Reactive Oxygen Species/metabolism

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Investigation of the reactive oxygen species metabolism during the life cycle of Fusarium graminearum

Investigation of the reactive oxygen species metabolism during the life cycle of Fusarium graminearum

cereal crops causing plant diseases such as Fusarium Head Blight in wheat. The infection process is mediated mainly via differentiation of fungal cells into complex multicellular organs, so called infection cushions (ICs). In previous work an RNAseq-based transcriptomic and functional analysis indicated major transcriptional rearrangements between ICs and non-invasive cells. Data analysis revealed that expression of enzymes involved in the metabolism of reactive oxygen species (ROS) was elevated in ICs. ROS are i teg al o po e ts of e e ae o i ell s eta olis a d a e fo ed as -products of oxygen-based cellular reactions. While being harmful to the cell structure when accumulating, ROS are also necessary for cellular functions serving as an important second messenger mediating cellular differentiation. Particularly, they are essential elements in plant-pathogen interactions, such as fungal infection processes. Only few ROS-related enzymes involved in these interactions are known to this day, however. The aim of this study was to gain further insights into the role of ROS and specific ROS-related enzymes, particularly secreted ones, in different aspects of the fungal life-cycle. Via gene deletions 9 monooxygenases (4 of them secreted), 5 secreted peroxidases, 2 secreted oxidases, 1 secreted dehydrogenase, 1 secreted reductase, 2 secreted cupredoxins, 3 metallothioneins, 1 NAD(P) transhydrogenase (NNT), and 1 secreted superoxide dismutase (SOD) were disrupted. Mutants were tested for virulence, vegetative growth, ROS-sensitivity, ROS-accumulation, and fertility. It could be shown that secreted peroxidases are involved in vegetative growth, ROS-accumulation, and fertility. Other ROS-related enzymes deleted in this study caused no effect on the tested parameters. This low number of phenotypes indicates a high resilience of F. graminearum against disruptions of its ROS-metabolism. It seems that the ROS-equilibrium which the fungus seeks to maintain during infection is a highly secured system, fortified by a large array of enzymes with redundant function. Further experiments for gaining insights into
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Reactive oxygen species (ROS) and lipid metabolism in idiopathic pulmonary fibrosis - role of peroxisomes in the pathogenesis of this devastating disease

Reactive oxygen species (ROS) and lipid metabolism in idiopathic pulmonary fibrosis - role of peroxisomes in the pathogenesis of this devastating disease

content secrete huge amounts of extracellular matrix. However, altered peroxisome functions in IPF pathogenesis have never been investigated. Proinflammatory mediators and reactive oxygen species (ROS) accumulation were shown as pathogenetic mechanisms of this yet incurable disease. Since peroxisomes are involoved in both the degradation of proinflammatory lipid mediators (eicosanoids) as well as ROS metabolism, alterations in the protective capacity of this organelle might contribute to the pathogenesis of IPF. In addition, children with Zellweger Syndrome, the most severe peroxisomal biogenesis defect, develop chronic liver fibrosis and cirrhosis, suggesting that the peroxisomal metabolism is essential for the protection against fibrotic organ degeneration. In the experimental part of this thesis the hypothesis was tested, 1) whether the peroxisomal compartment and corresponding gene expression is altered in IPF, 2) whether the downregulation of peroxisomal biogenesis and metabolism in IPF promotes further excessive secretion of extracellular matrix proteins and proinflammatory mediators and 3) whether proinflammatory and profibrotic cytokines influence peroxisomal abundance and metabolism. Moreover, the molecular mechanisms leading to the alterations of the peroxisomal compartment were investigated. In addition, a bleomycin induced lung fibrosis mouse model was used to analyze peroxisomal biogenesis, antioxidative and lipid metabolic proteins at various time-points after bleomycin treatment. The molecular mechanisms and specific involvement of peroxisomal proteins in TGF-E induced ECM production were investigated. Finally the effect of TGF-E1 on the peroxisomal
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Reactive Oxygen Species as Regulators of MDSC-Mediated Immune Suppression

Reactive Oxygen Species as Regulators of MDSC-Mediated Immune Suppression

MAIN TEXT Regulation of MDSCs by ROS A state of “oxidative stress” describes a situation where high levels of ROS -derived from cellular metabolism, toxic insults, or oxidative burst- outbalance the anti-oxidative system ( 8 ). This breakdown of cellular homeostasis results from mitochondrial dysfunction or increased metabolic activity, oncogene activity or infiltrating immune cells ( 8 ) and induces damage to lipids, proteins, carbohydrates and nucleic acids and can even lead to cell death ( 9 ). Excessive production of ROS molecules is associated with several inflammatory and pathologic conditions. For example, oxidative stress within the intestinal epithelium is thought to be involved in the pathogenesis of intestinal inflammation ( 10 ) and oxidative stress is also associated with neurodegenerative diseases ( 8 ). Furthermore, elevated rates of ROS can be observed in almost all cancers and are involved in tumor metastasis ( 11 ). On the other hand, emerging evidence suggests that ROS molecules serve as signaling intermediates that play central roles in several molecular pathways and also serve as central mediators of immune cells ( 12 ). Low levels of ROS are continuously generated under healthy cellular conditions, and are neutralized by the endogenous antioxidant machinery that is regulated by nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Nrf2 is retained and degraded in the cytosol by Kelch ECH associating protein 1 (Keap1) under basal conditions ( 13 ). Cellular stimuli such as oxidative stress lead to conformational changes in Keap1, which are followed by the release of Nrf2 from Keap1. Afterwards, Nrf2 translocates
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Reactive Oxygen Species Interact With NLRP3 Inflammasomes and Are Involved in the Inflammation of Sepsis: From Mechanism to Treatment of Progression

Reactive Oxygen Species Interact With NLRP3 Inflammasomes and Are Involved in the Inflammation of Sepsis: From Mechanism to Treatment of Progression

Shuai Zhao 1 * † , Fan Chen 2† , Qiliang Yin 3 , Dunwei Wang 1 , Wei Han 1 * ‡ and Yuan Zhang 1 * ‡ 1 Department of Anesthesiology, First Hospital of Jilin University, Changchun, China, 2 Department of Neurosurgery, University Medicine Greifswald, Greifswald, Germany, 3 Department of Oncology, First Hospital of Jilin University, Changchun, China Over the past 10 years, the crisis of sepsis has remained a great challenge. According to data from 2016, the sepsis-related mortality rate remains high. In addition, sepsis consumes extensive medical resources in intensive care units, and anti- inflammatory agents fail to improve sepsis-associated hyperinflammation and symptoms of immunosuppression. The specific immune mechanism of sepsis remains to be elucidated. Reactive oxygen species (ROS) are triggered by energy metabolism and respiratory dysfunction in sepsis, which not only cause oxidative damage to tissues and organelles, but also directly and indirectly promote NOD-, LRR-, and pyrin domain- containing protein 3 (NLRP3) inflammasome activation. NLRP3 inflammasomes enlarge the inflammatory response and trigger apoptosis of immune cells to exacerbate sepsis progression. Inhibiting the negative effects of ROS and NLRP3 inflammasomes therefore provides the possibility of reversing the excessive inflammation during sepsis. In this review, we describe the interaction of ROS and NLRP3 inflammasomes during sepsis, provide prevention strategies, and identify fields that need further study.
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Spin Biochemistry Modulates Reactive Oxygen Species (ROS) Production by Radio Frequency Magnetic Fields

Spin Biochemistry Modulates Reactive Oxygen Species (ROS) Production by Radio Frequency Magnetic Fields

¤ Current address: Research Center for Bioelectromagnetic Interaction at the Institute of Occupational Medicine, University Hospital RWTH Aachen, Aachen, Germany Introduction One of the greatest challenges in the field of chemical and physical biology is to bridge the knowledge gap between the atomic level and the cellular level [1]. Focused at the biological quantum/classical interface, an emerging field called quantum biology has promised to offer new and compelling insights into fundamental underlying cellular processes from the perspective of quantum phenomena [2,3]. Following this paradigm, we present a novel methodology for indirectly investigating possible quantum effects in biological systems by applied static and alternating magnetic fields that induce changes in magnetically sensitive free radical pairs in biochemical reactions. Some evidence shows the effects of such exposures on cellular morphology, growth curves, and protein expression, implying an underlying metabolic influence [4–7]. The effect of weak magnetic fields on cellular metabolic processes is not well understood and little is known about how magnetic fields influence reaction rates in oxidative metabolism [8–10]. This work aims to elucidate biological responses that are sensitive to radio frequency (RF) magnetic fields involving the production of reactive oxygen species (ROS), of which are born presumably from spin-correlated free radical pairs. In many biological processes, the reactivity of molecular oxygen and the formation of oxygen radical intermediates are a consequence of oxidative respiration [11,12]. Most organisms have developed protective enzyme systems that mediate ROS
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Reactive Oxygen Species as Regulators of MDSC-Mediated Immune Suppression

Reactive Oxygen Species as Regulators of MDSC-Mediated Immune Suppression

MAIN TEXT Regulation of MDSCs by ROS A state of “oxidative stress” describes a situation where high levels of ROS -derived from cellular metabolism, toxic insults, or oxidative burst- outbalance the anti-oxidative system ( 8 ). This breakdown of cellular homeostasis results from mitochondrial dysfunction or increased metabolic activity, oncogene activity or infiltrating immune cells ( 8 ) and induces damage to lipids, proteins, carbohydrates and nucleic acids and can even lead to cell death ( 9 ). Excessive production of ROS molecules is associated with several inflammatory and pathologic conditions. For example, oxidative stress within the intestinal epithelium is thought to be involved in the pathogenesis of intestinal inflammation ( 10 ) and oxidative stress is also associated with neurodegenerative diseases ( 8 ). Furthermore, elevated rates of ROS can be observed in almost all cancers and are involved in tumor metastasis ( 11 ). On the other hand, emerging evidence suggests that ROS molecules serve as signaling intermediates that play central roles in several molecular pathways and also serve as central mediators of immune cells ( 12 ). Low levels of ROS are continuously generated under healthy cellular conditions, and are neutralized by the endogenous antioxidant machinery that is regulated by nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Nrf2 is retained and degraded in the cytosol by Kelch ECH associating protein 1 (Keap1) under basal conditions ( 13 ). Cellular stimuli such as oxidative stress lead to conformational changes in Keap1, which are followed by the release of Nrf2 from Keap1. Afterwards, Nrf2 translocates
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The Effect of Glutathione Peroxidase-1 Knockout on Anticancer Drug Sensitivities and Reactive Oxygen Species in Haploid HAP-1 Cells

The Effect of Glutathione Peroxidase-1 Knockout on Anticancer Drug Sensitivities and Reactive Oxygen Species in Haploid HAP-1 Cells

4. Discussion The aim of this work was to assess the influence of the key antioxidative enzyme GPx1 on anticancer drug cytotoxicity. In this proof-of-concept study, we used a GPx1 knockout cell line, obtained by a CRISPR-Cas9 deletion of the only GPX1 gene in HAP-1 haploid human cancer cells, to analyze for differences in potency of widely used anticancer drugs to the parental line. Characterization of both cell lines showed slight differences in the morphology but no differences in size, doubling-time, viability or rates of metabolism. Our next focus was on the expression of various redox associated enzymes and intracellular GSH + GSSG content. It was anticipated that the knockout cell line would adapt to the loss of GPx1 function by increasing the expression of other antioxidant enzymes and/or GSH + GSSG. However, with the exception of a complete loss of GPx1 expression, we found no other significant alterations in the knockout cell line with respect to catalase, GPx4, peroxiredoxin-1 and -2 and thioredoxin-1 and -2. This suggests that under normal growth conditions, GPx1 is not essential for maintenance of a healthy redox balance. However, against our intuition we found a significant decrease in GSH + GSSG content in the knockout cells relative to the native cell line, suggesting a more complicated relationship between GPx1 and glutathione metabolism.
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Differential expression of islet glutaredoxin 1 and 5 with high reactive oxygen species production in a mouse model of diabesity

Differential expression of islet glutaredoxin 1 and 5 with high reactive oxygen species production in a mouse model of diabesity

hexokinase is saturated due to glucose overload. A recent study linked Grx to adenosine monophosphate-activated protein kinase (AMPK) activation and thereby stabilization of insu- lin secretion [ 54 ]. Consequently, Grx1 might support generation of new islets as well as growth of pre-existing islets, and further sustain islet metabolic activity in attempt to maintain glucose homeostasis and preserve insulin secretion capacity. In this study, Grx5 featured a significant reduction in both groups of mice, which was markedly more pronounced in db/db animals and correlated with fading insulin expression and rising blood glucose levels. The Grx5 enzyme is an important actor in composition of iron-sulfur clusters in the mitochondria [ 26 ]. Therefore, it is essential for a broad range of enzymes relying on these clusters, among which numerous have relevance for the respiratory chain [ 26 ]. Thus, the connection between Grx5 and oxidative phosphorylation might explain the co-occurrence of reduced insulin as well as Grx5 expression in this study. It has been reported that Grx5-deficiency increases the suscepti- bility to oxidative stress [ 25 ]. Furthermore, a lack of Grx5 enzyme was also correlated to cellular iron overload [ 69 ]. Iron is known to catalyze ROS production and thereby mediate apoptosis [ 70 ]. The link between metabolic stress and iron metabolism was shown in an in vivo model for diabetes mellitus type 2 with defective iron channels which featured stronger beta-cell viability [ 71 ]. Also, iron chelator treatment and dietary iron restriction had beneficial effects on glucose homeostasis in rodents [ 72 ]. Therefore, Grx5 might play a key role in main- taining mitochondrial functionality and prevent detrimental impact of iron accumulation. At the present time, the exact significance of reduced Grx1 and 5 levels in diabese db/db mice remains to be studied. Functional experiments will elucidate whether reduced redoxin levels are cause or result of impaired insulin secretion in islets of diabese animals. Regulators and effectors of islet redoxins have to be identified and modulation of redoxin expression should
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Involvement of Reactive Oxygen Species in the Induction of (5)-Ar-/?-Coumaroyloctopamine Accumulation by ß-l,3-Glucooligosaccharide Elicitors in Potato Tuber Tissues 

Involvement of Reactive Oxygen Species in the Induction of (5)-Ar-/?-Coumaroyloctopamine Accumulation by ß-l,3-Glucooligosaccharide Elicitors in Potato Tuber Tissues 

in the signal transduction pathway from stimula­ tion by lam inarin to the induction of p -C O accu­ mulation. Inhibition of both laminarin-induced p- CO biosynthesis and H 20 2 generation by DPI (Fig. lc, Table II) suggests that N A D PH oxidase is likely to be involved in this generation of ROS. In potato; it has already been dem onstrated that large am ounts of ROS are generated shortly after inoculation of incompatible pathogen or elicitor treatm ent (Doke, 1983). The produced ROS are thought to function as the signal for the induction of H R (Doke, 1985) and accumulation of sesquit- erpenoid phytoalexin including rishitin (Ellis et al., 1993). The present study indicates that p -C O bio­ synthesis is controlled by the same mechanism in­ volved in the defense responses in potato, al­ though it follows a totally distinct pathway from that of rishitin. Thus, it is likely that ROS can regu­ late the activities of a broad-range of enzymes in the secondary metabolism of potato. While ROS generation has also been described in various plant/pathogen or plant/elicitor interactions (Woj- taszek, 1997), their signaling function with respect to the induction of phytoalexin accumulation has been dem onstrated in parsley (Jabs et al., 1997) and soybean (A postol et al., 1989) suspension cul­ tures.
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Comparison of Eight Human Tumour Cell Lines and Their Responses to Low-Dose Reactive Oxygen Species

Comparison of Eight Human Tumour Cell Lines and Their Responses to Low-Dose Reactive Oxygen Species

5 translated via thiol-relays (mainly cysteine residues within proteins), a process called redox signalling.(Hanschmann et al., 2013) At high levels, ROS can overpowered the antioxidant capacity of the cell. This can directly cause cell demise by defective NFκB activation and alteration of mitochondrial outer membrane permeability, allowing the translocation of mitochondrial resident pro-apoptotic proteins to induce apoptosis. Alternatively, ROS can also serve signalling functions at high concentrations, for example in p62-mediated engagement of autophagy.(Carroll et al., 2018) Cancer cells often display an imbalance in either ROS production and removal, or redox signalling pathways.(Acharya et al., 2010, Cui, 2012, Gius and Spitz, 2006) It was one of the aims of this study to investigate the expression of a number of redox-proteins and redox enzymes involved in metabolism and redox- signalling pathways in response to mild exposure to exogenous ROS generated by physical plasmas.
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STIM-Orai Channels and Reactive Oxygen Species in the Tumor Microenvironment

STIM-Orai Channels and Reactive Oxygen Species in the Tumor Microenvironment

The importance of ROS for carcinogenesis immediately leads to the question of if there are ROS sources in the TME (Figure 4 ). Already 30 years ago, it was shown that cancer cells can induce pathologically increased ROS release [ 180 ]. However, analyzing ROS in the TME remains to be difficult, despite the fact that more and more techniques to measure different ROS are being developed (Table 1 ). A big challenge is that the unique TME is disrupted during preparation, leading to errors in analyses, in particular with regard to tumor cell metabolism. Furthermore, finding proper controls for in vitro studies is likewise challenging, as fast proliferating tumor cells can establish different ROS levels already due to their diverse metabolic state and not necessarily due to malignant transformation [ 181 ]. Nevertheless, several reliable studies have been performed to analyze ROS formation in the TME as reviewed in Reference [ 182 ]. The activation of oncogenes, the loss of tumor suppressor genes as well as mitochondrial DNA mutations and hypoxia may lead to an enhancement of ROS levels in tumor cells that further support carcinogenesis and malignancy [ 182 ]. Other publications further describe the same mechanisms to be responsible for the NOX-dependent ROS release by tumor cells [ 183 , 184 ].
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Regulation of cardiotrophin-1 expression during mouse embryonic stem cell differentiation by hypoxia and reactive oxygen species

Regulation of cardiotrophin-1 expression during mouse embryonic stem cell differentiation by hypoxia and reactive oxygen species

can regulate transcription. The functions of HIF-1 target genes have been divided into categories that include cell proliferation and viability, erythropoiesis and iron metabolism, as well as vascular development and remodeling. The expression of these genes is induced when oxygen tension decreases over physiological relevant ranges. To prevent the continuous overexpression of these genes, cells utilize prolyl hydroxylases [Hofer et al, 2001; Elkins et al, 2003; Huang and Bunn, 2003] to hydroxylate HIF-1α. Hydroxylation targets HIF-1α for binding to the von Hippel- Lindau protein (pVHL), which is the recognition component of an E3 ubiquitin protein ligase, and ubiquitination of HIF-1α. These results in the targeting of HIF-1α for destruction by the proteasome. Cells lacking functional pVHL cannot degrade HIF and thus overproduce mRNAs encoded by HIF target genes. Oxygenation of asparagine also blocks the recruitment of coactivating proteins [Lando et al, 2002]. Many researchers have shown that there is an increase in intracellular ROS levels during hypoxia [Chandel et al, 1998; Duranteau et al, 1998; Kulisz et al, 2002; Schaefer et al, 2003], indicating that redox signaling pathways may be involved in the regulation of hypoxia responsive genes. This hypothesis was supported by the fact that pro-oxidants, that induce an increase in intracellular ROS, stabilized and activated HIF-1α leading to the increased expression of various genes [Duyndam et
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Studies on Specific and General Defense Strategies against Reactive Oxygen Species in 'Bacillus subtilis'

Studies on Specific and General Defense Strategies against Reactive Oxygen Species in 'Bacillus subtilis'

active in the aerobic, upper layer. Similar to other soil-living Bacillus species, B. subtilis can be regarded as r-strategist that shows metabolic activation when nutrients become available (Sneath, 1986). In contrast to the exponential growth observed under laboratory conditions, in its natural ecosystem physical stress and nutrient limitation restrict the growth of populations to slow rates. The permanent variation of biotic and abiotic factors rather enforce the cellular system to focus on repeated adaptation in order to survive under hazardous environmental conditions (Kjelleberg, 1993; Morita, 1997). As a consequence of the effort to adjust the physiological state most economically, B. subtilis cells respectively ancestral cells, have developed highly complex response networks during their evolution. Adaptive networks. Bacterial cells may alter morphology, metabolism and motility in order to adapt to environmental fluctuations. The phenotypical responses are based on highly sophisticated systems to percept environmental signals which subsequently trigger changes in gene expression or protein synthesis. B. subtilis represents a group of bacteria with two outstanding adaptive strategies that are activated by nutrient limitations: sporulation and natural competence.
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The Reactive Sulfur Species Concept: 15 Years On

The Reactive Sulfur Species Concept: 15 Years On

In fact, there is a rather profound piece of underlying chemistry associated with many of these remedies. Most of them act via the modification of critical thiol residues in their respective target proteins, and this may result in widespread cellular signalling and feedback, as already mentioned in the context of Keap-1 modification, nuclear factor 2 (Nrf2) release and a subsequent antioxidant defence. Certain medical drugs, such as omeprazole and structurally related prazoles, also seem to function via such an oxidative mechanism [112,113]. Omeprazole is a proton pump inhibitor targeting a potassium dependent ATPase. The sulfoxide is used in the therapy of various gastrointestinal ulcers and becomes activated under acidic conditions to form a reactive sulfenic acid. The latter then reacts with a cysteine residue in the ATPase to form a disulfide, a process which irreversibly shuts down the enzyme and causes an increase in stomach pH. Other agents, such as clopidogrel, a drug used to prevent thrombosis, also become activated under certain conditions to form a reactive RSS which subsequently modifies specific target proteins via a disulfide bond. In the case of the antiplatelet agent clopidogrel, the reactive intermediate is not well defined in most literature on this topic, yet regardless of its exact nature it is able to modify P2Y12 and hence inhibit blot clotting and thrombosis. In contrast, 1,2-dithiole-3-thiones, such as the schistosomicide oltipraz, react without any prior activation. This compound, together with a range of structurally related 1,2-
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Early cadmium-induced effects on reactive oxygen species production, cell viability and membrane electrical potential in grapevine roots

Early cadmium-induced effects on reactive oxygen species production, cell viability and membrane electrical potential in grapevine roots

published by J anicka -r ussak et al. (2008). Conclusion The early effects of Cd on grapevine adventitious roots were found in cell viability and reactive oxygen species (ROS) production. Cd disturbed the plasma membrane (PM) integrity leading to the loss of the cell viability. This response was both concentration-dependent, occur- ring at the concentrations higher than 60 μM Cd (24 h), and time-dependent, occurring after the time period longer than 30 min (100 μM Cd). Similar concentration‑depend- ence was observed also in the production of both super- oxide anion (O·̄ 2 ) and hydrogen peroxide (H 2 O 2 ), which,
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OH-Radical-Type Reactive Oxygen Species: A Short Review on the Mechanisms of OH-Radical-and Peroxynitrite Toxicity 

OH-Radical-Type Reactive Oxygen Species: A Short Review on the Mechanisms of OH-Radical-and Peroxynitrite Toxicity 

O H has a very positive redox potential (close to +2V) and a life time of approximately 1 [isec thus reacting closely to the site of its generation producing “site specific” oxidative damage. The oxygen species O H is the major target of the anti­ oxidative power of phenolics: due to its kinetic properties, OH is a reactive oxygen species not under the control of specific enzymes and/or de­ toxification chains. Since superoxide is able to re- ductively release iron ions from transport mole­ cules such as ferritin or transferrin or from hemoglobin, Fenton- or Haber-Weiss-chemistry is of utmost relevance in a wealth of disease pro­ cesses such as inflammation.
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Erythrocyte metabolism, oxygen delivery, and hypertensive kidney disease

Erythrocyte metabolism, oxygen delivery, and hypertensive kidney disease

Theoretically, oxygen consumption and oxygen supply could be tweaked to improve renal oxygenation. In fact, mechanisms regulation renal oxygen consumption have been an important scientific focus in recent years. For example, worsened renal energy ef ficiency through mitochondrial uncoupling has been observed in diabetic kidney disease [8]. Conversely, more efficient mitochondria convey renal hypoxia toler- ance in animals [9]. In many organs, increased perfusion is the prime mechanism matching oxygen supply to increased oxygen demand. In the kidney, however, increased perfusion results in concomitant increases in glomerular solute filtration. Filtered solutes have to be reclaimed through
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Reactive oxygen species in iridium-based OER catalysts

Reactive oxygen species in iridium-based OER catalysts

assumed the product desorbs from the surface aer forming, an assumption we will show to be valid. It is then straightforward to compute the heat of reaction for this process for different types of oxygen species by way of DFT (see ESI† for details), as the energies of the gas phase reactant and product are constants and only the adsorption energy of the oxygen species involved in the reaction changes the heat evolved (using the positive sign convention of microcalorimetry). And while we do not know the structure of the amorphous IrO x , we can use model systems to
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OH-Radical-Type Reactive Oxygen Species Derived from Superoxide and Nitric Oxide: A Sensitive Method for their Determination and Differentiation 

OH-Radical-Type Reactive Oxygen Species Derived from Superoxide and Nitric Oxide: A Sensitive Method for their Determination and Differentiation 

Reactive Oxygen Species, Peroxynitrite, Fenton-Type Oxidants Reactive oxygen species are involved in many diseases where the radical species O H . peroxynitrite and the non-radical, hypochlorous acid, play an outstanding role. The formation of O H -type oxidants is essentially confined to a few types of reactions. The most prominent ones are the one-electron reduction of hydrogen peroxide by Fe2+ or Cu+- ions (Fenton- type reactions), reaction of hypochlorite with superoxide and finally formation and decay of peroxynitrite (O N O O H ), formed from superoxide and NO. In this communication we wish to report on a simple model system allowing to differentiate between these ROS: ethene formation from ACC is only detectable in the presence of hypochlorite (v. Kruedener et al.,
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The effect of reactive oxygen species and smoking on the spermatozoa quality and outcome of patients undergoing IVF/ICSI therapy

The effect of reactive oxygen species and smoking on the spermatozoa quality and outcome of patients undergoing IVF/ICSI therapy

induces DNA damage in spermatozoa and in generated preimplantation embryos. Also, nicotine at a concenteration of 10mM for 24 hours resulted in the formation of definite fragmentation which could be seen via electrophoresis as a characteristic ladder pattern and 5mM nicotine treatment for 24 hours showed week intensity of DNA laddering (Khae-hawn et al., 2005). Moreover, Cigarette smoking is significantly correlated with increased levels of seminal oxidative stress, as evidenced by a significant reduction in Reactive Oxygen Species-Total Antioxidant Capacity score (ROS-TAC). To strengthen the above hypothesis, it should be emphasized that cigarette smoke has been associated with increased frequency of aneuploidy in sperm (Twigg et al., 1998a;b), lower seminal plasma antioxidant levels and increased oxidative damage to DNA (Fraga et al., 1996; Shen et al., 1997). It is concluded that certain life style factors, such as tobacco smoking, may reduce the antioxidant capacity of seminal plasma and impair the secretion of accessory sex glands (Depuydt et al., 1996; Klinefelterand Hess, 1998). The seminal plasma protects spermatozoa from excessive ROS by means of small molecular weight free radical scavengers, such as Ascorbate and Tocopheral, Uric acid and ROS-metabolizing enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase (Alvarez and Storey, 1989). ROS-TAC scores decrease as a result of an imbalance between levels of ROS and antioxidants in semen (Sharma et al., 1999).
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