Egg case concentrate of Mantis religiosa abrogates the accumulation of cadmium in muscular and bone tissues of African catfish via activation of nitric oxide and myeloperoxidase activity

2020 ◽  
Author(s):  
J. K. Akintunde ◽  
I. A. Imhade ◽  
G. Oboh
Keyword(s):  
Nitric Oxide ◽  
African Catfish ◽  
Myeloperoxidase Activity ◽  
Mantis Religiosa ◽  
Egg Case

scholarly journals Reduced oxidative and nitrosative damage in murine experimental colitis in the absence of inducible nitric oxide synthase

Gut ◽  
1999 ◽  
Vol 45 (2) ◽  
pp. 199-209 ◽  
Author(s):  
B Zingarelli ◽  
C Szabó ◽  
A L Salzman
Keyword(s):  
Nitric Oxide ◽  
Nitrosative Stress ◽  
Experimental Colitis ◽  
Neutrophil Infiltration ◽  
Intercellular Adhesion Molecule ◽  
Myeloperoxidase Activity ◽  
Wild Type ◽  
Oxidative And Nitrosative Stress ◽  
Intense Staining ◽  
Genetic Ablation

BACKGROUNDOxidative and nitrosative stress have been implicated in the pathogenesis of inflammatory bowel diseases.AIMSTo study the role of nitric oxide (NO) derived from inducible NO synthase (iNOS) in an experimental model of murine enterocolitis.METHODSTrinitrobenzene sulphonic acid (TNBS) was instilled per rectum to induce a lethal colitis in iNOS deficient mice and in wild type controls. The distal colon was evaluated for histological evidence of inflammation, iNOS expression and activity, tyrosine nitration and malondialdehyde formation (as indexes of nitrosative and oxidative stress), myeloperoxidase activity (as index of neutrophil infiltration), and tissue localisation of intercellular adhesion molecule 1 (ICAM-1).RESULTSTNBS administration induced a high mortality and weight loss associated with a severe colonic mucosal erosion and ulceration, increased myeloperoxidase activity, increased concentrations of malondialdehyde, and an intense staining for nitrotyrosine and ICAM-1 in wild type mice. Genetic ablation of iNOS gene conferred to mice a significant resistance to TNBS induced lethality and colonic damage, and notably reduced nitrotyrosine formation and concentrations of malondialdehyde; it did not, however, affect neutrophil infiltration and intestinal ICAM-1 expression in the injured tissue.CONCLUSIONData show that activation of iNOS is required for nitrosative and oxidative damage in experimental colitis.

scholarly journals Modulation by Nitric Oxide of Cerebral Neutrophil Accumulation after Transient Focal Ischemia in Rats

2000 ◽  
Vol 20 (5) ◽  
pp. 812-819 ◽  
Author(s):  
Sophie Batteur-Parmentier ◽  
Isabelle Margaill ◽  
Michel Plotkine
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Neutrophil Infiltration ◽  
Focal Ischemia ◽  
Left Middle Cerebral Artery ◽  
No Production ◽  
Myeloperoxidase Activity ◽  
Transient Focal Ischemia

A beneficial role of nitric oxide (NO) after cerebral ischemia has been previously attributed to its vascular effects. Recent data indicate a regulatory role for NO in initial leukocyte-endothelial interactions in the cerebral microcirculation under basal and ischemic conditions. In this study, the authors tested the hypothesis that endogenous NO production during and/or after transient focal cerebral ischemia can also be neuroprotective by limiting the process of neutrophil infiltration and its deleterious consequences. Male Sprague-Dawley rats were subjected to 2 hours occlusion of the left middle cerebral artery and the left common carotid artery. The effect of NG-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg, intraperitoneally), an NO synthase inhibitor, was examined at 48 hours after ischemia on both infarct size and myeloperoxidase activity, an index of neutrophil infiltration. L-NAME given 5 minutes after the onset of ischemia increased the cortical infarct volume by 34% and increased cortical myeloperoxidase activity by 60%, whereas administration of L-NAME at 1, 7, and 22 hours of reperfusion had no effect. Such exacerbations of infarction and myeloperoxidase activity produced when L-NAME was given 5 minutes after the onset of ischemia were not observed in rats rendered neutropenic by vinblastine. These results suggest that after transient focal ischemia, early NO production exerts a neuroprotective effect by modulating neutrophil infiltration.

Pulmonary changes in a mouse model of combined burn and smoke inhalation-induced injury

2008 ◽  
Vol 105 (2) ◽  
pp. 678-684 ◽  
Author(s):  
Akio Mizutani ◽  
Perenlei Enkhbaatar ◽  
Aimalohi Esechie ◽  
Lillian D. Traber ◽  
Robert A. Cox ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Murine Model ◽  
Burn Injury ◽  
Total Body Surface Area ◽  
Inhalation Injury ◽  
Smoke Inhalation ◽  
Inos Mrna ◽  
Myeloperoxidase Activity ◽  
Smoke Inhalation Injury ◽  
Injury Group

The morbidity and mortality of burn victims increase when burn injury is combined with smoke inhalation. The goal of the present study was to develop a murine model of burn and smoke inhalation injury to more precisely reveal the mechanistic aspects of these pathological changes. The burn injury mouse group received a 40% total body surface area third-degree burn alone, the smoke inhalation injury mouse group received two 30-s exposures of cotton smoke alone, and the combined burn and smoke inhalation injury mouse group received both the burn and the smoke inhalation injury. Animal survival was monitored for 120 h. Survival rates in the burn injury group, the smoke inhalation injury group, and the combined injury group were 70%, 60%, and 30%, respectively. Mice that received combined burn and smoke injury developed greater lung damage as evidenced by histological changes (septal thickening and interstitial edema) and higher lung water content. These mice also displayed more severely impaired pulmonary gas exchange [arterial Po2(PaO2)/inspired O2fraction (FiO2) < 200]. Lung myeloperoxidase activity was significantly higher in burn and smoke-injured animals compared with the other three experimental groups. Plasma NO2−/NO3−, lung inducible nitric oxide synthase (iNOS) activity, and iNOS mRNA increased with injury; however, the burn and smoke injury group exhibited a higher response. Severity of burn and smoke inhalation injury was associated with more pronounced production of nitric oxide and accumulation of activated leukocytes in lung tissue. The murine model of burn and smoke inhalation injury allows us to better understand pathophysiological mechanisms underlying cardiopulmonary morbidity secondary to burn and smoke inhalation injury.

scholarly journals The effects of disodium pamidronate on human polymorphonuclear leukocytes and platelets: An in vitro study

2009 ◽  
Vol 14 (3) ◽  
Author(s):  
Eleonora Salvolini ◽  
Monia Orciani ◽  
Arianna Vignini ◽  
Roberto Primio ◽  
Laura Mazzanti
Keyword(s):  
Nitric Oxide ◽  
In Vitro Study ◽  
Protective Mechanism ◽  
No Production ◽  
Myeloperoxidase Activity ◽  
Inflammatory Processes ◽  
Anti Inflammatory ◽  
Constitutive Nitric Oxide Synthase

AbstractRecent reports have indicated that, as well as having antiresorptive effects, bisphosphonates could have an application as anti-inflammatory drugs. Our aim was to investigate whether this anti-inflammatory action could be mediated by the nitric oxide (NO) released by the leukocytes migrating to the site of inflammation. In particular, we investigated in vitro the intracellular calcium concentration ([Ca2+]i), the level of NO released by PMN and platelets, and the PMN myeloperoxidase activity after incubation with disodium pamidronate, since there was a postulated modulatory effect of this aminosubstituted bisphosphonate on leukocytes both in vitro and in vivo. Our data shows that the pamidronate treatment provoked a significant increase in the [Ca2+]i parallel to the enhancement in NO release, suggesting a possible activation of constitutive nitric oxide synthase, while the myeloperoxidase activity was significantly reduced. In conclusion, we hypothesized that treatment with pamidronate could stimulate NO-production by cells present near the bone compartment, thus constituting a protective mechanism against bone resorption occurring during inflammation. In addition, PMN- and platelet-derived NO could act as a negative feed-back signal to restrict the inflammatory processes.

scholarly journals ANTI-INFLAMMATORY ACTIVITY OF PARTIALLY PURIFIED LECTIN FROM PRAECITRULLUS FISTULOSUS PHLOEM EXUDATES.

2019 ◽  
Vol 12 (1) ◽  
pp. 91
Author(s):  
Madhu Cs ◽  
Sharada Ac
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Activity ◽  
No Production ◽  
Myeloperoxidase Activity ◽  
Mice Model ◽  
Ammonium Sulfate Precipitation ◽  
Edema Volume ◽  
Anti Inflammatory ◽  
Praecitrullus Fistulosus ◽  
Inflammatory Effect

Objective: The objective of the present study is to determine the anti-inflammatory effect of a partially purified lectin from phloem exudates againstpaw edema mice model.Methods: Partially purified lectin was prepared by phloem exudates in phosphate buffer saline followed by ammonium sulfate precipitation anddialysis. Anti-inflammatory activity was determined against carrageenan-induced mice model and inhibition of nitric oxide (NO) production wasdetermined.Results: Partially purified lectin exhibited promising anti-inflammatory activity at 50 mg/kg b.w. by reducing the edema volume significantly up to64% (**p<0.01) against control mice. Decrease in myeloperoxidase activity and NO production in paw exudates was observed up to 55.90 (*p<0.05)and 47.22% (*p<0.05), respectively, and this supports the anti-inflammatory property of the partially purified lectin.Conclusion: This finding indicated that further studies needed to purify and characterize a novel lectin from Praecitrullus fistulosus for elucidating themolecular mechanism of anti-inflammatory activity.

Taurine Ameliorates Thyroid Hypofunction and Renal Injury in L-NAME-Induced Hypertensive Rats

Drug Research ◽  
2018 ◽  
Vol 69 (02) ◽  
pp. 83-92 ◽  
Author(s):  
Isaac Adedara ◽  
Sanmi Alake ◽  
Laide Olajide ◽  
Mercy Adeyemo ◽  
Temitayo Ajibade ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Thyroid Stimulating Hormone ◽  
Antioxidant Enzyme Activities ◽  
Myeloperoxidase Activity ◽  
Hypertensive Rats ◽  
Nitric Oxide Synthase Inhibitor ◽  
Reference Drug ◽  
Male Wistar Rats ◽  
Synthase Inhibitor

AbstractThere is a growing global interest in hypertension due to its associated complications including renal dysfunction in patients. The thyroid system reportedly regulates renal function in both animal and human. The present study investigated the therapeutic efficacy of taurine on renal and thyroid dysfunctions in hypertensive rats. Hypertension was induced by oral administration of nitric oxide synthase inhibitor, N-nitro L-arginine-methyl-ester (L-NAME), at 40 mg/kg body weight to the male Wistar rats for 14 consecutive days. The hypertensive rats were subsequently treated with either taurine (100 and 200 mg/kg) or reference drug atenolol (10 mg/kg) for another 14 consecutive days. Hypertensive rats showed renal damage evidenced by elevated plasma creatinine and urea levels when compared with normotensive control rats. Furthermore, L-NAME-induced hypertensive rats showed decreased circulatory concentrations of thyroid stimulating hormone, thyroxine, triiodothyronine and the ratio of triiodothyronine to thyroxine. The marked decrease in the renal antioxidant enzyme activities and nitric oxide level was accompanied by significant increase in myeloperoxidase activity and biomarkers of oxidative stress in hypertensive rats. Histological examination of kidneys from hypertensive rats revealed congestion of blood vessels, hemorrhagic lesion and disorganized glomerular structure. However, treatment with taurine or atenolol significantly reversed the suppression of thyroid function, ameliorated renal oxidative stress and histopathological lesions in L-NAME-induced hypertensive rats. Taurine may be a useful chemotherapeutic supplement in enhancing renal and thyroid functions in hypertensive patients.

Role of nitric oxide in hypoxia-induced colonic dysfunction in the neonatal rat

1997 ◽  
Vol 272 (4) ◽  
pp. G760-G769 ◽  
Author(s):  
J. F. Brown ◽  
B. L. Tepperman
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Protein Content ◽  
No Synthase ◽  
Neonatal Rat ◽  
Myeloperoxidase Activity ◽  
Neonatal Rats ◽  
Colonic Tissue ◽  
Colonic Injury

In addition to being an important mediator in the regulation of intestinal integrity, nitric oxide (NO), when produced in large quantities by the inducible isoform of NO synthase, can also be cytotoxic. The aim of this study was to examine the role of NO in hypoxia-induced colonic injury in neonatal rats. Rats (10-12 days old) were exposed to a hypoxic environment of 14% O2-86% N2 for 30 min. NO synthase activity in colonic tissue was measured via the conversion of L-[14C]arginine to L-[14C]citrulline. Epithelial permeability was assessed by measuring the plasma-to-lumen flux of [3H]mannitol or the luminal protein content of colonic lavage. The role of neutrophils was assessed by pretreatment with antineutrophil serum (200 microl/kg ip) and measurement of tissue myeloperoxidase activity. Hypoxia resulted in an elevation in the activity of the inducible Ca2+-independent isoform of NO synthase in colonic tissue, which was maximal between 4 and 6 h posthypoxia and was associated with an increase in myeloperoxidase activity, [3H]mannitol flux, luminal protein content, and histological damage. These effects were attenuated by pretreatment with dexamethasone or the NO synthase inhibitors aminoguanidine and N(G)-nitro-L-arginine methyl ester, whereas the inactive stereoisomer N(G)-nitro-D-arginine methyl ester was without effect. Pretreatment with antineutrophil serum significantly reduced circulating neutrophils, myeloperoxidase activity, and Ca2+-independent NO synthase activity. These findings demonstrate that hypoxia-induced colonic injury in neonatal rats is associated with elevated NO synthase activity, which is related to an increase in neutrophil infiltration.

scholarly journals Experimental Model of Zymosan-Induced Arthritis in the Rat Temporomandibular Joint: Role of Nitric Oxide and Neutrophils

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Hellíada Vasconcelos Chaves ◽  
Ronaldo de Albuquerque Ribeiro ◽  
André Mattos Brito de Souza ◽  
Antonio Alfredo Rodrigues e Silva ◽  
Antoniella Souza Gomes ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Temporomandibular Joint ◽  
Myeloperoxidase Activity ◽  
Plasma Extravasation ◽  
Neutrophil Accumulation ◽  
Histological Changes ◽  
Leucocyte Migration ◽  
Nos Inhibitors ◽  
Oxide Synthase

Aims. To establish a new model of zymosan-induced temporomandibular joint (TMJ) arthritis in the rat and to investigate the role of nitric oxide.Methods. Inflammation was induced by an intra-articular injection of zymosan into the left TMJ. Mechanical hypernociception, cell influx, vascular permeability, myeloperoxidase activity, nitrite levels, and histological changes were measured in TMJ lavages or tissues at selected time points. These parameters were also evaluated after treatment with the nitric oxide synthase (NOS) inhibitors L-NAME or 1400 W.Results. Zymosan-induced TMJ arthritis caused a time-dependent leucocyte migration, plasma extravasation, mechanical hypernociception, and neutrophil accumulation between 4 and 24 h. TMJ immunohistochemical analyses showed increased inducible NOS expression. Treatment with L-NAME or 1400 W inhibited these parameters.Conclusion. Zymosan-induced TMJ arthritis is a reproducible model that may be used to assess both the mechanisms underlying TMJ inflammation and the potential tools for therapies. Nitric oxide may participate in the inflammatory temporomandibular dysfunction mechanisms.

Methylene Blue Inhibits the Inflammatory Process of the Acetic Acid-Induced Colitis in Rat Colonic Mucosa

2015 ◽  
Vol 100 (11-12) ◽  
pp. 1364-1374 ◽  
Author(s):  
Soykan Dinc ◽  
Muzaffer Caydere ◽  
Giray Akgul ◽  
Erdinc Yenidogan ◽  
Semra Hucumenoglu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Acetic Acid ◽  
Clinical Problem ◽  
Treated Group ◽  
Male Rats ◽  
Myeloperoxidase Activity ◽  
Sprague Dawley ◽  
Biochemical Alterations ◽  
Inflammatory Bowel

Inflammatory bowel disease is a serious health problem. Although it has been widely investigated, treatment of inflammatory bowel diseases currently remains a challenging clinical problem. Overproduction of nitric oxide has been demonstrated to cause tissue damage and inflammation. In this study, the effect of methylene blue (MB), a well-known inhibitor of nitric oxide synthesis, was investigated in acetic acid (AA)-induced colitis model in Sprague-Dawley rats. Eighty male rats were randomized into 4 groups (control, control MB, colitis, colitis + MB). AA was applied to groups 3 and 4. MB was added into groups 2 and 4. Three days later, animals were killed and the 8 cm distal colonic segment was resected, and the specimens were examined using macroscopical, histological, and biochemical methods. The results of the macroscopic and microscopic examination showed that in group 4 the mucosal damage and inflammation score was significantly lower than group 3. Increased intestinal permeability in acetic acid-administered group was significantly reversed by MB application. Myeloperoxidase activity and malondialdehyde levels increased significantly, while superoxide dismutase and catalase activities were suppressed after AA-administration. These biochemical parameters were reversed in MB-treated group. Administration of acetic acid resulted in increased levels of tumor necrosis factor-α, interleukin-1β, interleukin-6, total nitrite/nitrate levels, and nitric oxide synthase activity. These biochemical alterations were also significantly reversed by MB application. In conclusion, our results indicate that MB decreases the level of nitric oxide and decreases inflammation in acetic acid-induced colitis.

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