scholarly journals Oxidative stress in animals: a pathophysiologist's view

2020 ◽  
Vol 2020 (4) ◽  
pp. 10-18
Author(s):  
Dmitriy Gildikov
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Antioxidant System ◽  
Review Article ◽  
Publication Activity ◽  
Pathophysiological Mechanism ◽  
Oxygen Species ◽  
The World ◽  
Intracellular Oxidative Stress

In the review article, from the modern standpoint, oxidative stress is considered as a universal pathophysiological mechanism of the vast majority of diseases in animals. A brief review of the publication activity in the world on this topic; the significance of reactive oxygen species in the physiology and development of intracellular oxidative stress, the role of etiological factors that initiate their hyperproduction are presented, as well the methods of detecting oxidative stress are characterizited. General concepts of the antioxidant system of the animal body are examined, and the pathophysiological targets of oxidative stress in animals are generalized.

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.

MRP1 Plays a Role in Regulating Hematopoietic Stem Cell Oxidative Stress and Differentiation Via MRP1-Dependent Gsh Efflux

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 1223-1223
Author(s):  
Cassandra J Reiling ◽  
Dianna Howard ◽  
Christian M Paumi
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Stem Cell ◽  
Oxygen Species ◽  
Self Renewal ◽  
Hematopoietic Stem ◽  
Intracellular Ros ◽  
Intracellular Oxidative Stress

Abstract Abstract 1223 Hematopoietic stem cells (HSCs) are currently used therapeutically to treat diseases such as leukemia; however, a greater understanding in both the molecular and environmental requirements for HSCs self-renewal will hopefully increase the success rate of these therapeutic uses. It is increasingly evident that reactive oxygen species (ROS) and cellular oxidative stress play an important role in HSC self-renewal and differentiation. Therefore a better understanding of intracellular oxidative stress regulation is critical to increasing transplant success and increasing successful treatment of Leukemia. Our studies take aim at determining the role of multidrug resistance-associated protein 1 (MRP1) in regulating intracellular ROS in HSC's. MRP1 is expressed at slightly higher levels in HSCs than in mature blood cells. The expression pattern of MRP1 in HSCs suggests a possible role in hematopoietic stem cell integrity and differentiation. A major function of MRP1 is to help maintain the oxidative balance of the cell by transporting reduced glutathione (GSH), oxidized glutathione (GSSG), and glutathione-4-hydroxy-nonenal (HNE-SG) conjugates out of the cell. We have hypothesized that MRP1-dependent efflux of GSH and GSSG in HSC increases intracellular reactive oxygen species (ROS) resulting in a loss of self-renewing and increased differentiation of HSCs. In our current studies we have used C57BL/6 FVB and Mrp1-disrupted FVB [Mrp1 (−/−)] mice to investigate the role of MRP1 in HSC differentiation. Our experiments have revealed an increase in LT-HSC and ST-HSC and a corresponding decrease in MPP's in the MRP1 −/− mice as compared to WT matched controls. To determine if MRP1 plays a role in regulating HSC intracellular oxidative stress levels via GSH and GSSG efflux, we measured cellular oxidative stress as a function of DCF-DA and relative GSH levels as a function of glutathione-monochlorobimane (GS-MCB) conjugate fluorescence by flow cytometry. Our studies revealed higher intracellular ROS in WT mice as compared to MRP1 −/− mice and decreased GS-MCB in our WT mice as compared to the MRP1 −/− mice. Taken together the DCF-DA and MCB assays support our hypothesis that MRP1-dependent efflux of GSH/GSSG decreases cellular GSH resulting in higher level of ROS. Our hypothesis is further supported by analysis of lineage marked cells (Lin+), which showed a distinct differentiation pattern between the cells derived from WT and MRP1−/− bone marrow (BM). These studies are supported by results from colony forming cell (CFC) assays. Interestingly, analysis of whole blood did not result in a robust phenotype with regards to leukocytes; however, we found an increase in the number of platelets in MRP1−/− mice when compared to the WT. The increase in platelets is an intriguing result under further investigation. In light of our recent results we have initiated long-term transplant assays to determine if MRP1 does indeed play a role in HSC differentiation and self-renewal. If our hypothesis is true as suggested by our current studies then we expect that expression of MRP1 will negatively effect the ability of HSC's to successfully transplant in the long-term. Overall our data supports our hypothesis that MRP1-dependent efflux of GSH and GSSG in HSC increases intracellular ROS thereby decreasing HSC self-renewing potential and increasing HSC differentiation. Disclosures: No relevant conflicts of interest to declare.

scholarly journals The role of oxidative/nitrosative stress in pathogenesis of paracetamol-induced toxic hepatitis

2010 ◽  
Vol 63 (11-12) ◽  
pp. 827-832 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic ◽  
Rada Jesic-Vukicevic
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Kupffer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Severe Liver ◽  
Hepatocellular Necrosis

Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito?chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu?cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion radicals through the enzyme nicotinamide adenine dinucleotide phosphate oxidase. Hydrogen peroxide, which is influenced by the neutrophil-derived enzyme myeloperoxidase, generates hypochlorus acid as a potent oxidant. Role of peroxynitrite in paracetamol-induced oxidative stress. Superoxide can react with nitric oxide to form peroxynitrite, as a potent oxidant. Nitrotyrosine is formed by the reaction of tyrosine with peroxynitrite in paracetamol hepatotoxicity. Conclusion. Overdose of paracetamol may produce severe liver injury with hepatocellular necrosis. The most important mechanisms of cell injury are metabolic activation of paracetamol, glutathione depletion, alkylation of proteins, especially mitochondrial proteins, and formation of reactive oxygen/nitrogen species.

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.

Flavonoids, the Family of Plant-derived Antioxidants making inroads into Novel Therapeutic Design against IR-induced Oxidative Stress in Parkinson’s Disease

2021 ◽  
Vol 19 ◽  
Author(s):  
Tapan Behl ◽  
Gagandeep Kaur ◽  
Aayush Sehgal ◽  
Gokhan Zengin ◽  
Sukhbir Singh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Ionizing Radiation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Radiation Induced ◽  
Novel Therapeutic

Background: Ionizing radiation from telluric sources is unceasingly an unprotected pitfall to humans. Thus, the foremost contributors to human exposure are global and medical radiations. Various pieces of evidences assembled during preceding years reveal the pertinent role of ionizing radiation-induced oxidative stress in the progression of neurodegenerative insults such as Parkinson’s disease, which have been contributing to increased proliferation and generation of reactive oxygen species. Objective: This review delineates the role of ionizing radiation-induced oxidative stress in Parkinson’s disease and proposes novel therapeutic interventions of flavonoid family offering effective management and slowing down the progression of Parkinson’s disease. Method: Published papers were searched via MEDLINE, PubMed, etc. published to date for in-depth database collection. Results: The potential of oxidative damage may harm the non-targeted cells. It can also modulate the functions of central nervous system, such as protein misfolding, mitochondria dysfunction, increased levels of oxidized lipids, and dopaminergic cell death, which accelerates the progression of Parkinson’s disease at the molecular, cellular, or tissue levels. In Parkinson’s disease, reactive oxygen species exacerbate the production of nitric oxides and superoxides by activated microglia, rendering death of dopaminergic neuronal cell through different mechanisms. Conclusion: Rising interest has extensively engrossed on the clinical trial designs based on the plant derived family of antioxidants. They are known to exert multifarious impact either way in neuroprotection via directly suppressing ionizing radiation-induced oxidative stress and reactive oxygen species production or indirectly increasing the dopamine levels and activating the glial cells.

scholarly journals Effect of Blueberry Anthocyanins Malvidin and Glycosides on the Antioxidant Properties in Endothelial Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Wuyang Huang ◽  
Yunming Zhu ◽  
Chunyang Li ◽  
Zhongquan Sui ◽  
Weihong Min
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Functional Food ◽  
Functional Role ◽  
Antioxidant Properties ◽  
Heme Oxygenase 1 ◽  
Oxygen Species ◽  
Good Resource

The objective of this research was to survey the antioxidant functional role of the main anthocyanins of blueberries in endothelial cells. Changes on the reactive oxygen species (ROS), xanthine oxidase-1 (XO-1), superoxide dismutase (SOD), and heme oxygenase-1 (HO-1) in cells of malvidin and the two glycosides were investigated. The results showed that these anthocyanins decreased the levels of ROS and XO-1 but increased the levels of SOD and HO-1. Glycosides improved the antioxidant capacity of malvidin to a great extent. The changes in the antioxidant properties of malvidin-3-glucoside were more pronounced than malvidin-3-galactoside. Variation in levels of malvidin-3-glucoside and malvidin-3-galactoside had a significant impact on antioxidant properties to different extents. It indicates that blueberries are a good resource of anthocyanins, which can protect cells from oxidative deterioration and use blueberry as a potential functional food to prevent diseases related to oxidative stress.

scholarly journals The copper chaperone CcsA coupling with superoxide dismutase SodA mediates oxidative stress response in Aspergillus fumigatus

2021 ◽  
Author(s):  
Wenlong Du ◽  
Pengfei Zhai ◽  
Shuai Liu ◽  
Yuanwei Zhang ◽  
Ling Lu
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Stress Response ◽  
Aspergillus Fumigatus ◽  
Fungal Pathogens ◽  
Oxidative Stress Response ◽  
Superoxide Dismutases ◽  
Oxygen Species ◽  
Oxidative Response

Superoxide dismutases (SODs) are important metalloenzymes that protect fungal pathogens against the toxic effects of reactive oxygen species (ROS) generated by host defense mechanisms during the infection process. The activation of Cu/Zn-SOD1 is found to be dependent on its c haperone Ccs1 ( c opper c haperone for S OD1). However, the role of Ccs1 ortholog in the human pathogen Aspergillus fumigatus and how these SODs coordinate to mediate oxidative stress response remain elusive. Here, we demonstrated that A. fumigatus CcsA, a Saccharomyces cerevisiae Ccs1 ortholog, is required for cells in response to oxidative response and the activation of Sod1. Deletion of ccsA resulted in increased ROS accumulation and enhanced sensitivity to oxidative stress due to loss of SodA activity. Molecular characterization of CcsA revealed that the conserved CXC motif is required not only for the physical interaction with SodA but also for the oxidative stress adaption. Notably, addition of Mn 2+ or overexpression of cytoplasmic Mn-SodC could rescue the defects of the ccsA or sodA deletion mutant, indicating the important role of Mn 2+ and Mn-SodC in ROS detoxification; however, deletion of CcsA-SodA complex could not affect A. fumigatus virulence. Collectively, our findings demonstrate that CcsA functions as a Cu/Zn-Sod1 chaperone that participates in the adaptation to oxidative stress in A. fumigatus and provide a better understanding of the CcsA-SodA complex-mediated oxidative stress response in filamentous fungi. IMPORTANCE Reactive oxygen species (ROS) produced by phagocytes have been reported to participate in the killing of fungal pathogens. Superoxide dismutases (SODs) are considered to be the first defense line against superoxide anions. Characterizing the regulatory mechanisms of SOD activation is important for understanding how fungi adapt to oxidative stress in hosts. Our findings demonstrated that CcsA functions as a SodA chaperone in A. fumigatus and that the conserved CXC motif within CcsA is required for its interaction with SodA and the CcsA-SodA-mediated oxidative response. These data may provide new insights into how fungal pathogens adapt to oxidative stress via the CcsA-SodA complex.

scholarly journals The role of oxidative stress in alcoholic liver injury

2009 ◽  
Vol 62 (11-12) ◽  
pp. 547-553 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Kupffer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Alcoholic Liver Injury ◽  
Chronic Ethanol Consumption

Introduction. Oxidative stress plays an important role in pathogenesis of alcoholic liver injury. The main source of free oxygen species is cytochrome P450-dependent monooxygenase, which can be induced by ethanol. Role of cytochrome P4502E1 in ethanol-induced oxidative stress. Reactive oxygen species produced by this enzyme are more important in intracellular oxidative damage compared to species derived from activated phagocytes. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in alcohol-induced oxidative stress. Production of mitochondrial reactive oxygen species is increased, and glutathione content is decreased in chronically ethanolfed animals. Oxidative stress in mitochondria leads to mitochondrial DNA damage and has a dual effect on apoptosis. Role of Kupffer cells in alcohol-induced liver injury. Chronic ethanol consumption is associated with increased release of endotoxin from gut lumen into portal circulation. Endotoxin activates Kupffer cells, which then release proinflammatory cytokines and oxidants. Role of neutrophils in alcohol-induced liver injury. Alcoholic liver injury leads to the accumulation of neutrophils, which release reactive oxygen species and lysosomal enzymes and contribute to hepatocyte damage and necrosis. Role of nitric oxide in alcohol-induced oxidative stress. High amounts of nitric oxide contribute to the oxidative damage, mainly by generating peroxynitrites. Role of antioxidants in ethanol-induced oxidative stress. Chronic ethanol consumption is associated with reduced liver glutathione and ?-tocopherol level and with reduced superoxide dismutase, catalase and glutathione peroxidase activity. Conclusion. Oxidative stress in alcoholic liver disease is a consequence of increased production of oxidants and decreased antioxidant defense in the liver.

Sign in / Sign up

Export Citation Format

Share Document