During pneumococcal pneumonia, NADPH oxidase-derived reactive oxygen species are redundant for host defense but limit neutrophil recruitment and survival. Decreased NADPH oxidase-dependent reactive oxygen species production is well tolerated and improves disease outcome during pneumococcal pneumonia by removing neutrophils from the tight constraints of reactive oxygen species-mediated regulation.. ...
Asthma is a chronic inflammatory airway disease induced by many environmental factors. The inhalation of allergens and pollutants promote the reactive oxygen species (ROS) production leading to airway inflammation, hyper-responsiveness and remodeling in allergic asthma. The effects of asthma medications on ROS production are unclear. The present study investigated the anti-ROS effects of current asthma medications including inhaled corticosteroid (ICS; budesonide and fluticasone), leukotriene receptor antagonist (LTRA; montelukast), long acting β2 agonists (LABAs; salmeterol and formoterol) and a new extra-LABA (indacaterol). The human monocyte cell line THP-1 cells were pre-treated with different concentrations of the asthma medications at different time-points after hydrogen peroxide (H2O2) stimulation. H2O2 production was measured with DCFH-DA by flow cytometry. Montelukast, fluticasone and salmeterol suppressed H2O2-induced ROS production. Indacaterol enhanced H2O2-induced ROS production.
Toyokuni, S. (1999), Reactive oxygen species-induced molecular damage and its application in pathology. Pathology International, 49: 91-102. doi: 10.1046/j.1440-1827.1999.00829.x ...
Mitochondria are the major cellular producers of reactive oxygen species (ROS), and mitochondrial ROS production increases steeply with increased proton-motive force. The uncoupling proteins (UCP1, UCP2, and UCP3) and adenine nucleotide translocase induce proton leak in response to exogenously added fatty acids, superoxide, or lipid peroxidation products. "Mild uncoupling" by these proteins may provide a negative feedback loop to decrease proton-motive force and attenuate ROS production. Using wild-type and Ucp3(-/-) mice, we found that native UCP3 actively lowers the rate of ROS production in isolated energized skeletal muscle mitochondria, in the absence of exogenous activators. The estimated specific activity of UCP3 in lowering ROS production was 90 to 500 times higher than that of the adenine nucleotide translocase. The mild uncoupling hypothesis was tested by measuring whether the effect of UCP3 on ROS production could be mimicked by chemical uncoupling. A chemical uncoupler mimicked the ...
Dysregulation of apoptosis is a prime hallmark of leukemia. Therefore, drugs which restore the sensitivity of leukemic cells to apoptotic stimuli are promising candidates in the treatment of leukemia. The main objective of this dissertation was to examine the antileukemic effect of sanguinarine, in vitro, and to further examine the signaling mechanisms that may be involved. This study demonstrates that in human leukemic cells, sanguinarine activates a caspase-dependent apoptotic cell death pathway that is characterized by reactive oxygen species-dependent ceramide generation, and subsequent inhibition of Akt signaling pathway. In addition, sanguinarine also induces reactive oxygen species-dependent glutathione depletion and activation of extracellular signal-regulated kinase1/2. Moreover, inhibition of reactive oxygen species generation, using reactive oxygen species scavengers and antioxidants, significantly abrogates sanguinarine-induced ceramide generation, Akt dephosphorylation, extracellular signal
... : Effect of CAgNCs on ROS production in V. tapetis cells. Intracellular ROS generation was determined by the flow cytometry using H2DCFDA. A: concentration dependent ROS production; B: time dependant ROS production ...
The Impact of Various Reactive Oxygen Species on the Formation of Neutrophil Extracellular Traps. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
In this study PI3-kinase was found to play a role in regulating NADPH oxidase-generated superoxide in platelets, altering the bioactivity of platelet NO that contributes to platelet disaggregation. The progressive reversal of aggregation following initial aggregation as the result of PI3-kinase inhibition in stimulated platelets is consistent with the findings of previous studies.2 Given that disaggregation resulting from PI3-kinase inhibition in TRAP-stimulated platelets correlated with a dose-dependent inhibition of the integrin GPIIb-IIIa activation,2 the activation of PI3-kinase is considered essential for maintaining GPIIb-IIIa in its activated state to sustain aggregation. Likewise, the ability of NO donors to induce platelet disaggregation has been linked to the diminished activation of GPIIb-IIIa and fibrinogen binding.29 The stimulation of platelets induces a conformational change in GPIIb-IIIa (inside-out signaling) leading to the binding of soluble fibrinogen and the onset of platelet ...
Reactive oxygen species (ROS) are constantly generated and eliminated in the biological system, and play important roles in a variety of normal biochemical functions and abnormal pathological processes (16). Mitochondria are considered the major source of cellular ROS (and are likely to play a significant role in ROS stress in cancer cells (17). Although, increased ROS stress in cancer cells may provide therapeutic strategies by further increasing ROS to kill cancer cells using pharmacological agents (18), ROS take part in survival signal activation and under persistent endogenous ROS stress cells become resistant (19). In the present study E2 was shown that be able to increased OVCAR-3 cell proliferation, which is evident by increased cell viability. It also induced intracellular ROS generation in a dose dependent manner. Interestingly, the optimal dose of E2 which was most effective on cell viability, caused the highest ROS generation in these cell. On the other hand, treatment of cells with ...
AIMS/HYPOTHESIS: The aim of this study was to perform a detailed analysis of cytokine toxicity in the new human EndoC- H1 beta cell line. METHODS: The expression profile of the antioxidative enzymes in the new human EndoC- H1 beta cells was characterised and compared with that of primary beta cells in the human pancreas. The effects of proinflammatory cytokines on reactive oxygen species formation, insulin secretory responsiveness and apoptosis of EndoC- H1 beta cells were determined. RESULTS: EndoC- H1 beta cells were sensitive to the toxic action of proinflammatory cytokines. Glucose-dependent stimulation of insulin secretion and an increase in the ATP/ADP ratio was abolished by proinflammatory cytokines without induction of IL-1 expression. Cytokine-mediated caspase-3 activation was accompanied by reactive oxygen species formation and developed more slowly than in rodent beta cells. Cytokines transiently increased the expression of unfolded protein response genes, without inducing endoplasmic ...
In the present study, we have demonstrated that the function of both BKCa and SKCa channels in uterine arteries of pregnant animals is suppressed by heightened oxidative stress during chronic hypoxia. Our results suggest that chronic hypoxia-induced oxidative stress exerts its adverse effect on KCa channel-mediated relaxations of uterine arteries through suppressing steroid hormone-induced upregulation of KCa channel activities. These findings provide strong evidence that heightened ROS is a common mechanism to impair BKCa and SKCa channel function in uterine arteries and contributes to the dysfunction of uterine circulation caused by chronic hypoxia during gestation.. Consistent with our previous studies,6 the present finding that both NS1619- and NS309-induced relaxations of uterine arteries were significantly attenuated by chronic hypoxia in pregnant animals, further suggesting that chronic hypoxia downregulates both BKCa and SKCa channel activities. However, the molecular mechanisms ...
Background: During myocardial ischemia/reperfusion injury, a burst of reactive oxygen species (ROS) is considered to occur at the onset of reperfusion and cause cardiomyocyte death through the loss of mitochondrial membrane potential (ΔΨm), but there are evidences against this concept. We aimed to visualize the dynamic changes of ROS during ischemia/reperfusion in intact rat hearts using two-photon laser scanning microscopy.. Methods and Results: Langendorff-perfused rat hearts were loaded with 5-(and -6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate acetyl-ester and tetramethylrhodamine ethyl-ester, fluorescent indicators of ROS and ΔΨm, respectively. Under the two-photon excitation, spatio-temporal changes of ROS and ΔΨm in response to ischemia/reperfusion were simultaneously monitored at cellular level. As soon as ischemia started, ROS level of each cell began to increase, despite maintained ΔΨm. Importantly, the rate of ROS accumulation during the early phase of ...
We provided evidence in the present report suggesting that treatment of the BEAS-2B cells with continuous low concentration of As3+ induces cell transformation and that the capacity of ROS generation in the transformed cells was severely compromised. Such a reduction in ROS generation seems to be responsible for fast proliferation, anchorage-independent growth, and resistance to As3+ toxicity of the transformed cells. A sustained alternative activation of NF-κB might contribute to the fast and anchorage-independent growth of these cells due to reduced ROS generation. The fast growth of the transformed cells could be reversed by either resuming the ROS production through SOD2/catalase inhibition or gene silencing of NF-κB p105/50.. ROS have long been viewed as major contributors to oxidative injury and DNA damage of tissues or cells (22). A sustained oxidative injury and unrepaired damage on DNA will be carcinogenic due to accumulation of genetic mutations that either activate oncogenes or ...
Scientists have identified a new type of anti-inflammatory compound that may be useful in treating a wide range of conditions, including neurodegenerative and autoimmune diseases. These compounds inhibit the enzyme Nox2, part of a family of enzymes responsible for producing reactive oxygen species.
OBJECTIVE: To obtain further insight into the mechanism underlying the vasodilator effect of nebivolol. Since oxidative inactivation of nitric oxide (NO) is regarded as an important cause of its decreased biological activity, we studied (1) the effect of nebivolol on some oxidative parameters in essential hypertensive patients; (2) the effect of plasma of nebivolol-treated patients on reactive oxygen species production and NO availability in endothelial cells. METHODS: A total of 20 healthy subjects and 20 matched essential hypertensive patients treated with atenolol or nebivolol according to a double-blind, randomized design participated in the study. We measured low-density lipoprotein (LDL) and plasma hydroperoxides, 8-isoprostanes, oxidized LDL, susceptibility of LDL to oxidation (lag phase) and LDL vitamin E and the effect of plasma of nebivolol- and atenolol-treated patients on reactive oxygen species production and NO availability in endothelial cells exposed to oxidative stress. RESULTS: ...
Schoultz I, McKay CM, Graepel R, Phan VC, Wang A, Soderholm J, McKay DM. Indomethacin-induced translocation of bacteria across enteric epithelia is reactive oxygen species-dependent and reduced by vitamin C. Am J Physiol Gastrointest Liver Physiol 303: G536-G545, 2012. First published June 14, 2012; doi:10.1152/ajpgi.00125.2012.-The enteric epithelium must absorb nutrients and water and act as a barrier to the entry of luminal material into the body; this barrier function is a key component of innate immunity. Nonsteroidal anti-inflammatory drug (NSAID)-induced enteropathy occurs via inhibition of prostaglandin synthesis and perturbed epithelial mitochondrial activity. Here, the direct effect of NSAIDs [indomethacin, piroxicam (cyclooxygenase 1 and 2 inhibitors), and SC-560 (a cyclooxygenase 1 inhibitor)] on the barrier function of human T84 epithelial cell line monolayers was assessed by transepithelial electrical resistance (TER) and internalization and translocation of a commensal Escherichia ...
Reactive oxygen species are produced during normal ovarian function, and they may also be produced as a result of toxicant metabolism. Our earlier work demonstrated a role for reactive oxygen species in mediating spontaneous apoptosis in follicles deprived of hormonal support and apoptosis caused by exposure to ovarian toxicants. We discovered that reactive oxygen species increased in ovarian follicles cultured without gonadotropin support prior to any increase in endpoints of apoptosis and that follicle stimulating hormone stimulated synthesis of the antioxidant glutathione (GSH) and suppressed the rise in reactive oxygen species. We further showed that GSH depletion in cultured follicles reversed the protective, suppressive effect of follicle stimulating hormone on reactive oxygen species and on apoptosis. This work provides evidence that the protective effects of follicle stimulating hormone are mediated in part via upregulation of GSH synthesis. We also showed that increased generation of ...
Am J Clin Exp Urol 2013;1(1):39-52 www.ajceu.us /ISSN:2330-1910/AJCEU1311005 Original Article Prostate-associated gene 4 (PAGE4) protects cells against stress by elevating p21 and suppressing reactive oxygen species production Yu Zeng1,3, Dong Gao1, John J Kim1,5, Takumi Shiraishi1, Naoki Terada1, Yoshiyuki Kakehi4, Chuize Kong3, Robert H Getzenberg1, Prakash Kulkarni1,2 Department of Urology, The James Buchanan Brady Urological Institute, 2Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland; 3Department of Urology, Institute of Urology, The First Hospital, China Medical University, Shenyang, China; 4Department of Urology, Kagawa University Faculty of Medicine, Kita-gun, Kagawa, Japan; 5Current address: University of California, Berkeley and University of California, San Francisco Graduate Program in Bioengineering, USA 1 Received November 28, 2013; Accepted December 22, 2013; Epub December 25, 2013; Published December 30, 2013 Abstract: Background: It is ...
... Free Radic Res. 2019 Oct 21;:1-11 Authors: Guo J, Xu H, Liu S, Wang Z, Dai Y, Lu J, Zheng S, Xu D, Zhou J, Ke L, Cheng X, Xu M, Zhang X, Guo Y, Lin Y, Ding W, Gao G, Wang H, Chen Q, Yu X, Chen H, Qin L, Sun X, Li Z, Zheng S, Wang J, Cheng Y, Qiu S, Hu Y, Huang P, Lin C, Wu Q, Li Y, Chen T, Shaw C,...
Rationale: Cardiac lipotoxicity, characterized by increased uptake, oxidation and accumulation of lipid intermediates, contributes to cardiac dysfunction in obesity and diabetes. However, mechanisms linking lipid overload and mitochondrial dysfunction are incompletely understood. Objective: To elucidate the mechanisms for mitochondrial adaptations to lipid overload in postnatal hearts in vivo. Methods and Results: Using a transgenic mouse model of cardiac lipotoxicity overexpressing long-chain acyl-CoA synthetase 1 in cardiomyocytes, we show that modestly increased myocardial fatty acid uptake leads to mitochondrial structural remodeling with significant reduction in minimum diameter. This is associated with increased palmitoyl-carnitine oxidation and increased reactive oxygen species (ROS) generation in isolated mitochondria. Mitochondrial morphological changes and elevated ROS generation are also observed in palmitate-treated neonatal rat ventricular cardiomyocytes (NRVCs). Palmitate exposure ...
Poster (2013, September 11). Neutrophils (PMNs) produce reactive oxygen species (ROS) to kill pathogenic agents. After appropriate stimulation, leading to the activation of protein kinase C (PKC), the cytosolic subunits of the NADPH ... [more ▼]. Neutrophils (PMNs) produce reactive oxygen species (ROS) to kill pathogenic agents. After appropriate stimulation, leading to the activation of protein kinase C (PKC), the cytosolic subunits of the NADPH oxidase (Nox2) are phosphorylated and translocated to the membrane flavocytochrome b558, forming the active enzyme which produces superoxide anion (O2●-). From O2●- derives H2O2 used by the PMNs myeloperoxidase (MPO) to form strong oxidant species. Many human and animal pathologies with fatal issue are associated with uncontrolled activation of PMNs. The modulation of enzymes implied in ROS production is thus a primary target to manage excessive inflammatory events. For this purpose, we evaluated the effects of NDS27, a water-soluble salt of ...
Traditionally, reactive oxygen species (ROS) have been regarded as toxic by-products of aerobic metabolism. However, in recent years it has become apparent that plants actively produce ROS as signalling molecules. ROS are able to mediate adaptive responses to various environmental stresses as well as processes such as stomatal closure and development. Downstream signalling events that are modulated by ROS include calcium mobilisation, protein phosphorylation and gene expression. This study investigated signalling proteins acting downstream of ROS, in order to understand how ROS are perceived and transduced to elicit such a wide range of responses. To establish a molecular profile provoked by ROS, a microarray experiment of Arabidopsis plants exposed to exogenous H(_2)O(_2) was analysed. Of the 895 differentially expressed transcripts, a substantial proportion had predicted functions in cell rescue and defence, including heat shock, disease resistance and antioxidant genes. Genes encoding ...
The production of ROS is known to be increased in diabetic patients (20), and such an increase may contribute to the development of diabetes complications (21,22). In addition, we previously proposed that hyperglycemia-induced ROS production from the mitochondria electron transport chain was a key event in the development of diabetes complications (6,23). In this study, we first confirmed that metformin, which has been reported to exert a possible additional benefit in the prevention of diabetes complications independently of its antihyperglycemic effect (8,24,25), inhibited the hyperglycemia-induced intracellular ROS production as measured by H2DCF-DA and the mtROS production as measured by the MitoTracker Red probe (26). The fluorescence of H2DCF-DA indicates intracellular ROS production (7). In contrast, the reduced MitoTracker Red probe can specifically detect mtROS, since this probe accumulates inside mitochondria and is oxidized predominantly by reactions involving hydrogen peroxide ...
Oxygen is one of the most important molecules on Earth mainly because of the biochemical symmetry of oxygenic photosynthesis and aerobic respiration that can maintain homeostasis within our planet's biosphere. Oxygen can also produce toxic molecules, reactive oxygen species (ROS). ROS play a dual role in biological systems, since they can be either harmful or beneficial to living systems. They can be considered a double-edged sword because at moderate concentrations, nitric oxide (NO•), superoxide anion, and related reactive oxygen species play an important role as regulatory mediators in signalling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and re-establish redox homeostasis. On the other hand, overproduction of ROS has the potential to cause damage. In the recent decades, ROS has become a focus of interest in most biomedical disciplines and many types of clinical research. Increasing evidence from research on several diseases ...
How to measure reactive oxygen species using a specific fluorescent dye/indicato - posted in Biochemistry: When a fluorescent dye/indicator is added to a cell culture to show the ROS in the culture, how can the amount of reactive oxygen species be estimated or determined? Is there an easy method, possibly not costly? Thanks for the responses!
Background: Increasing evidence indicates that mitochondrial-derived reactive oxygen species (ROS) and cellular apoptosis contribute to the pathogenesis of cardiac dysfunction. Mitochondrial thioredoxin (Trx2) is a key protein regulating cellular redox and survival, However, but its role in normal cardiac growth has not been determined.. Methods and Results: We have generated cardiac-specific Trx2 knockout mice (Trx2-cKO) to determine the physiological importance of the Trx2 system in the heart. Trx2-cKO mice developed a spontaneous dilated cardiomyopathy at 1 month of age with increased heart size, fibrosis, reduced ventricular wall thickness, and progressive contractile dysfunction, resulting in death due to heart failure by 4 months of age. Cardiac changes in Trx2-cKO mice were accompanied by disruption of mitochondrial integrity and function, as evident by alterations in mitochondrial number, ultrastructure, membrane potential and ATP production. Increases in ASK1 signaling and ROS ...
Estrogen-mediated high reactive oxygen species (ROS) tolerance plays an important role in driving carcinogenesis. ROS overproduction acts as the significant effector to increase genomic instability...
The aim of this study was to determine the relationship between proliferation inhibition and the production of reactive oxygen species (ROS) induced by Licochalcone A (LCA). Cell viability was evaluated using sulforhodamine B (SRB) assay. Intracellul
Click to launch & play an online audio visual presentation by Dr. Zhi-Qing Zhao on Reactive oxygen species and myocardial apoptosis, part of a collection of online lectures.
Elevated cellular reactive species, which can be produced by diabetic serum conditions such as elevated inflammatory cytokines, lipotoxicity or glucotoxicity contribute to islet beta cell dysfunction and cell death. Cellular pathways that result in beta cell oxidative stress are poorly resolved. In this study, stimulation of human donor islets, primary mouse islets or homogeneous beta cell lines with a cocktail of inflammatory cytokines (TNFα, IL-1β, and INFγ) significantly induced NADPH oxidase-1 (NOX-1) gene expression (p,0.05). This pro-inflammatory cytokine cocktail concomitantly induced loss of islet glucose stimulated insulin response (p,0.05), elevated expression of MCP-1 (p,0.01), increased cellular reactive oxygen species (ROS) and induced cell death. Inhibitors of NADPH oxidase, apocynin and diphenyleneiodonium, and a dual selective NOX1/4 inhibitor, blocked ROS generation (p,0.01) and induction of MCP-1 (p,0.05) by pro-inflammatory cytokines in beta cells. It has previously been ...
The role of miR-451 in certain cardiac diseases was recently reported including ischemia/reperfusion and hypertrophic cardiomyopathy. Oxidative stress is known to involve in the above diseases. Currently the relationship between miR-451 and cardiac oxidative stress is unknown. We thus hypothesize that miR-451 act as a key mediator for cardiac hypertrophy via regulating myocardial ROS level and antioxidant pathways. We first compared the heart/body weight (HW/BW) ratio between age- & gender-matched miR-451 knockout (KO) and wild-type (WT) mice. Increase of HW/BW was found in KO mice (6.1±0.1 vs 4.8±0.1 mg/g in WT, p,0.01). Expression of fetal genes ANF (2.9-fold↑) and β-MHC (4.0-fold↑) was also significantly increased in KO hearts, as well as the ROS level (2.3-fold↑, p,0.05) in KO hearts. Consistently, both the protein expression and activation levels of the oxidation-regulating gene Nrf2 decreased the same extent (~33%↓, p,0.05) in KO hearts. In contrast, the protein expression of ...
Hypothalamus is a key area involved in the control of metabolism and food intake via the integrations of numerous signals (hormones, neurotransmitters, metabolites) from various origins. These factors modify hypothalamic neurons activity and generate adequate molecular and behavioral responses to control energy balance. In this complex integrative system, a new concept has been developed in recent years, that includes reactive oxygen species (ROS) as a critical player in energy balance. ROS are known to act in many signaling pathways in different peripheral organs, but also in hypothalamus where they regulate food intake and metabolism by acting on different types of neurons, including proopiomelanocortin (POMC) and agouti-related protein (AgRP)/neuropeptide Y (NPY) neurons. Hypothalamic ROS release is under the influence of different factors such as pancreatic and gut hormones, adipokines (leptin, apelin,...), neurotransmitters and nutrients (glucose, lipids,...). The sources of ROS production are
Oxidative stress figures prominently in retinal diseases, including diabetic retinopathy, and glaucoma. Ligands for σ1R, a unique transmembrane protein localized to the endoplasmic reticulum, mitochondria, and nuclear and plasma membranes, have profound retinal neuroprotective properties in vitro and in vivo. Studies to determine the mechanism of σ1R-mediated retinal neuroprotection have focused mainly on neurons. Little is known about the effects of σ1R on Müller cell function, yet these radial glial cells are essential for homeostatic support of the retina. Here we investigated whether σ1R mediates the oxidative stress response of Müller cells using wild-type (WT) and σ1R-knockout (σ1RKO) mice. We observed increased endogenous reactive oxygen species (ROS) levels in σ1RKO Müller cells compared to WT, which was accompanied by decreased expression of Sod1, catalase, Nqo1, Hmox1, Gstm6, and Gpx1. The protein levels of SOD1, CAT, NQO1, and GPX1 were also significantly decreased. The ...
We demonstrate in this article that 10 weeks of exposure to concentrated ambient PM2.5 potentiates hypertension in response to AII and alters vasoconstrictor/vasodilator sensitivity. These alterations were accompanied by increased NAD(P)H oxidase and NOS-dependent generation of O2·− and upregulation of the RhoA/ROCK pathway.. Because exposure to PM2.5 alone did not alter BP, we did not pursue additional investigations in the PM2.5 group alone and investigated the impact of PM2.5 in conjunction with AII. An additional reason to examine the effect of PM2.5 in conjunction with AII is prior observations by us and others that suggest that PM2.5 has minimal effects by itself, but actively synergizes with other risk factors to influence outcomes.3,6,9,10 Our data are consistent with this notion and suggest that although PM2.5 by itself had no discernible impact on BP, has an important effect in potentiating it, presumably by "sensitizing" the vasculature. The AII infusion model is a well ...
The article by Sukumar et al. (1) published in a recent issue of Diabetes concludes that the type 2 NADPH oxidase (Nox2) plays a critical role in insulin resistance-related endothelial dysfunction. However, in our opinion it is too premature to draw these conclusions when looking at the entire body of available literature. The authors show in two different genetic mouse models of insulin resistance a blunted endothelium-dependent aortic relaxation to acetylcholine that can be reversed to normal both in vitro and in vivo by applying the peptide gp91ds-tat, which interferes with protein-protein interactions during Nox2 activation. Similarly, knockout of Nox2 in one of the genetic models of insulin resistance improved aortic vascular function and reduced reactive oxygen species formation in pulmonary tissues. The effects of the other vascular Nox isoforms in the mouse, Nox1 and 4, were not studied.. Our group has recently studied all Nox isoforms in one model of diabetic vascular complications ...
Our data show that disulfide bonds between C-terminal cysteines link ASIC1a subunits. This was a surprising discovery because previous data showed that the C terminus was not required to form an ASIC1 structure (4), and we found that C-terminal cysteines were not needed to produce ASIC1a trimers on the cell surface or to generate functional channels. However, the C-terminal cysteines were a target for the oxidant H2O2; it induced inter-subunit links, reducing the amount of ASIC1a present on the cell surface and the H+-activated current.. Our data, combined with previous studies, indicate that H2O2 and other oxidants can regulate ASIC1a in at least 2 ways. Earlier work showed that oxidants decreased current amplitude, and the studies suggested that the modification was in the extracellular or transmembrane domains of ASIC1a (26, 27). We found a similar response to H2O2, an endogenous reactive oxygen species. Because H2O2 inhibited an ASIC1a variant that lacked intracellular cysteines, our data ...
In our studies, we showed that inhibition of LPS-stimulated ROS production in BMDM also selectively inhibited the production of PGD2, but not its isomer PGE2. LPS-induced PGD2 production in BMDM was mediated via H-PGDS isomerase, but not L-PGDS. LPS-induced H-PGDS-mediated PGD2 production was sensitive to and dependent on the NOX-generated ROS in BMDM. In contrast, the LPS-induced PGE2 production in BMDM was ROS independent.. To our knowledge, this is the first report of the role of ROS in differential regulation of LPS-induced PGD2 and PGE2 production. The novel finding of our study is that the modulation of intracellular ROS levels in macrophages could selectively regulate LPS-induced production of PGD2, but not PGE2. Therefore, it is impossible that the ROS or any NOX/ROS inhibitors exert their selective effects on PGD2 production via the modification of COX-2 enzyme in BMDM. If there is any modifications of the COX-2 protein expression or its enzyme activity by the above inhibitors or H2O2, ...
Exposure to radiation can lead to deficits in cognitive function, including impairments in hippocampal-dependent learning and memory. However, not all individuals exposed to irradiation develop cognitive impairments, suggesting the involvement of genetic risk factors. Apolipoprotein E (apoE), a protein important for neuronal repair, might influence susceptibility to developing radiation-induced cognitive impairments. Humans express three major apoE isoforms, apoE2, apoE3 and apoE4. Compared to apoE3, apoE4 increases the risk to develop Alzheimers disease while apoE2 decreases this risk. ApoE4 is also associated with cognitive deficits following neurotrauma. Moreover, deficiency of apolipoprotein E (apoE) in mice worsens cognitive impairments following irradiation. There might also be sex differences in the risk for developing radiation-induced cognitive impairments. In both humans and rodents, females are more susceptible to the effects of irradiation on cognition than males. The neur
Mary Beckman http://sageke.sciencemag.org/cgi/content/abstract/sageke;2001/9/nw30 Key Words: oxidative stress isp-1 reactive oxygen species life-span worm. Abstract: Some people think stress kills--and the image of the businessman nearly popping his jugular isnt all theyre thinking about. Researchers have long pursued the connection between oxidative stress and aging. While generating the adenosine triphosphate that powers the cell, mitochondria also give birth to the byproduct superoxide, a highly reactive oxygen radical that can damage other molecules. To protect the cell, resident enzymes turn superoxide into the slightly less obnoxious peroxide and then into innocuous water--but they dont neutralize it all. Some researchers propose that the havoc wreaked by these reactive oxygen species (ROS) promotes aging (see "The Two Faces of Oxygen"), based in part on observations that an antioxidant drug and mutations that disrupt global energy-producing activities can extend worm and yeast ...
The activation of nuclear factor of activated T cells 5(NFAT5), a well-known osmoprotective factor, can be induced by isotonic stimuli, such as activated Toll-like receptors (TLRs). It is unclear, however, how NFAT5 discriminates between isotonic and hypertonic stimuli. In this study we identified a novel context-dependent suppression of NFAT5 target gene expression in RAW 264.7 macrophages stimulated with lipopolysaccharide (LPS) or a high salt (NaCl) concentration. Although LPS and NaCl both used NFAT5 as a core transcription factor, these stimuli mutually inhibited distinct sets of NFAT5 targets within the cells. Although reactive oxygen species (ROS) are essential for this inhibition, the source of ROS differed depending on the context: mitochondria for high salt and xanthine oxidase for TLRs. Specifically, the high salt-induced suppression of interleukin-6 (IL-6) production was mediated through the ROS-induced inhibition of NFAT5 binding to the IL-6 promoter. The context-dependent ...
Generation of reactive oxygen species in murine macrophages.To assess the influence of mono-MP on the generation of intracellular oxidative stress in macrophage
1. Sugar can suppress your immune system.. 2. Sugar upsets the mineral relationships in the body.. 3. Sugar can cause juvenile delinquencey in children.. 4. Sugar eaten pregnancy and lactation can influence muscle force production in offspring, which can affect an individuals ability to exercise.. 5. Sugar in soda, when consumed by children, results in the children drinking less milk.. 6. Sugar can elevate glucose and insulin responses and return them to fasting levels slower in oral contraceptive users.. 7. Sugar can increase reactive oxygen species (ROS), which can damage cells and tissues.. 8. Sugar can cause hyperactivity, anxiety, inability to concentrate and crankiness in children.. 9. Sugar can produce a significant rise in triglycerides.. 10. Sugar reduces the bodys ability to defend against bacterial infection.. 11. Sugar causes a decline in tissue elasticity and function - the more sugar you eat, the more elasticity and function you lose.. 12. Sugar reduces high-density lipoproteins ...
A receptor called TRPM2 acts as an ROS sensor or gauge inside the neutrophil. When ROS levels are low, the neutrophil is on the move, looking for infections to fight. As the neutrophil nears a wound site and begins to encounter foreign particles or bacteria, it engulfs them and generates a killing burst of ROS to destroy the captured enemy. TRPM2 senses these consistent, high levels of ROS inside the cell and puts the neutrophil in park, so the cell stays in place to continue killing invading microbes. The neutrophil senses a dramatic increase in reactive oxygen species as it gets closer to the wound site, and this triggers the shutdown of the migration of the cell, said Jingsong Xu, assistant professor of pharmacology in the UIC College of Medicine and corresponding author on the paper. Once the neutrophil ceases moving, it just kills one bacteria or pathogen after another - and can concentrate on doing its job of cleaning up the site, Xu said. To shut down migration, TRPM2 must be ...
Hydrogen water as a new therapeutic antioxidant has been widely used in living organisms under stress. In this study, we applied nanobubble (NB) technology to hydrogen water. The antioxidant capacity of hydrogen NB water was studied with respect to different reactive oxygen species (ROS) both in vit …
Negative regulator of reactive oxygen species (ROS) that limits ROS production by phagocytes during inflammatory response, thereby playing a role during host defense. Acts via direct interaction with CYBB/NOX2 monomer that impairs interaction between CYBB/NOX2 and CYBA/p22-phox and formation of a stable NOX2 complex (By similarity). May play a critical role in desensitizing TLR signaling through inhibition of Toll-like receptor-mediated NF-kappa-B activation and cytokine production.
Reactive Oxygen Species in Plants: Boon Or Bane - Revisiting the Role of ROS begins by presenting the basic introduction to ROS and deciphers the detailed knowledge in ROS research. It then examines the broad range of ROS signaling mechanisms as well as how they may be beneficial for plants and human beings. This book also describes both the bane and boon aspects of ROS with their impact on plants, and how the recent revelations have compelled us to rethink ROS turning from stressors to plant regulators ...
Exendin-4 Protects Mitochondria from Reactive Oxygen Species Induced Apoptosis in Pancreatic Beta Cells. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Pharmacological approaches also suggest that different parts of the overall ROS production in response to infection appear to be mediated by different mechanisms. Though the involvement of an NADPH oxidase has been predominant in most cases (Bolwell et al., 1998; Grant et al., 2000b; Torres and Dangl, 2005), both NADPH oxidases and cell wall peroxidases might mediate ROS production in response to the same pathogen (Grant et al., 2000a). A more detailed temporal resolution of the activity of each system may reveal that the pools of ROS produced by each mechanism do not functionally overlap. For example, differential effects of DPI on ROS accumulation during the HR- and MAMP-mediated basal defense responses were reported, with the latter being considerably less attenuated by DPI (Soylu et al., 2005). These results suggest that alternative mechanisms might be activated to produce ROS during some basal defense responses, while NADPH oxidases might have later effects following R-mediated pathogen ...
Pharmacological approaches also suggest that different parts of the overall ROS production in response to infection appear to be mediated by different mechanisms. Though the involvement of an NADPH oxidase has been predominant in most cases (Bolwell et al., 1998; Grant et al., 2000b; Torres and Dangl, 2005), both NADPH oxidases and cell wall peroxidases might mediate ROS production in response to the same pathogen (Grant et al., 2000a). A more detailed temporal resolution of the activity of each system may reveal that the pools of ROS produced by each mechanism do not functionally overlap. For example, differential effects of DPI on ROS accumulation during the HR- and MAMP-mediated basal defense responses were reported, with the latter being considerably less attenuated by DPI (Soylu et al., 2005). These results suggest that alternative mechanisms might be activated to produce ROS during some basal defense responses, while NADPH oxidases might have later effects following R-mediated pathogen ...
Annexin A2 (AnxA2) is a multi-functional and -compartmental protein whose subcellular localisation and functions are tightly regulated by its post-translational modifications. AnxA2 and its Tyr23-phosphorylated form (pTyr23AnxA2) are involved in malignant cell transformation, metastasis and angiogenesis. Here, we show that H2O2 exerts rapid, simultaneous and opposite effects on the Tyr23 phosphorylation status of AnxA2 in two distinct compartments of rat pheochromocytoma (PC12) cells. Reactive oxygen species induce dephosphorylation of pTyr23AnxA2 located in the PML bodies of the nucleus, whereas AnxA2 associated with F-actin at the cell cortex is Tyr23 phosphorylated. The H2O2-induced responses in both compartments are transient and the pTyr23AnxA2 accumulating at the cell cortex is subsequently incorporated into vesicles and then released to the extracellular space. Blocking nuclear export by leptomycin B does not affect the nuclear pool of pTyr23AnxA2, but increases the amount of total AnxA2 ...