Mitochondrial reactive oxygen species are involved in chemoattractant-induced oxidative burst and degranulation of human neutrophils in vitro

2017 ◽  
Vol 96 (3) ◽  
pp. 254-265 ◽  
Author(s):  
Nina Vorobjeva ◽  
Anastasia Prikhodko ◽  
Ivan Galkin ◽  
Olga Pletjushkina ◽  
Roman Zinovkin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Oxidative Burst ◽  
Reactive Oxygen ◽  
Human Neutrophils ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species

scholarly journals Nitroglycerine causes mitochondrial reactive oxygen species production: In vitro mechanistic insights

2007 ◽  
Vol 23 (12) ◽  
pp. 990-992 ◽  
Author(s):  
Tommaso Gori ◽  
Andreas Daiber ◽  
Giuseppe Di Stolfo ◽  
Silvia Sicuro ◽  
Saverio Dragoni ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Species Production

scholarly journals Elesclomol-induced increase of mitochondrial reactive oxygen species impairs glioblastoma stem-like cell survival and tumor growth

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Mariachiara Buccarelli ◽  
Quintino Giorgio D’Alessandris ◽  
Paola Matarrese ◽  
Cristiana Mollinari ◽  
Michele Signore ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Molecular Mechanisms ◽  
Reactive Oxygen ◽  
Strong Increase ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species

Abstract Background Glioblastoma (GBM) is the most common and aggressive primary malignant brain tumor in adults, characterized by a poor prognosis mainly due to recurrence and therapeutic resistance. It has been widely demonstrated that glioblastoma stem-like cells (GSCs), a subpopulation of tumor cells endowed with stem-like properties is responsible for tumor maintenance and progression. Moreover, it has been demonstrated that GSCs contribute to GBM-associated neovascularization processes, through different mechanisms including the transdifferentiation into GSC-derived endothelial cells (GdECs). Methods In order to identify druggable cancer-related pathways in GBM, we assessed the effect of a selection of 349 compounds on both GSCs and GdECs and we selected elesclomol (STA-4783) as the most effective agent in inducing cell death on both GSC and GdEC lines tested. Results Elesclomol has been already described to be a potent oxidative stress inducer. In depth investigation of the molecular mechanisms underlying GSC and GdEC response to elesclomol, confirmed that this compound induces a strong increase in mitochondrial reactive oxygen species (ROS) in both GSCs and GdECs ultimately leading to a non-apoptotic copper-dependent cell death. Moreover, combined in vitro treatment with elesclomol and the alkylating agent temozolomide (TMZ) enhanced the cytotoxicity compared to TMZ alone. Finally, we used our experimental model of mouse brain xenografts to test the combination of elesclomol and TMZ and confirmed their efficacy in vivo. Conclusions Our results support further evaluation of therapeutics targeting oxidative stress such as elesclomol with the aim of satisfying the high unmet medical need in the management of GBM.

scholarly journals Ultraviolet light A irradiation induces immunosuppression associated with the generation of reactive oxygen species in human neutrophils

2016 ◽  
Vol 09 (01) ◽  
pp. 1650001 ◽  
Author(s):  
Cunbo Li ◽  
Xuechen Shi ◽  
Mincai Chen ◽  
Guangxue Xu ◽  
Xinglei Su ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ultraviolet Light ◽  
Inflammatory Responses ◽  
Reactive Oxygen ◽  
Human Neutrophils ◽  
Oxygen Species ◽  
Immune Functions ◽  
Uva Irradiation ◽  
Underlying Mechanisms

Ultraviolet blood irradiation has been used as a physical therapy to treat many nonspecific diseases in clinics; however, the underlying mechanisms remain largely unclear. Neutrophils, the first line of host defense, play a crucial role in a variety of inflammatory responses. In the present work, we investigated the effects of ultraviolet light A (UVA) on the immune functions of human neutrophils at the single-cell level by using an inverted fluorescence microscope. N-Formyl-methionyl-leucyl-phenylalanine (FMLP), a classic physiological chemotactic peptide, was used to induce a series of immune responses in neutrophils in vitro. FMLP-induced calcium mobilization, migration, and phagocytosis in human neutrophils was significantly blocked after treatment with 365[Formula: see text]nm UVA irradiation, demonstrating the immunosuppressive effects of UVA irradiation on neutrophils. Similar responses were also observed when the cells were pretreated with H2O2, a type of reactive oxygen species (ROS). Furthermore, UVA irradiation resulted in an increase in NAD(P)H, a member of host oxidative stress in cells. Taken together, our data indicate that UVA irradiation results in immunosuppression associated with the production of ROS in human neutrophils.

Effect of Pyridone Carboxylic Acid Anti-microbials on the Generation of Reactive Oxygen Species In Vitro

1996 ◽  
Vol 24 (4) ◽  
pp. 345-351 ◽  
Author(s):  
H Akamatsu ◽  
Y Niwa ◽  
H Sasaki ◽  
Y Matoba ◽  
Y Asada ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Xanthine Oxidase ◽  
Reactive Oxygen ◽  
Human Neutrophils ◽  
Oxygen Species ◽  
Oxidase System ◽  
Superoxide Radical Anion ◽  
A Cell ◽  
Inflammatory Action

The effects of ofloxacin, ciprofloxacin and balofloxacin on the reactive oxygen species (ROS) levels generated by human neutrophils was examined in vitro; ROS generated in a cell-free, xanthine–xanthine oxidase system was also assessed. The species investigated were superoxide radical anion (O2−), hydrogen peroxide (H2O2) and hydroxyl radical (OH·). Both ofloxacin and ciprofloxacin markedly decreased the levels of O2−, H2O2 and OH· generated by human neutrophils. On the other hand, these drugs did not affect any of the ROS examined in the xanthine-xanthine oxidase system. Balofloxacin showed no significant effect on ROS generated by either system. The present study indicates that ofloxacin and ciprofloxacin may exert an anti-inflammatory action by reducing the potent ROS species excessively generated by neutrophils at the sites of inflammation.

scholarly journals Pharmacological intervention with oxidative burst in human neutrophils

2017 ◽  
Vol 10 (2) ◽  
pp. 56-60 ◽  
Author(s):  
Rado Nosáľ ◽  
Katarína Drábiková ◽  
Viera Jančinová ◽  
Tatiana Mačičková ◽  
Jana Pečivová ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Oxidative Burst ◽  
Rank Order ◽  
Reactive Oxygen ◽  
Natural Antioxidants ◽  
Pharmacological Intervention ◽  
Human Neutrophils ◽  
Oxygen Species ◽  
Free System ◽  
Immunological Responses

AbstractIn this study we investigated the effect of five therapeutically used drugs and four natural polyphenolic compounds on the mechanism of oxidative burst of human neutrophils concerning their participation in the generation of reactive oxygen species (ROS). The compounds investigated decreased the oxidative burst of whole blood in the rank order of potency: N-feruloylserotonin > quercetin > curcumin > arbutin > dithiaden > carvedilol. The generation of intracellular reactive oxygen species in isolated neutrophils decreased in the same rank order, while carvedilol was ineffective. Scavenging of extracellular oxygen radicals followed the rank order of potency: N-feruloylserotonin > curcumin > quercetin > dithiaden. Arbutin and carvedilol had no effect. All compounds tested increased the activity of caspase-3 in cell-free system indicating a positive effect on apoptosis of neutrophils. Activation of protein kinase C was significantly decreased by dithiaden, curcumin, quercetin and N-feruloylserotonin. Carvedilol, dithiaden, quercetin and arbutin reduced activated neutrophil myeloperoxidase release more significantly compared with their less pronounced effect on superoxide generation The presented results are indicative of pharmacological intervention with neutrophils in pathological processes. Of particular interest was the effect of natural compounds. Intracellular inhibition of oxidative burst in isolated neutrophils by the drugs tested and natural antioxidants has to be further analysed since ROS play an important role in immunological responses of neutrophils.

scholarly journals Mitochondria-Targeted Antioxidant SkQ1 Improves Dermal Wound Healing in Genetically Diabetic Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Ilya A. Demyanenko ◽  
Vlada V. Zakharova ◽  
Olga P. Ilyinskaya ◽  
Tamara V. Vasilieva ◽  
Artem V. Fedorov ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Wound Healing ◽  
Smooth Muscle Actin ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
Mitochondrial Reactive Oxygen Species ◽  
Genetically Diabetic Mice

Oxidative stress is widely recognized as an important factor in the delayed wound healing in diabetes. However, the role of mitochondrial reactive oxygen species in this process is unknown. It was assumed that mitochondrial reactive oxygen species are involved in many wound-healing processes in both diabetic humans and animals. We have applied the mitochondria-targeted antioxidant 10-(6′-plastoquinonyl)decyltriphenylphosphonium (SkQ1) to explore the role of mitochondrial reactive oxygen species in the wound healing of genetically diabetic mice. Healing of full-thickness excisional dermal wounds in diabetic C57BL/KsJ-db−/db− mice was significantly enhanced after long-term (12 weeks) administration of SkQ1. SkQ1 accelerated wound closure and stimulated epithelization, granulation tissue formation, and vascularization. On the 7th day after wounding, SkQ1 treatment increased the number of α-smooth muscle actin-positive cells (myofibroblasts), reduced the number of neutrophils, and increased macrophage infiltration. SkQ1 lowered lipid peroxidation level but did not change the level of the circulatory IL-6 and TNF. SkQ1 pretreatment also stimulated cell migration in a scratch-wound assay in vitro under hyperglycemic condition. Thus, a mitochondria-targeted antioxidant normalized both inflammatory and regenerative phases of wound healing in diabetic mice. Our results pointed to nearly all the major steps of wound healing as the target of excessive mitochondrial reactive oxygen species production in type II diabetes.

scholarly journals Attenuating Effect of Chlorella Extract on NLRP3 Inflammasome Activation by Mitochondrial Reactive Oxygen Species

2021 ◽  
Vol 8 ◽  
Author(s):  
Yuya Nakashima ◽  
Kazuhito Gotoh ◽  
Soichi Mizuguchi ◽  
Daiki Setoyama ◽  
Yurie Takata ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nlrp3 Inflammasome ◽  
Reactive Oxygen ◽  
Food Supplement ◽  
Inflammasome Activation ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Nlrp3 Inflammasome Activation

The NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasome has been linked to the pathogenesis of a wide variety of human diseases. Although many drugs and inhibitors have been developed to treat NLRP3-associated diseases, only limited clinical data support their efficacy and safety. Chlorella, a unicellular green alga that is widely and safely used as a food supplement, contains various antioxidants. In this study, we obtained a fat-soluble extract from Chlorella (CE) and demonstrated that it reduced NLRP3 inflammasome activation by inhibiting mitochondrial reactive oxygen species and caspase-1 activation. In addition, CE supplementation attenuated lipopolysaccharide-induced interleukin 1β transcription through activation of hypoxia-inducible factor 1α in vitro and in vivo. As Chlorella is a safe and useful food supplement, it may be a practical pharmacological approach for treating NLRP3-driven diseases.

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