thought to be due to lack of consensus of optimal therapeutic doses, lack of reliable markers indicating which patient is to benefit from therapy and the chemical complexity of antioxidants in vivo. Current treatments for atherosclerosis include HMG-CoA reductase inhibitors which directly target low-density lipoproteins to tackle atherosclerotic plaque formation. Conclusion: HMG-CoA reductase inhibitors are not enough for the treatment of atherosclerosis given the complexity of the disease which has immune, musculoskeletal, genetic and hematologic aspects besides the involvement of lipids and lipoproteins. Therefore, other pharmacologic targets such as the PCSK9 enzyme and NFK- β should be researched in depth as possible treatments for atherosclerosis.

scholarly journals Evidence for the Important ¬Role of Oxidative Stress in the Pathogenesis of Acne

2019 ◽  
Vol 8 ◽  
pp. 1291
Author(s):  
Sina Kardeh ◽  
Seyed arman Moein ◽  
Mohammad Reza Namazi ◽  
Bahareh Kardeh
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Acne Vulgaris ◽  
Reactive Oxygen ◽  
Peroxisome Proliferator ◽  
Oxygen Species ◽  
Oxidative Stress Biomarkers ◽  
Peroxisome Proliferator Activated Receptor ◽  
Oxidative Biomarkers

Acne vulgaris is a common inflammatory skin disorder which is recognizable by dermatological lesions and scars. In addition to some pathogenetic factors such as hyperkeratinization, upregulated sebum secretion, and immunoinflammatory reactions, recent studies have also connected oxidative stress to the pathogenesis of acne vulgaris. In this article, we will briefly review clinical studies that interrogated alterations in oxidative stress biomarkers by a systematic search conducted in PubMed, Web of Science, and Scopus using “acne”, “oxidative stress”, and “reactive oxygen species” keywords. Overall, studies have shown that oxidative biomarkers (e.g. lipid peroxidation final products) are higher in acne vulgaris lesions. A significant positive correlation has also been noted between acne severity and oxidative biomarkers. In contrast, diminished levels of antioxidant enzymes (e.g. superoxide dismutase and catalase) have been observed in acne. We propose four probable mechanisms for the role of reactive oxygen species (ROS) in acne pathogenesis. We believe that ROS can contribute significantly to the acne vulgaris pathobiology via toll-like receptor (TLR), peroxisome proliferator-activated receptor (PPAR), mTOR pathway, and innate immune system, resulting in inflammation by alterations in the generation of several proinflammatory cytokines including IL-1, IL-8, and TNF-a.[GMJ. 2019;8:e1291]

scholarly journals Therapeutic Strategies for Oxidative Stress-Related Cardiovascular Diseases: Removal of Excess Reactive Oxygen Species in Adult Stem Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Hyunyun Kim ◽  
Jisoo Yun ◽  
Sang-Mo Kwon
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Stem Cell ◽  
Cardiovascular Diseases ◽  
Progenitor Cells ◽  
Adult Stem Cells ◽  
Reactive Oxygen ◽  
Therapeutic Strategies ◽  
Oxygen Species

Accumulating evidence indicates that acute and chronic uncontrolled overproduction of oxidative stress-related factors including reactive oxygen species (ROS) causes cardiovascular diseases (CVDs), atherosclerosis, and diabetes. Moreover ROS mediate various signaling pathways underlying vascular inflammation in ischemic tissues. With respect to stem cell-based therapy, several studies clearly indicate that modulating antioxidant production at cellular levels enhances stem/progenitor cell functionalities, including proliferation, long-term survival in ischemic tissues, and complete differentiation of transplanted cells into mature vascular cells. Recently emerging therapeutic strategies involving adult stem cells, including endothelial progenitor cells (EPCs), for treating ischemic CVDs have highlighted the need to control intracellular ROS production, because it critically affects the replicative senescence ofex vivoexpanded therapeutic cells. Better understanding of the complexity of cellular ROS in stem cell biology might improve cell survival in ischemic tissues and enhance the regenerative potentials of transplanted stem/progenitor cells. In this review, we will discuss the nature and sources of ROS, drug-based therapeutic strategies for scavenging ROS, and EPC based therapeutic strategies for treating oxidative stress-related CVDs. Furthermore, we will discuss whether primed EPCs pretreated with natural ROS-scavenging compounds are crucial and promising therapeutic strategies for vascular repair.

Are reactive oxygen species important mediators of vascular dysfunction?

2019 ◽  
Vol 15 ◽  
Author(s):  
Gabriel T. do Vale ◽  
Carlos R. Tirapelli
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Vascular Dysfunction ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Metabolism ◽  
Ros Generation ◽  
Oxygen Species ◽  
Promising Alternative

Reactive oxygen species (ROS) are reactive derivatives of oxygen metabolism. The ROS generation can be mediated by distinctive enzymatic systems including NADPH oxidases. The components of this enzyme are expressed in endothelial and vascular smooth muscle cells, adventitial fibroblasts, and infiltrating monocytes/macrophages. Oxidative stress is a molecular dysregulation in ROS generation/elimination, which plays a key role in the development of vascular dysfunction in distinctive conditions including hypertension. It is characterized by vascular inflammation, a loss of NO bioavailability and endothelial dysfunction. Considering that oxidative stress is a key mediator of vascular dysfunction, antioxidant therapy with classic antioxidants seemed to be a promising alternative for the treatment of vascular diseases. In this sense, some commonly used drugs for the treatment of cardiovascular diseases such as angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor AT1 antagonists showed antioxidant effects that might have contributed, at least in part, to the beneficial effects of these drugs on the treatment of cardiovascular diseases. The effectiveness of these drugs shows that ROS are in fact important mediators of vascular dysfunction and that angiotensin II plays a critical role in such response.

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