scholarly journals The role of oxidative stress during inflammatory processes

2014 ◽  
Vol 395 (2) ◽  
pp. 203-230 ◽  
Author(s):  
Jérôme Lugrin ◽  
Nathalie Rosenblatt-Velin ◽  
Roumen Parapanov ◽  
Lucas Liaudet
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Cellular Response ◽  
Current Knowledge ◽  
High Mobility ◽  
Nuclear Factor Κb ◽  
Redox Biology ◽  
Inflammatory Processes ◽  
Reactive Oxidant ◽  
Endogenous Antioxidant

Abstract The production of various reactive oxidant species in excess of endogenous antioxidant defense mechanisms promotes the development of a state of oxidative stress, with significant biological consequences. In recent years, evidence has emerged that oxidative stress plays a crucial role in the development and perpetuation of inflammation, and thus contributes to the pathophysiology of a number of debilitating illnesses, such as cardiovascular diseases, diabetes, cancer, or neurodegenerative processes. Oxidants affect all stages of the inflammatory response, including the release by damaged tissues of molecules acting as endogenous danger signals, their sensing by innate immune receptors from the Toll-like (TLRs) and the NOD-like (NLRs) families, and the activation of signaling pathways initiating the adaptive cellular response to such signals. In this article, after summarizing the basic aspects of redox biology and inflammation, we review in detail the current knowledge on the fundamental connections between oxidative stress and inflammatory processes, with a special emphasis on the danger molecule high-mobility group box-1, the TLRs, the NLRP-3 receptor, and the inflammasome, as well as the transcription factor nuclear factor-κB.

scholarly journals Antioxidants: Pharmacothearapeutic Boon for Diabetes

2021 ◽  
Author(s):  
Varuna Suresh ◽  
Amala Reddy ◽  
Pavithra Muthukumar ◽  
Thendarl Selvam
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Cellular Response ◽  
Cell Function ◽  
Glucose Variability ◽  
Diabetic Rats ◽  
Long Term Effects ◽  
Free Radical Damage ◽  
Cellular Defense ◽  
Elevated Glucose

Glucose-induced oxidative stress can be found related to “glucose variability” and “glucose memory”. The irregular low and elevated glucose conditions cause damage to endothelial cell function than a steady, constant rise in level of glucose. Activation of PKC, NADPH oxidases, and mitochondrial oxidants are some of the pathways exhibited as a result of this aggravated cellular response. Regarding glucose memory, long after the normalization elevated level of glucose in the endothelial cells of diabetic rats and culture, a existance or ‘memory’ of induced basement membrane mRNA is expressed. This demonstrates that glucose causes dangerous long-term effects beyond the hyperglycemia period. Oxidative stress give rise to glucotoxicity and lipotoxicity which are phenomena’s related to diabetes. Following the pathogenesis of diabetes, hyperglycemia and hyperlipidemia exerts a supplementary toxic effect on the beta-cells. So, hyperglycemia can be considered as a requirement for the destructive effects of lipotoxicity. Thus glucolipotoxicity can be considered as a substitute for lipotoxicity which relates the detrimental correlation between lipids and beta-cell function. Generally, the antioxidant pharmacotherapy can be coupled with drugs to boost the natural cellular defense mechanisms as the naturally existing antioxidant components, which neutralizes free radical damage. This considers antioxidant a boon tool for pharmacotherapeutic agent.

scholarly journals Squalene: More than a Step toward Sterols

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 688 ◽  
Author(s):  
Marco Micera ◽  
Alfonso Botto ◽  
Federica Geddo ◽  
Susanna Antoniotti ◽  
Cinzia Margherita Bertea ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Cardiovascular Diseases ◽  
Defense Mechanisms ◽  
Current Knowledge ◽  
Ex Vivo ◽  
Antioxidant Properties ◽  
Metabolic Intermediate ◽  
Cellular Models

Squalene (SQ) is a natural triterpene widely distributed in nature. It is a metabolic intermediate of the sterol biosynthetic pathway and represents a possible target in different metabolic and oxidative stress-related disorders. Growing interest has been focused on SQ’s antioxidant properties, derived from its chemical structure. Strong evidence provided by ex vivo models underline its scavenging activity towards free radicals, whereas only a few studies have highlighted its effect in cellular models of oxidative stress. Given the role of unbalanced free radicals in both the onset and progression of several cardiovascular diseases, an in depth evaluation of SQ’s contribution to antioxidant defense mechanisms could represent a strategic approach in dealing with these pathological conditions. At present experimental results overall show a double-edged sword role of squalene in cardiovascular diseases and its function has to be better elucidated in order to establish intervention lines focused on its features. This review aims to summarize current knowledge about endogenous and exogenous sources of SQ and to point out the controversial role of SQ in cardiovascular physiology.

scholarly journals Carnosine Prevents Aβ-Induced Oxidative Stress and Inflammation in Microglial Cells: A Key Role of TGF-β1

Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 64 ◽  
Author(s):  
Giuseppe Caruso ◽  
Claudia Fresta ◽  
Nicolò Musso ◽  
Mariaconcetta Giambirtone ◽  
Margherita Grasso ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Microglial Cells ◽  
Neuronal Cultures ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Aβ Oligomers ◽  
Endogenous Antioxidant ◽  
Tgf Β1

Carnosine (β-alanyl-L-histidine), a dipeptide, is an endogenous antioxidant widely distributed in excitable tissues like muscles and the brain. Carnosine is involved in cellular defense mechanisms against oxidative stress, including the inhibition of amyloid-beta (Aβ) aggregation and the scavenging of reactive species. Microglia play a central role in the pathogenesis of Alzheimer’s disease, promoting neuroinflammation through the secretion of inflammatory mediators and free radicals. However, the effects of carnosine on microglial cells and neuroinflammation are not well understood. In the present work, carnosine was tested for its ability to protect BV-2 microglial cells against oligomeric Aβ1-42-induced oxidative stress and inflammation. Carnosine prevented cell death in BV-2 cells challenged with Aβ oligomers through multiple mechanisms. Specifically, carnosine lowered the oxidative stress by decreasing NO and O2−• intracellular levels as well as the expression of iNOS and Nox enzymes. Carnosine also decreased the secretion of pro-inflammatory cytokines such as IL-1β, simultaneously rescuing IL-10 levels and increasing the expression and the release of TGF-β1. Carnosine also prevented Aβ-induced neurodegeneration in mixed neuronal cultures challenged with Aβ oligomers, and these neuroprotective effects were completely abolished by SB431542, a selective inhibitor of the type-1 TGF-β receptor. Our data suggest a multimodal mechanism of action of carnosine underlying its protective effects on microglial cells against Aβ toxicity with a key role of TGF-β1 in mediating these protective effects.

scholarly journals Capillary Blood GSH Level Monitoring, Using an Electrochemical Method Adapted for Micro Volumes

Molecules ◽  
2018 ◽  
Vol 23 (10) ◽  
pp. 2504 ◽  
Author(s):  
Zaneta Buchtova ◽  
Zuzana Lackova ◽  
Jiri Kudr ◽  
Zdenek Zitka ◽  
Jan Skoda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Green Tea ◽  
Defense Mechanisms ◽  
Sample Volume ◽  
Capillary Blood ◽  
Stress Monitoring ◽  
Short Term ◽  
Cell Defense ◽  
Short Term Study ◽  
Endogenous Antioxidant

Glutathione (γ-glutamyl-cysteinyl-glycine; also known as GSH) is an endogenous antioxidant that plays a crucial role in cell defense mechanisms against oxidative stress. It is thus not surprising that this molecule can serve as a biomarker for oxidative stress monitoring. As capillary blood is a highly accessible target for biomarking, it is a valuable bodily fluid for diagnosing human GSH levels. This study focused on the optimization of GSH measurements from micro volumes of capillary blood prior to using electrochemical detection. The optimization of experimental parameters, including the sample volume and its stability, was performed and evaluated. Moreover, we tested the optimized method as part of a short-term study. The study consisted of examining 10 subjects within 96 h of their consumption of high amounts of antioxidants, attained from a daily dose of 2 g/150 mL of green tea. The subjects’ capillary blood (5 μL) was taken at 0 h, 48 h, and 96 h for subsequent analysis. The short-term supplementation of diet with green tea showed an increase of GSH pool by approximately 38% (between 0 and 48 h) within all subjects.

scholarly journals Oxidative Stress and Antioxidants in Atherosclerosis Development and Treatment

Biology ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 60 ◽  
Author(s):  
Anastasia V. Poznyak ◽  
Andrey V. Grechko ◽  
Varvara A. Orekhova ◽  
Yegor S. Chegodaev ◽  
Wei-Kai Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Current Knowledge ◽  
Chronic Inflammatory Disease ◽  
Therapeutic Properties ◽  
Atherosclerosis Development ◽  
Reactive Oxidant ◽  
Key Events ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Atherosclerosis can be regarded as chronic inflammatory disease affecting the arterial wall. Despite the recent progress in studying the pathogenesis of atherosclerosis, some of the pathogenic mechanisms remain to be fully understood. Among these mechanisms is oxidative stress, which is closely linked to foam cells formation and other key events in atherosclerosis development. Two groups of enzymes are involved in the emergence of oxidative stress: Pro-oxidant (including NADPH oxidases, xanthine oxidases, and endothelial nitric oxide synthase) and antioxidant (such as superoxide dismutase, catalases, and thioredoxins). Pro-oxidant enzymes in normal conditions produce moderate concentrations of reactive oxidant species that play an important role in cell functioning and can be fully utilized by antioxidant enzymes. Under pathological conditions, activities of both pro-oxidant and antioxidant enzymes can be modified by numerous factors that can be relevant for developing novel therapies. Recent studies have explored potential therapeutic properties of antioxidant molecules that are capable to eliminate oxidative damage. However, the results of these studies remain controversial. Other perspective approach is to inhibit the activity of pro-oxidant enzymes and thus to slow down the progression of atherosclerosis. In this review we summarized the current knowledge on oxidative stress in atherosclerosis and potential antioxidant approaches. We discuss several important antioxidant molecules of plant origin that appear to be promising for treatment of atherosclerosis.

scholarly journals Novel Insights into the Vasoprotective Role of Heme Oxygenase-1

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Emanuela Marcantoni ◽  
Luigia Di Francesco ◽  
Melania Dovizio ◽  
Annalisa Bruno ◽  
Paola Patrignani
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Vascular Wall ◽  
Heme Oxygenase 1 ◽  
Antiinflammatory Effect ◽  
Atherosclerotic Lesions ◽  
Inflammatory Processes ◽  
Cox 2 ◽  
Endogenous Antioxidant

Cardiovascular risk factors contribute to enhanced oxidative stress which leads to endothelial dysfunction. These events trigger platelet activation and their interaction with leukocytes and endothelial cells, thus contributing to the induction of chronic inflammatory processes at the vascular wall and to the development of atherosclerotic lesions and atherothrombosis. In this scenario, endogenous antioxidant pathways are induced to restrain the development of vascular disease. In the present paper, we will discuss the role of heme oxygenase (HO)-1 which is an enzyme of the heme catabolism and cleaves heme to form biliverdin and carbon monoxide (CO). Biliverdin is reduced enzymatically to the potent antioxidant bilirubin. Recent evidence supports the involvement of HO-1 in the antioxidant and antiinflammatory effect of cyclooxygenase(COX)-2-dependent prostacyclin in the vasculature. Moreover, the role of HO-1 in estrogen vasoprotection is emerging. Finally, possible strategies to develop novel therapeutics against cardiovascular disease by targeting the induction of HO-1 will be discussed.

scholarly journals Oxidant/Antioxidant Imbalance in Alzheimer’s Disease: Therapeutic and Diagnostic Prospects

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Joanna Wojsiat ◽  
Katarzyna Marta Zoltowska ◽  
Katarzyna Laskowska-Kaszub ◽  
Urszula Wojda
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Defense Mechanisms ◽  
Current Knowledge ◽  
Ros Generation ◽  
Molecular Change ◽  
Molecular Alterations ◽  
Change Characteristics ◽  
Clinical Continuum

Alzheimer’s disease (AD) is the most common cause of dementia and a great socioeconomic burden in the aging society. Compelling evidence demonstrates that molecular change characteristics for AD, such as oxidative stress and amyloidβ(Aβ) oligomerization, precede by decades the onset of clinical dementia and that the disease represents a biological and clinical continuum of stages, from asymptomatic to severely impaired. Nevertheless, the sequence of the early molecular alterations and the interplay between them are incompletely understood. This review presents current knowledge about the oxidative stress-induced impairments and compromised oxidative stress defense mechanisms in AD brain and the cross-talk between various pathophysiological insults, with the focus on excessive reactive oxygen species (ROS) generation and Aβoverproduction at the early stages of the disease. Prospects for AD therapies targeting oxidant/antioxidant imbalance are being discussed, as well as for the development of novel oxidative stress-related, blood-based biomarkers for early, noninvasive AD diagnostics.

Anti-carcinogenic action of curcumin by activation of antioxidant defence system and inhibition of NF-κB signalling in lymphoma-bearing mice

2011 ◽  
Vol 32 (2) ◽  
pp. 161-170 ◽  
Author(s):  
Laxmidhar Das ◽  
Manjula Vinayak
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Antioxidant Enzymes ◽  
Morphological Changes ◽  
Nuclear Factor Κb ◽  
Antioxidant Defence ◽  
Defence System ◽  
Antioxidant Defence System ◽  
Endogenous Antioxidant ◽  
Endogenous Antioxidant Defence

NF-κB (nuclear factor κB) plays a significant role in inflammation, immunity, cell proliferation, apoptosis and malignancy. ROS (reactive oxygen species) are among the most important regulating factors of NF-κB. Intracellular ROS are mainly regulated by an endogenous antioxidant defence system. Any disruption of redox balance leads to oxidative stress, which causes a number of pathological conditions including inflammation and malignancy. Increased metabolic activity in cancerous cells leads to oxidative stress, which is further enhanced due to depletion of the endogenous antioxidant defence system. However, the activation and signalling of NF-κB are reported to be inhibited by overexpression and induced activity of antioxidant enzymes. Therefore the present study focuses on the correlation between the endogenous antioxidant defence system, ROS and NF-κB activation during lymphoma growth in mice. The study highlights the anti-carcinogenic role of curcumin by modulation of NF-κB activation and oxidative stress via the endogenous antioxidant defence system. Oxidative stress was monitored by lipid peroxidation, protein carbonylation and antioxidant enzyme activity. NF-κB-mediated signalling was tested by DNA-binding activity. The results reflect that intracellular production of H2O2 in oxidative tumour micro-environment regulates NF-κB activation. Curcumin inhibits oxidative state in the liver of lymphoma-bearing mice by enhancing the transcription and activities of antioxidant enzymes, which in turn modulate activation of NF-κB, leading to a decrease in lymphoma growth. Morphological changes as well as cell proliferation and cell survival assays confirmed reduced lymphoma growth. Thus curcumin contributes to cancer prevention by disrupting the vicious cycle of constant ROS production, responsible for a high oxidative micro-environment for tumour growth.

Increased thioredoxin-1 production in human naturally occurring regulatory T cells confers enhanced tolerance to oxidative stress

Blood ◽  
2011 ◽  
Vol 117 (3) ◽  
pp. 857-861 ◽  
Author(s):  
Dimitrios Mougiakakos ◽  
C. Christian Johansson ◽  
Regina Jitschin ◽  
Martin Böttcher ◽  
Rolf Kiessling
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Regulatory T Cells ◽  
Defense Mechanisms ◽  
Redox Regulation ◽  
Feedback Inhibition ◽  
Inflammatory Diseases ◽  
Nuclear Factor Κb ◽  
Effector Cells ◽  
Thioredoxin 1

Abstract Levels of regulatory T cells (Tregs) are increased in different cancer types as well as in inflammatory diseases, such as rheumatoid arthritis. Treg accumulation may result from aberrant proliferation and trafficking as well as greater resilience to oxidative stress compared with conventional T cells. This enhanced antioxidative capacity of Tregs possibly serves as feedback inhibition during inflammation and prevents uncontrolled immune reactions by favoring survival of suppressor rather than effector cells. In this study, we demonstrate that human Tregs express and secrete higher levels of thioredoxin-1, a major antioxidative molecule. Thioredoxin-1 has an essential role in maintaining their surface thiol density as the first line of antioxidative defense mechanisms and is sensitive to proinflammatory stimuli, mainly tumor necrosis factor-α, in a nuclear factor-κB-dependent fashion. The antiapoptotic and oncogenic potential of (secreted) Trx-1 suggests that it may exert effects in Tregs beyond redox regulation.

scholarly journals NADPH Oxidases and Their Role in Atherosclerosis

Biomedicines ◽  
2020 ◽  
Vol 8 (7) ◽  
pp. 206 ◽  
Author(s):  
Anastasia V. Poznyak ◽  
Andrey V. Grechko ◽  
Varvara A. Orekhova ◽  
Victoria Khotina ◽  
Ekaterina A. Ivanova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vascular Remodeling ◽  
Current Knowledge ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Current View ◽  
Nadph Oxidases ◽  
Inflammatory Processes ◽  
Atherosclerosis Development ◽  
Initiating Factors

The current view on atherosclerosis positions it as a multifactorial disorder that results from the interplay between lipid metabolism disturbances and inflammatory processes. Oxidative stress is proven to be one of the initiating factors in atherosclerosis development, being implicated both in the inflammatory response and in atherogenic modifications of lipoproteins that facilitate lipid accumulation in the arterial wall. The hallmark of oxidative stress is the elevated level of reactive oxygen species (ROS). Correspondingly, the activity of major ROS-generating enzymes, including nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, xanthine oxidases, and cyclooxygenases, is an important element in atherosclerosis development. In particular, the role of NADPH oxidases in atherosclerosis development has become a subject of intensive research. Aberrant activity of NADPH oxidases was shown to be associated with cardiovascular disease in humans. With regard to atherosclerosis, several important pathological components of the disease development, including endothelial dysfunction, inflammation, and vascular remodeling, involve aberrations in NADPH oxidases functioning. In humans, NADPH oxidases are represented by four isoforms expressed in vascular tissues, where they serve as the main source of ROS during atherogenesis. Moreover, recent studies have demonstrated their impact on vascular remodeling processes. Interestingly, one of the NADPH oxidase isoforms, NOX4, was shown to have an atheroprotective effect. Despite the growing evidence of the crucial involvement of NADPH oxidases in atherosclerosis pathogenesis, the available data still remains controversial. In this narrative review, we summarize the current knowledge of the role of NADPH oxidases in atherosclerosis and outline the future directions of research.

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