scholarly journals Graphene and graphene oxide induce ROS production in human HaCaT skin keratinocytes: the role of xanthine oxidase and NADH dehydrogenase

Nanoscale ◽  
2018 ◽  
Vol 10 (25) ◽  
pp. 11820-11830 ◽  
Author(s):  
Marco Pelin ◽  
Laura Fusco ◽  
Cristina Martín ◽  
Silvio Sosa ◽  
Javier Frontiñán-Rubio ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Graphene Oxide ◽  
Xanthine Oxidase ◽  
Nadh Dehydrogenase ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Mitochondrial Depolarization ◽  
Skin Keratinocytes

Graphene based nanomaterials induce a reactive oxygen species-mediated mitochondrial depolarization, caused by the activation of NADH dehydrogenase and xanthine oxidase.

Reactive oxygen species modulate HIF-1 mediated PAI-1 expression: involvement of the GTPase Rac1

2003 ◽  
Vol 89 (05) ◽  
pp. 926-935 ◽  
Author(s):  
Utta Berchner-Pfannschmidt ◽  
Christoph Wotzlaw ◽  
Robbert Cool ◽  
Joachim Fandrey ◽  
Helmut Acker ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Plasminogen Activator Inhibitor ◽  
Dominant Negative ◽  
Mrna Levels ◽  
Ros Production ◽  
Oxygen Species ◽  
Plasminogen Activator Inhibitor 1 ◽  
Pai 1

SummaryThe hypoxia-inducible transcription factor HIF-1 mediates upregulation of plasminogen activator inhibitor-1 (PAI-1) expression under hypoxia. Reactive oxygen species (ROS) have also been implicated in PAI-1 gene expression. However, the role of ROS in HIF-1-mediated regulation of PAI-1 is not clear. We therefore investigated the role of the GTPase Rac1 which modulates ROS production in the pathway leading to HIF-1 and PAI-1 induction.Overexpression of constitutively activated (RacG12V) or dominant-negative (RacT17N) Rac1 increased or decreased, respectively, ROS production. In RacG12V-expressing cells, PAI-1 mRNA levels as well as HIF-1α nuclear presence were reduced under normoxia and hypoxia whereas expression of RacT17N resulted in opposite effects. Treatment with the antioxidant pyrrolidinedithiocarbamate or coexpression of the redox factor-1 restored HIF-1 and PAI-1 promoter activity in RacG12V-cells. In contrast, NFκB activation was enhanced in RacG12V-cells, but abolished by RacT17N. Thus, these findings suggest a mechanism explaining modified fibrinolysis and tissue remodeling in an oxidized environment.

scholarly journals Oxidative stress in marathon runners: interest of antioxidant supplementation

2006 ◽  
Vol 96 (S1) ◽  
pp. S31-S33 ◽  
Author(s):  
Mari-Carmen Gomez-Cabrera ◽  
Agustín Martínez ◽  
Gustavo Santangelo ◽  
Federico V. Pallardó ◽  
Juan Sastre ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Xanthine Oxidase ◽  
Cell Signalling ◽  
Reactive Oxygen ◽  
Peripheral Blood Lymphocytes ◽  
Signalling Pathways ◽  
Marathon Running ◽  
Oxygen Species ◽  
Marathon Runners

We have recently reported that xanthine oxidase is involved in the generation of free radicals in exhaustive exercise. Allopurinol, an inhibitor of xanthine oxidase, prevents it. The aim of the present work was to elucidate the role of exercise-derived reactive oxygen species in the cell signalling pathways involved in the adaptation to exercise in man. We have found that exercise causes an increase in the activity of plasma xanthine oxidase and an activation of NF-κB in peripheral blood lymphocytes after marathon running. This activation is dependent on free radical formation in exercise: treatment with allopurinol completely prevents it. In animal models, we previously showed that NF-κB activation induced by exhaustive physical exercise leads to an increase in the expression of superoxide dismutase, an enzyme involved in antioxidant defence. We report evidence in man that reactive oxygen species act as signals in exercise as decreasing their formation prevents activation of important signalling pathways which can cause useful adaptations in cells.

scholarly journals Production, Signaling, and Scavenging Mechanisms of Reactive Oxygen Species in Fruit–Pathogen Interactions

2019 ◽  
Vol 20 (12) ◽  
pp. 2994 ◽  
Author(s):  
Ying Wang ◽  
Dongchao Ji ◽  
Tong Chen ◽  
Boqiang Li ◽  
Zhanquan Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Pathogenic Fungi ◽  
Ros Production ◽  
Oxygen Species ◽  
Ros Homeostasis ◽  
Molecular Damage ◽  
Different Levels ◽  
In Cells

Reactive oxygen species (ROS) play a dual role in fruit–pathogen interaction, which largely depends on their different levels in cells. Fruit recognition of a pathogen immediately triggers an oxidative burst that is considered an integral part of the fruit defense response. ROS are also necessary for the virulence of pathogenic fungi. However, the accumulation of ROS in cells causes molecular damage and finally leads to cell death. In this review, on the basis of data regarding ROS production and the scavenging systems determining ROS homeostasis, we focus on the role of ROS in fruit defense reactions against pathogens and in fungi pathogenicity during fruit–pathogen interaction.

scholarly journals RNAi-Mediated Down-Regulation of Dicer-Like 2 and 4 Changes the Response of ‘Moneymaker’ Tomato to Potato Spindle Tuber Viroid Infection from Tolerance to Lethal Systemic Necrosis, Accompanied by Up-Regulation of miR398, 398a-3p and Production of Excessive Amount of Reactive Oxygen Species

Viruses ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 344 ◽  
Author(s):  
Takahiro Suzuki ◽  
Sho Ikeda ◽  
Atsushi Kasai ◽  
Akito Taneda ◽  
Misato Fujibayashi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Potato Spindle Tuber Viroid ◽  
Ros Production ◽  
Oxygen Species ◽  
Superoxide Dismutase 1 ◽  
Systemic Necrosis ◽  
Viroid Infection ◽  
Infected Line

To examine the role of RNA silencing in plant defenses against viroids, a Dicer-like 2 and 4 (DCL2&4)–double knockdown transgenic tomato plant line, 72E, was created. The expression of endogenous SlDCL2s and SlDCL4 in line 72E decreased to about a half that of the empty cassette line, EC. When challenged with potato spindle tuber viroid (PSTVd), line 72E showed significantly higher levels of PSTVd accumulation early in the course of the infection and lethal systemic necrosis late in the infection. The size distribution of PSTVd-derived small RNAs was significantly different with the number of RNAs of 21 and 22 nucleotides (nt) in line 72E, at approximately 66.7% and 5% of those in line EC, respectively. Conversely, the numbers of 24 nt species increased by 1100%. Furthermore, expression of the stress-responsive microRNA species miR398 and miR398a-3p increased 770% and 868% in the PSTVd-infected line 72E compared with the PSTVd-infected EC. At the same time, the expression of cytosolic and chloroplast-localized Cu/Zn-superoxide dismutase 1 and 2 (SOD1 and SOD2) and the copper chaperon for SOD (CCS1) mRNAs, potential targets of miR398 or 398a-3p, decreased significantly in the PSTVd-infected line 72E leaves, showing necrosis. In concert with miR398 and 398a-3p, SODs control the detoxification of reactive oxygen species (ROS) generated in cells. Since high levels of ROS production were observed in PSTVd-infected line 72E plants, it is likely that the lack of full dicer-likes (DCL) activity in these plants made them unable to control excessive ROS production after PSTVd infection, as disruption in the ability of miR398 and miR398a-3p to regulate SODs resulted in the development of lethal systemic necrosis.

scholarly journals Reactive Oxygen Species: A Promising Therapeutic Target for SDHx-Mutated Pheochromocytoma and Paraganglioma

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3769
Author(s):  
Katerina Hadrava Hadrava Vanova ◽  
Chunzhang Yang ◽  
Leah Meuter ◽  
Jiri Neuzil ◽  
Karel Pacak
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Ros Scavenging ◽  
Promising Therapeutic Target ◽  
Ros Accumulation ◽  
Intracellular Ros

Pheochromocytoma (PHEO) and paraganglioma (PGL) are rare neuroendocrine tumors derived from neural crest cells. Germline variants in approximately 20 PHEO/PGL susceptibility genes are found in about 40% of patients, half of which are found in the genes that encode succinate dehydrogenase (SDH). Patients with SDH subunit B (SDHB)-mutated PHEO/PGL exhibit a higher likelihood of developing metastatic disease, which can be partially explained by the metabolic cell reprogramming and redox imbalance caused by the mutation. Reactive oxygen species (ROS) are highly reactive molecules involved in a multitude of important signaling pathways. A moderate level of ROS production can help regulate cellular physiology; however, an excessive level of oxidative stress can lead to tumorigenic processes including stimulation of growth factor-dependent pathways and the induction of genetic instability. Tumor cells effectively exploit antioxidant enzymes in order to protect themselves against harmful intracellular ROS accumulation, which highlights the essential balance between ROS production and scavenging. Exploiting ROS accumulation can be used as a possible therapeutic strategy in ROS-scavenging tumor cells. Here, we focus on the role of ROS production in PHEO and PGL, predominantly in SDHB-mutated cases. We discuss potential strategies and approaches to anticancer therapies by enhancing ROS production in these difficult-to-treat tumors.

scholarly journals Overexpression of ATG5 Gene Makes Granulocyte-Like HL-60 Susceptible to Release Reactive Oxygen Species

2020 ◽  
Vol 21 (15) ◽  
pp. 5194 ◽  
Author(s):  
Agnieszka Mroczek ◽  
Adrianna Cieloch ◽  
Aneta Manda-Handzlik ◽  
Weronika Kuźmicka ◽  
Angelika Muchowicz ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Fluorescent Microscopy ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Extracellular Traps ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Proliferation And Apoptosis

Neutrophils represent the first line of defense against pathogens using various strategies, such as phagocytosis, production of reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) formation. Recently, an autophagy-independent role of autophagy related (ATG) gene 5 in immune cells, including neutrophils, was emphasized. Our aim was to investigate the role of ATG5 protein in neutrophils’ antimicrobial functions, proliferation and apoptosis. To this end, we used genetically modified human promyelocytic leukemia (HL-60) cells overexpressing ATG5, differentiated toward granulocyte-like cells with all-trans retinoic acid (ATRA) and dimethylformamide. The level of differentiation, phagocytosis, proliferation and apoptosis were determined by flow cytometry. ROS production and NETs release was assessed by fluorometry and fluorescent microscopy. ATG5 gene expression was evaluated by real-time PCR, whereas the protein level of ATG5 and LC3-II was determined by Western blot. We did not observe the induction of autophagy in differentiated HL-60 cells overexpressing ATG5. The increased expression of ATG5 affects the differentiation of HL-60 cells with ATRA, ROS production and phagocytosis. However, we did not detect changes in NETs release. Moreover, ATG5 protects differentiated HL-60 cells from apoptosis but does not cause changes in proliferation rate.

Role of reactive oxygen species in acetylcholine-induced preconditioning in cardiomyocytes

1999 ◽  
Vol 277 (6) ◽  
pp. H2504-H2509 ◽  
Author(s):  
Zhenhai Yao ◽  
Jiankun Tong ◽  
Xiaohui Tan ◽  
Changqing Li ◽  
Zuohui Shao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Ventricular Myocytes ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Intracellular Signals ◽  
Dichlorofluorescin Diacetate ◽  
Flow Through

We examined the ability of ACh to mimic ischemic preconditioning in cardiomyocytes and the role of ATP-sensitive potassium (KATP) channels and mitochondrial reactive oxygen species (ROS) in mediating this effect. Chick embryonic ventricular myocytes were studied in a flow-through chamber while flow rate, pH,[Formula: see text], and[Formula: see text] were controlled. Cell viability was quantified with propidium iodide (5 μM), and production of ROS was measured using 2′,7′-dichlorofluorescin diacetate. Data were expressed as means ± SE. Preconditioning with 10 min of ischemia followed by 10 min of reoxygenation or 10 min of ACh (1 mM) followed by a drug-free period before 1 h of ischemia and 3 h of reoxygenation reduced cell death to the same extent [preconditioning 19 ± 2% ( n = 6, P < 0.05) ACh 21 ± 5% ( n = 6, P < 0.05) vs controls 42 ± 5% ( n = 9)]. Like preconditioning, ACh increased ROS production threefold before ischemia [0.60 ± 0.16 ( n = 7, P< 0.05) vs. controls, 0.16 ± 0.03 ( n = 6); arbitrary units]. Protection and increased ROS production during ACh preconditioning were abolished with 5-hydroxydecanoate (5-HD, 100 μM), a selective mitochondrial KATP channel antagonist, and the thiol reductant 2-mercaptopropionyl glycine (2-MPG, 1 mM), an antioxidant [cell death: 5-HD+ACh 37 ± 7% ( n = 5), 2-MPG+ACh 47 ± 6% ( n = 6); ROS signals: 5-HD+ACh 0.09 ± 0.03 ( n = 5), 2-MPG+ACh 0.01 ± 0.04 ( n = 4)]. In addition, ACh-induced ROS signaling was blocked by the mitochondrial site III electron transport inhibitor myxothiazol (0.02 ± 0.07, n = 5). These results demonstrate that activation of mitochondrial KATPchannels and increased ROS production from mitochondria are important intracellular signals that participate in ACh-induced preconditioning in cardiomyocytes.

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