Bacterial Genetic Approach to the Study of Reactive Oxygen Species Production in Galleria mellonella During Salmonella Infection

Over the last decade, an increasing number of reports presented Galleria mellonella larvae as an important model to study host-pathogen interactions. Coherently, increasing information became available about molecular mechanisms used by this host to cope with microbial infections but few of them dealt with oxidative stress. In this work, we addressed the role of reactive oxygen species (ROS) produced by the immune system of G. mellonella to resist against Salmonella enterica, an intracellular pathogen responsible for a wide range of infections. We confirmed that Salmonella was pathogen for G. mellonella and showed that it had to reach a minimal bacterial load within the hemolymph to kill the larvae. ROS production by G. mellonella was revealed by the virulence defects of Salmonella mutants lacking catalases/peroxiredoxins or cytoplasmic superoxide dismutases, both strains being highly sensitive to these oxidants. Finally, we used bacterial transcriptional fusions to demonstrate that hydrogen peroxide (H2O2) was produced in the hemolymph of Galleria during infection and sensed by S. enterica. In line with this observation, the H2O2-dependent regulator OxyR was found to be required for bacterial virulence in the larvae. These results led us to conclude that ROS production is an important mechanism used by G. mellonella to counteract bacterial infections and validate this host as a relevant model to study host-pathogen interactions.

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Hypoxia-induced reactive oxygen species formation in skeletal muscle

Journal of Applied Physiology ◽

10.1152/japplphysiol.01298.2006 ◽

2007 ◽

Vol 102 (6) ◽

pp. 2379-2388 ◽

Cited By ~ 213

Author(s):

Thomas L. Clanton

Keyword(s):

Reactive Oxygen Species ◽

Skeletal Muscle ◽

Molecular Mechanisms ◽

Cell Injury ◽

Cell Function ◽

Contractile Activity ◽

Reactive Oxygen ◽

Hypoxic Exposure ◽

Ros Production ◽

Oxygen Species

The existence of hypoxia-induced reactive oxygen species (ROS) production remains controversial. However, numerous observations with a variety of methods and in many cells and tissue types are supportive of this idea. Skeletal muscle appears to behave much like heart in that in the early stages of hypoxia there is a transient elevation in ROS, whereas in chronic exposure to very severe hypoxia there is evidence of ongoing oxidative stress. Important remaining questions that are addressed in this review include the following. Are there levels of Po2 in skeletal muscle, typical of physiological or mildly pathophysiological conditions, that are low enough to induce significant ROS production? Does the ROS associated with muscle contractile activity reflect imbalances in oxygen uptake and demand that drive the cell to a more reduced state? What are the possible molecular mechanisms by which ROS may be elevated in hypoxic skeletal muscle? Is the production of ROS in hypoxia of physiological significance, both with respect to cell signaling pathways promoting cell function and with respect to damaging effects of long-term exposure? Discussion of these and other topics leads to general conclusions that hypoxia-induced ROS may be a normal physiological response to imbalance in oxygen supply and demand or environmental stress and may play a yet undefined role in normal response mechanisms to these stimuli. However, in chronic and extreme hypoxic exposure, muscles may fail to maintain a normal redox homeostasis, resulting in cell injury or dysfunction.

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β-Aminobutyric Acid Primes an NADPH Oxidase–Dependent Reactive Oxygen Species Production During Grapevine-Triggered Immunity

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-23-8-1012 ◽

2010 ◽

Vol 23 (8) ◽

pp. 1012-1021 ◽

Cited By ~ 43

Author(s):

Carole Dubreuil-Maurizi ◽

Sophie Trouvelot ◽

Patrick Frettinger ◽

Alain Pugin ◽

David Wendehenne ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Nadph Oxidase ◽

Molecular Mechanisms ◽

Reactive Oxygen ◽

Aminobutyric Acid ◽

Ros Production ◽

Oxygen Species ◽

Defense Gene Expression ◽

Diphenylene Iodonium ◽

Signaling Events

The molecular mechanisms underlying the process of priming are poorly understood. In the present study, we investigated the early signaling events triggered by β-aminobutyric acid (BABA), a well-known priming-mediated plant resistance inducer. Our results indicate that, in contrast to oligogalacturonides (OG), BABA does not elicit typical defense-related early signaling events nor defense-gene expression in grapevine. However, in OG-elicited cells pretreated with BABA, production of reactive oxygen species (ROS) and expression of the respiratory-burst oxidase homolog RbohD gene were primed. In response to the causal agent of downy mildew Plasmopara viticola, a stronger ROS production was specifically observed in BABA-treated leaves. This process was correlated with an increased resistance. The NADPH oxidase inhibitor diphenylene iodonium (DPI) abolished this primed ROS production and reduced the BABA-induced resistance (BABA-IR). These results suggest that priming of an NADPH oxidase–dependent ROS production contributes to BABA-IR in the Vitis-Plasmopara pathosystem.

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Bufalin Induces Reactive Oxygen Species Dependent Bax Translocation and Apoptosis in ASTC-a-1 Cells

Evidence-based Complementary and Alternative Medicine ◽

10.1093/ecam/nep082 ◽

2011 ◽

Vol 2011 ◽

pp. 1-12 ◽

Cited By ~ 21

Author(s):

Lei Sun ◽

Tongsheng Chen ◽

Xiaoping Wang ◽

Yun Chen ◽

Xunbin Wei

Keyword(s):

Reactive Oxygen Species ◽

Cell Death ◽

Molecular Mechanisms ◽

Caspase 3 ◽

Temporal Dynamics ◽

Reactive Oxygen ◽

Ros Generation ◽

Ros Production ◽

Oxygen Species ◽

Induced Apoptosis

Bufalin has been shown to induce cancer cell death through apoptotic pathways. However, the molecular mechanisms are not well understood. In this study, we used the confocal fluorescence microscopy (CFM) to monitor the spatio-temporal dynamics of reactive oxygen species (ROS) production, Bax translocation and caspase-3 activation during bufalin-induced apoptosis in living human lung adenocarcinoma (ASTC-a-1) cells. Bufalin induced ROS production and apoptotic cell death, demonstrated by Hoechst 33258 staining as well as flow cytometry analysis. Bax redistributed from cytosol to mitochondria from 12 to 48 h after bufalin treatment in living cells expressed with green fluorescent protein Bax. Treatment with the antioxidantN-acetyl-cysteine (NAC), a ROS scavenger, inhibited ROS generation and Bax translocation and led to a significant protection against bufalin-induced apoptosis. Our results also revealed that bufalin induced a prominent increase of caspase-3 activation blocked potently by NAC. Taken together, bufalin induced ROS-mediated Bax translocation, mitochondrial permeability transition and caspase-3 activation, implying that bufalin induced apoptosis via ROS-dependent mitochondrial death pathway in ASTC-a-1 cells.

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Long-term caloric restriction increases UCP3 content but decreases proton leak and reactive oxygen species production in rat skeletal muscle mitochondria

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00435.2004 ◽

2005 ◽

Vol 289 (3) ◽

pp. E429-E438 ◽

Cited By ~ 107

Author(s):

Lisa Bevilacqua ◽

Jon J. Ramsey ◽

Kevork Hagopian ◽

Richard Weindruch ◽

Mary-Ellen Harper

Keyword(s):

Reactive Oxygen Species ◽

Reactive Oxygen ◽

Whole Body ◽

Proton Leak ◽

Protonmotive Force ◽

Ros Production ◽

Oxygen Species ◽

Wide Range ◽

Species Production

Calorie restriction (CR) without malnutrition increases life span and delays the onset of a variety of diseases in a wide range of animal species. However, the mechanisms responsible for the retardation of aging with CR are poorly understood. We proposed that CR may act, in part, by inducing a hypometabolic state characterized by decreased reactive oxygen species (ROS) production and mitochondrial proton leak. Here, we examine the effects of long-term CR on whole animal energetics as well as muscle mitochondrial energetics, ROS production, and ROS damage. CR was initiated in male FBNF1 rats at 6 mo of age and continued for 12 or 18 mo. Mean whole body V̇o2 was 34.6 ( P < 0.01) and 35.6% ( P < 0.001) lower in CR rats than in controls after 12 and 18 mo of CR, respectively. Body mass-adjusted V̇o2 was 11.1 and 29.5% lower (both P < 0.05) in CR rats than in controls after 12 and 18 mo of CR. Muscle mitochondrial leak-dependent (State 4) respiration was decreased after 12 mo compared with controls; however, after 18 mo of CR, there were slight but not statistically significant differences. Proton leak kinetics were affected by 12 mo of CR such that leak-dependent respiration was lower in CR mitochondria only at protonmotive force values exceeding 170 mV. Mitochondrial H2O2 production and oxidative damage were decreased by CR at both time points and increased with age. Muscle UCP3 protein content increased with long-term CR, consistent with a role in protection from ROS but inconsistent with the observed decrease or no change in proton leak.

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Cytochrome P450-dependent reactive oxygen species (ROS) production contributes to Mn3O4 nanoparticle-caused liver injury

RSC Advances ◽

10.1039/c8ra05633a ◽

2018 ◽

Vol 8 (65) ◽

pp. 37307-37314 ◽

Cited By ~ 1

Author(s):

Zongkai Yue ◽

Xiao Zhang ◽

Qilin Yu ◽

Lu Liu ◽

Xiaomeng Zhou

Keyword(s):

Reactive Oxygen Species ◽

Cytochrome P450 ◽

Liver Injury ◽

Reactive Oxygen ◽

Molecular Adsorption ◽

Ros Production ◽

Oxygen Species ◽

Wide Range

Mn3O4 nanoparticles (NPs) are one of the most important nanomaterials, and have a wide range of applications (i.e., catalysis, solar-electron transformation and molecular adsorption).

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Adrenomedullin Regulates Cellular Glutathione Content via Modulation of γ-Glutamate-Cysteine Ligase Catalytic Subunit Expression

Endocrinology ◽

10.1210/en.2005-0895 ◽

2006 ◽

Vol 147 (3) ◽

pp. 1357-1364 ◽

Cited By ~ 19

Author(s):

Jee-Youn Kim ◽

Ji-Hye Yim ◽

Jin-Ho Cho ◽

Jin-Hwan Kim ◽

Jeong-Hun Ko ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Molecular Mechanisms ◽

Ischemia Reperfusion ◽

Reactive Oxygen ◽

Catalytic Subunit ◽

Oxygen Species ◽

Glutamate Cysteine Ligase ◽

Hypoxic Injury ◽

Wide Range

Adrenomedullin (AM) participates in a wide range of physiological and pathological processes including vasorelaxation, angiogenesis, cancer promotion, and apoptosis. Recently, it has been reported that AM protects a variety of cells against oxidative stress induced by stressors such as hypoxia, ischemia/reperfusion, and hydrogen peroxide through the phosphatidylinositol 3-kinase (PI3K)-dependent pathway. However, the molecular mechanisms underlying the pathway of cell survival against hypoxic injury are largely unknown. In an effort to investigate the survival mechanism against hypoxic injury, we studied the effects of AM on cellular levels of reactive oxygen species, well-known mediators of cell death after oxidative stress, and the mechanism involved in the regulation of reactive oxygen species levels. Here, we show that AM increases γ-glutamate-cysteine ligase (γ-GCL) activity under both hypoxic and normoxic conditions, resulting in an up-regulation of cellular glutathione levels to more than 2-fold higher than basal expression. In addition, we demonstrate that AM induces concentration-dependent expression of the catalytic subunit of γ-GCL (γ-GCLC) at the mRNA and protein levels through the activation of the γ-GCLC promoter fragment sequence from −597 to −320. However, when treated with the PI3K inhibitors, the effects of AM on γ-GCLC expression were completely abrogated, suggesting that a PI3K pathway linked AM with the transcriptional activation of the γ-GCLC promoter. Taken together, our data suggests that AM participates in the regulation of cellular redox status via glutathione synthesis. These results may explain, in part, the mechanism by which AM protects cells against oxidative stress.

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Extracellular reactive oxygen species production by lichens

The Lichenologist ◽

10.1017/s0024282905014921 ◽

2005 ◽

Vol 37 (5) ◽

pp. 397-407 ◽

Cited By ~ 13

Author(s):

Richard Peter BECKETT ◽

Farida V. MINIBAYEVA ◽

Zsanett LAUFER

Keyword(s):

Reactive Oxygen Species ◽

High Stress ◽

Reactive Oxygen ◽

Ros Production ◽

Oxygen Species ◽

Biotic Stresses ◽

Intracellular Ros ◽

Wide Range ◽

Ros Formation ◽

Species Production

This review discusses the production of reactive oxygen species (ROS) by lichens and their possible roles. All organisms produce ROS, and production is increased by many abiotic and biotic stresses. Intracellular ROS production is generally considered to be harmful, and a variety of enzymic and non-enzymic scavenging systems exist to detoxify them. However, extracellular ROS formation has been suggested to play ‘positive roles’, particularly in the response of organisms to stress. Given their high stress tolerance, it is rather surprising that studies on extracellular ROS production by lichens have just started. Surveys of a wide range of lichens have shown that constitutively high rates of extracellular superoxide production occur in the Suborder Peltigerineae, but production appears to be absent in other groups. In some members of the Peltigerineae ROS production is stimulated by desiccation and wounding. It seems probable that the enzymes that produce the superoxide are laccases, based on first the types of substrates that lichens can break down, and second the dependence of the breakdown of these substrates on pH, temperature and the presence of inhibitors. While much more work is needed, we suggest that physiological roles of extracellular ROS production will be found to include defence against pathogens, melanization, and lignin breakdown.

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Reactive Oxygen Species in Acute Lymphoblastic Leukaemia: Reducing Radicals to Refine Responses

Antioxidants ◽

10.3390/antiox10101616 ◽

2021 ◽

Vol 10 (10) ◽

pp. 1616

Author(s):

Abdul Mannan ◽

Zacary P Germon ◽

Janis Chamberlain ◽

Jonathan R Sillar ◽

Brett Nixon ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Acute Lymphoblastic Leukaemia ◽

Lymphoblastic Leukaemia ◽

Molecular Mechanisms ◽

Chemotherapy Resistance ◽

Reactive Oxygen ◽

Ros Production ◽

Oxygen Species ◽

Therapeutic Approaches ◽

T Lymphoblasts

Acute lymphoblastic leukaemia (ALL) is the most common cancer diagnosed in children and adolescents. Approximately 70% of patients survive >5-years following diagnosis, however, for those that fail upfront therapies, survival is poor. Reactive oxygen species (ROS) are elevated in a range of cancers and are emerging as significant contributors to the leukaemogenesis of ALL. ROS modulate the function of signalling proteins through oxidation of cysteine residues, as well as promote genomic instability by damaging DNA, to promote chemotherapy resistance. Current therapeutic approaches exploit the pro-oxidant intracellular environment of malignant B and T lymphoblasts to cause irreversible DNA damage and cell death, however these strategies impact normal haematopoiesis and lead to long lasting side-effects. Therapies suppressing ROS production, especially those targeting ROS producing enzymes such as the NADPH oxidases (NOXs), are emerging alternatives to treat cancers and may be exploited to improve the ALL treatment. Here, we discuss the roles that ROS play in normal haematopoiesis and in ALL. We explore the molecular mechanisms underpinning overproduction of ROS in ALL, and their roles in disease progression and drug resistance. Finally, we examine strategies to target ROS production, with a specific focus on the NOX enzymes, to improve the treatment of ALL.

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