scholarly journals Reactive oxygen species (ros) scavenger exhibits antinociceptive properties in the rat (sprague-dawley) formalin test

2006 ◽  
Vol 53 (1) ◽  
pp. 26406-26406
Author(s):  
Won Hyung Lee ◽  
Young Ho Lee
Keyword(s):  
Reactive Oxygen Species ◽  
Formalin Test ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Sprague Dawley ◽  
Ros Scavenger

scholarly journals Efek Ekstrak Etanol Daun Gedi Merah (Abelmoschus Manihot (L.) Medik) Terhadap Kadar Superoxide Dismutase Dan Malondialdehyde Jaringan Ginjal Tikus Model Diabetes Melitus Tipe 2

2020 ◽  
Vol 8 (2) ◽  
pp. 83
Author(s):  
Ahmad Fuadi ◽  
Yoyon Arif ◽  
Yudi Purnomo
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Multiple Dose ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Sprague Dawley ◽  
Per Oral ◽  
One Way Anova ◽  
Diabetes Melitus

Hiperglikemia pada Diabetes Melitus (DM) meningkatkan produksi Reactive Oxygen Species (ROS) dan berperan terhadap risiko komplikasi nefropati diabetik. Daun gedi merah (Abelmoschus manihot (L.) Medik) berkhasiat sebagai antidiabetik dan antioksidan tetapi penelitian ekstrak etanol daun gedi merah (EEDGM) untuk mencegah nefropati diabetik belum banyak dilaporkan. Penelitian ini bertujuan untuk mengetahui efek EEDGM terhadap kadar SOD dan MDA ginjal tikus model DM.Metode: Tikus Sprague dawley jantan usia 4-6 minggu dikelompokan menjadi 2 kelompok kontrol dan 3 kelompok perlakuan (n=25 ekor). Tikus DM dibuat dengan diet tinggi lemak-fruktosa (DTLF) dan streptozotocin (STZ) 25 mg/kgBB i.p multiple dose. Ekstrak etanol daun gedi merah (EEDGM) diberikan per oral selama 4 minggu. Kadar SOD dan MDA ginjal diukur menggunakan SOD rat kit dan MDA rat kit. Hasil dianalisa dengan One Way Anova dilanjutkan dengan uji BNT (p<0,05).Hasil: Pemberian EEDGM dosis 800 mg/kgBB menghambat penurunan kadar SOD jaringan ginjal dengan persentase sekitar 60% dibandingkan KDM (p<0,05). Pemberian EEDGM dosis 400 mg/kgBB menghambat peningkatan kadar MDA jaringan ginjal dengan persentase sekitar 20% dibandingkan KDM (p<0,05). Induksi DTLF dan STZ menurunkan kadar SOD jaringan ginjal dengan persentase sekitar 40% dan meningkatkan kadar MDA jaringan ginjal dengan persentase sekitar 30%.Kesimpulan: Pemberian EEDGM dapat menghambat penurunan kadar SOD dan peningkatan kadar MDA jaringan ginjal tikus model DM.

scholarly journals Reactive oxygen species are required for spore-wall formation in Physcomitrella patens

Botany ◽  
2020 ◽  
Vol 98 (10) ◽  
pp. 575-587
Author(s):  
Fazle Rabbi ◽  
Karen S. Renzaglia ◽  
Neil W. Ashton ◽  
Dae-Yeon Suh
Keyword(s):  
Reactive Oxygen Species ◽  
Physcomitrella Patens ◽  
Reactive Oxygen ◽  
Spore Wall ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Normal Wall ◽  
Spore Walls ◽  
Ros Scavenger ◽  
Spine Structure

A robust spore wall was a key requirement for terrestrialization by early plants. Sporopollenin in spore and pollen grain walls is thought to be polymerized and cross-linked to other macromolecular components, partly through oxidative processes involving H2O2. Therefore, we investigated effects of scavengers of reactive oxygen species (ROS) on the formation of spore walls in the moss Physcomitrella patens (Hedw.) Bruch, Schimp & W. Gümbel. Exposure of sporophytes, containing spores in the process of forming walls, to ascorbate, dimethylthiourea, or 4-hydroxy-TEMPO prevented normal wall development in a dose, chemical, and stage-dependent manner. Mature spores, exposed while developing to a ROS scavenger, burst when mounted in water on a flat slide under a coverslip (a phenomenon we named “augmented osmolysis” because they did not burst in phosphate-buffered saline or in water on a depression slide). Additionally, the walls of exposed spores were more susceptible to alkaline hydrolysis than those of the control spores, and some were characterized by discontinuities in the exine, anomalies in perine spine structure, abnormal intine and aperture, and occasionally, wall shedding. Our data support the involvement of oxidative cross-linking in spore-wall development, including sporopollenin polymerization or deposition, as well as a role for ROS in intine/aperture development.

Antioxidant effect of pomegranate extract in reducing acute inflammation due to myringotomy

2011 ◽  
Vol 125 (4) ◽  
pp. 370-375 ◽  
Author(s):  
V Kahya ◽  
A Meric ◽  
M Yazici ◽  
M Yuksel ◽  
A Midi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Acute Inflammation ◽  
Histological Study ◽  
Reactive Oxygen ◽  
Inflammatory Cells ◽  
Oxygen Species ◽  
Sprague Dawley ◽  
Randomised Study ◽  
Sprague Dawley Rats ◽  
Reactive Oxygen Species Concentration

AbstractObjective:To assess the effect of pomegranate extract on acute inflammation due to myringotomy.Design:Prospective, randomised study.Subjects:Thirty Sprague–Dawley rats were divided into three groups. Group one constituted controls. Group two underwent myringotomy. Group three underwent myringotomy and also received 100 µl/day pomegranate extract, via gavage, one day before and two days after surgery. Following sacrifice 48 hours after myringotomy, the animals' right ears were used to determine the concentration of reactive oxygen species, using the chemiluminescence method; left ears were used for histological study.Results:Reactive oxygen species levels were significantly decreased in group three compared with group two (p < 0.01). The density of inflammatory cells in group three was significantly less than that in group two (p < 0.01). Lamina propria thickness and vessel density were also significantly decreased in group three compared with group two (p < 0.01).Conclusion:Our results indicate that oral pomegranate extract decreases reactive oxygen species concentration and acute inflammation in the tympanic membrane after myringotomy.

scholarly journals Mitochondrial uncoupling does not decrease reactive oxygen species production after ischemia-reperfusion

2014 ◽  
Vol 307 (7) ◽  
pp. H996-H1004 ◽  
Author(s):  
Ricardo Quarrie ◽  
Daniel S. Lee ◽  
Levy Reyes ◽  
Warren Erdahl ◽  
Douglas R. Pfeiffer ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Sprague Dawley ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Ros ◽  
Ros Formation

Cardiac ischemia-reperfusion (IR) leads to myocardial dysfunction by increasing production of reactive oxygen species (ROS). Mitochondrial H+ leak decreases ROS formation; it has been postulated that increasing H+ leak may be a mechanism of decreasing ROS production after IR. Ischemic preconditioning (IPC) decreases ROS formation after IR, but the mechanism is unknown. We hypothesize that pharmacologically increasing mitochondrial H+ leak would decrease ROS production after IR. We further hypothesize that IPC would be associated with an increase in the rate of H+ leak. Isolated male Sprague-Dawley rat hearts were subjected to either control or IPC. Mitochondria were isolated at end equilibration, end ischemia, and end reperfusion. Mitochondrial membrane potential (mΔΨ) was measured using a tetraphenylphosphonium electrode. Mitochondrial uncoupling was achieved by adding increasing concentrations of FCCP. Mitochondrial ROS production was measured by fluorometry using Amplex-Red. Pyridine dinucleotide levels were measured using HPLC. Before IR, increasing H+ leak decreased mitochondrial ROS production. After IR, ROS production was not affected by increasing H+ leak. H+ leak increased at end ischemia in control mitochondria. IPC mitochondria showed no change in the rate of H+ leak throughout IR. NADPH levels decreased after IR in both IPC and control mitochondria while NADH increased. Pharmacologically, increasing H+ leak is not a method of decreasing ROS production after IR. Replenishing the NADPH pool may be a means of scavenging the excess ROS thereby attenuating oxidative damage after IR.

Abstract 91: Inhibition of Toll-like Receptor 4 Suppresses Reactive Oxygen Species Generation in Diabetic Vasculature

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Maria Alicia Carrillo-Sepulveda ◽  
Camilla Wenceslau ◽  
R. Clinton Webb
Keyword(s):  
Reactive Oxygen Species ◽  
Vascular Dysfunction ◽  
Reactive Oxygen Species Generation ◽  
Vascular Complications ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Oxygen Species ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Tlr4 Signaling

Reactive oxygen species (ROS) are augmented in diabetes and play a central role in vascular dysfunction. TLR4, a key component of the innate immune system, is elevated during diabetes; however, the mechanistic link between TLR4, ROS, and vascular dysfunction remains elusive. Our previous results show that under high glucose (HG), TLR4 is upregulated in vascular smooth muscle cells (VSMCs) and mediates HG-induced ROS production. We hypothesized that TLR4 augments ROS in diabetic resistance vessels, which contributes to vascular dysfunction. To test our hypothesis, streptozotocin (STZ)-induced diabetic Sprague-Dawley rats (65mg/kg; 5weeks) were treated with 50ug/day of CLI-095, an inhibitor of TLR4, over 14 days. Glucose levels were increased (390±13 vs. 97±8.2mg/dL control) and body weight decreased (310±38.4 vs. 385±21g control) in the STZ group. These effects were unchanged by CLI-095 treatment. Mesenteric resistance arteries (MRA) from STZ rats exhibited impaired acetylcholine-induced relaxation (35.26±4.38% vs. 81.83±2.61% control, p<0.05), and CLI-095 treatment ameliorated this effect (71.99±3.48%, p<0.05). Moreover, dihydroethidium staining showed that the increase in ROS due to STZ (1.8 fold vs. control, p<0.05) was attenuated after CLI-095 treatment (1.6 fold vs. STZ, p<0.05). To test if TLR4 signaling is activated in MRA from the STZ rats, MyD88 protein levels, a downstream adaptor molecule, were measured. Arteries from the STZ rats showed increased expression of MyD88 (1.6 fold vs. control, p<0.05) which was reduced after CLI-095 treatment (1.2 fold vs. STZ, p<0.05). Finally, we assessed if TLR4 signaling in VSMCs following HG treatment is altered. Immunoprecipitation showed that HG did not alter the interaction between TLR4 and MyD88 in endothelial cells. In contrast, HG conditions increased TLR4 and MyD88 interaction in VSMCs. Concurrently, HG-induced activation of NFKB in VSMCs was diminished in cells pre-treated with CLI-095. Together our data suggest that activation of TLR4 signaling in VSMCs leads to ROS generation thereby contributing to a reduction in nitric oxide bioavailabitity contributing to endothelial dysfunction in diabetes. Thus, TLR4 is a putative target for the treatment of diabetic vascular complications.

scholarly journals Autophagy controls reactive oxygen species homeostasis in guard cells that is essential for stomatal opening

2019 ◽  
Vol 116 (38) ◽  
pp. 19187-19192 ◽  
Author(s):  
Shota Yamauchi ◽  
Shoji Mano ◽  
Kazusato Oikawa ◽  
Kazumi Hikino ◽  
Kosuke M. Teshima ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stomatal Closure ◽  
Reactive Oxygen ◽  
Guard Cells ◽  
Stomatal Opening ◽  
Glycolate Oxidase ◽  
Oxygen Species ◽  
Ros Accumulation ◽  
Intracellular Ros ◽  
Ros Scavenger

Reactive oxygen species (ROS) function as key signaling molecules to inhibit stomatal opening and promote stomatal closure in response to diverse environmental stresses. However, how guard cells maintain basal intracellular ROS levels is not yet known. This study aimed to determine the role of autophagy in the maintenance of basal ROS levels in guard cells. We isolated the Arabidopsis autophagy-related 2 (atg2) mutant, which is impaired in stomatal opening in response to light and low CO2 concentrations. Disruption of other autophagy genes, including ATG5, ATG7, ATG10, and ATG12, also caused similar stomatal defects. The atg mutants constitutively accumulated high levels of ROS in guard cells, and antioxidants such as ascorbate and glutathione rescued ROS accumulation and stomatal opening. Furthermore, the atg mutations increased the number and aggregation of peroxisomes in guard cells, and these peroxisomes exhibited reduced activity of the ROS scavenger catalase and elevated hydrogen peroxide (H2O2) as visualized using the peroxisome-targeted H2O2 sensor HyPer. Moreover, such ROS accumulation decreased by the application of 2-hydroxy-3-butynoate, an inhibitor of peroxisomal H2O2-producing glycolate oxidase. Our results showed that autophagy controls guard cell ROS homeostasis by eliminating oxidized peroxisomes, thereby allowing stomatal opening.

Specific inhibition of mitochondrial oxidative stress suppresses inflammation and improves cardiac function in a rat pneumonia-related sepsis model

2012 ◽  
Vol 302 (9) ◽  
pp. H1847-H1859 ◽  
Author(s):  
Qun S. Zang ◽  
Hesham Sadek ◽  
David L. Maass ◽  
Bobbie Martinez ◽  
Lisha Ma ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Vitamin E ◽  
Antioxidant Capacity ◽  
Membrane Integrity ◽  
Reactive Oxygen ◽  
Myocardial Inflammation ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Sprague Dawley ◽  
Sepsis Model

Using a mitochondria-targeted vitamin E (Mito-Vit-E) in a rat pneumonia-related sepsis model, we examined the role of mitochondrial reactive oxygen species in sepsis-mediated myocardial inflammation and subsequent cardiac contractile dysfunction. Sepsis was produced in adult male Sprague-Dawley rats via intratracheal injection of S. pneumonia (4 × 106colony formation units per rat). A single dose of Mito-Vit-E, vitamin E, or control vehicle, at 21.5 μmol/kg, was administered 30 min postinoculation. Blood was collected, and heart tissue was harvested at various time points. Mito-Vit-E in vivo distribution was confirmed by mass spectrometry. In cardiac mitochondria, Mito-Vit-E improved total antioxidant capacity and suppressed H2O2generation, whereas vitamin E offered little effect. In cytosol, both antioxidants decreased H2O2levels, but only vitamin E strengthened antioxidant capacity. Mito-Vit-E protected mitochondrial structure and function in the heart during sepsis, demonstrated by reduction in lipid and protein oxidation, preservation of mitochondrial membrane integrity, and recovery of respiratory function. While both Mito-Vit-E and vitamin E suppressed sepsis-induced peripheral and myocardial production of proinflammatory cytokines (tumor necrosis factor-α, interleukin-1β, and interleukin-6), Mito-Vit-E exhibited significantly higher efficacy ( P < 0.05). Stronger anti-inflammatory action of Mito-Vit-E was further shown by its near-complete inhibition of sepsis-induced myeloperoxidase accumulation in myocardium, suggesting its effect on neutrophil infiltration. Echocardiography analysis indicated that Mito-Vit-E ameliorated cardiac contractility of sepsis animals, shown by improved fractional shortening and ejection fraction. Together, our data suggest that targeted scavenging of mitochondrial reactive oxygen species protects mitochondrial function, attenuates tissue-level inflammation, and improves whole organ activities in the heart during sepsis.

scholarly journals Reactive oxygen species mediate arachidonic acid-induced dilation in porcine coronary microvessels

2003 ◽  
Vol 285 (6) ◽  
pp. H2309-H2315 ◽  
Author(s):  
Christine L. Oltman ◽  
Neal L. Kane ◽  
Francis J. Miller ◽  
Arthur A. Spector ◽  
Neal L. Weintraub ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Arachidonic Acid ◽  
Coronary Arteries ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cox Inhibitors ◽  
Ros Scavenger ◽  
Krebs Buffer

Reactive oxygen species (ROS) have been proposed to mediate vasodilation in the microcirculation. We investigated the role of ROS in arachidonic acid (AA)-induced coronary microvascular dilation. Porcine epicardial coronary arterioles (110 ± 4 μm diameter) were mounted onto pipettes in oxygenated Krebs buffer. Vessels were incubated with vehicle or 1 mM Tiron (a nonselective ROS scavenger), 250 U/ml polyethylene-glycolated (PEG)-superoxide dismutase (SOD; an [Formula: see text] scavenger), 250 U/ml PEG-catalase (a H2O2 scavenger), or the cyclooxygenase (COX) inhibitors indomethacin (10 μM) or diclofenac (10 μM) for 30 min. After endothelin constriction (30–60% of resting diameter), cumulative concentrations of AA (10–10–10–5 M) were added and internal diameters measured by video microscopy. AA (10–7 M) produced 37 ± 6% dilation, which was eliminated by the administration of indomethacin (4 ± 7%, P < 0.05) or diclofenac (–8 ± 8%, P < 0.05), as well as by Tiron (–4 ± 5%, P < 0.05), PEG-SOD (–10 ± 6%, P < 0.05), or PEG-catalase (1 ± 4%, P < 0.05). Incubation of small coronary arteries with [3H]AA resulted in the formation of prostaglandins, which was blocked by indomethacin. In separate studies in microvessels, AA induced concentration-dependent increases in fluorescence of the oxidant-sensitive probe dichlorodihydrofluorescein diacetate, which was inhibited by pretreatment with indomethacin or by SOD + catalase. We conclude that in porcine coronary microvessels, COX-derived ROS contribute to AA-induced vasodilation.

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