Effect of a normal protein diet on oxidative stress and organ damage in malnourished rats

This study was designed to evaluate biomarkers of oxidative stress in rats with or without aerobic exercise during recovery from protein malnutrition. From the 30th to the 90th day of life, male Wistar rats were fed a low protein diet (LP + 6%) followed by a normal protein diet (NP = 17%) until the 120th day and separated in two groups: sedentary (S) and exercise trained (E = swimming 1h/day, 5 days/week, with from the 90th to the 120th day). Rats fed a normal protein diet were used as controls. Results showed that physical exercise had beneficial effects on body weight gain during nutrition rehabilitation. Erythrocytes catalase and glutathione reductase (biomarkers of the antioxidant system) were significantly reduced in all groups in comparison to the sedentary control group. The plasma concentration of TBARs (biomarkers of the oxidative damage) was also lower in the recovered rats, suggesting that the improvement in body growth after nutritional rehabilitation with physical exercise could be related to a decrease in the oxidative stress level.

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Protective Effects of GYY4137 on Renal Ischaemia/Reperfusion Injury through Nrf2-Mediated Antioxidant Defence

Kidney & Blood Pressure Research ◽

10.1159/000509933 ◽

2021 ◽

pp. 1-9

Author(s):

Hongmei Zhao ◽

Yun Qiu ◽

Yichen Wu ◽

Hong Sun ◽

Sumin Gao

Keyword(s):

Oxidative Stress ◽

Reperfusion Injury ◽

Nuclear Translocation ◽

Organ Damage ◽

Related Factor ◽

Protective Effects ◽

Ischaemia Reperfusion Injury ◽

Renal Ischaemia ◽

Ischaemia Reperfusion ◽

Renal Histology

Introduction/Aims: Hydrogen sulfide (H2S) is considered to be the third most important endogenous gasotransmitter in organisms. GYY4137 is a long-acting donor for H2S, a gas transmitter that has been shown to prevent multi-organ damage in animal studies. We previously reported the effect of GYY4137 on cardiac ischaemia reperfusion injury (IRI) in diabetic mice. However, the role and mechanism of GYY4137 in renal IRI are poorly understood. The aims of this study were to determine whether GYY4137 can effectively alleviate the injury induced by renal ischaemia reperfusion and to explore its possible mechanism. Methods: Mice received right nephrectomy and clipping of the left renal pedicle for 45 min. GYY4137 was administered by intraperitoneal injection for 2 consecutive days before the operation. The model of hypoxia/reoxygenation injury was established in HK-2 cells, which were pre-treated with or without GYY4137. Renal histology, function, apoptosis, and oxidative stress were measured. Western blot was used to measure the target protein after renal IRI. Results: The results indicated that GYY4137 had a clear protective effect on renal IRI as reflected by the attenuation of renal dysfunction, renal tubule injury, and apoptosis. Moreover, GYY4137 remarkably reduced renal IRI-induced oxidative stress. GYY4137 significantly elevated the nuclear translocation of nuclear factor-erythroid-2-related factor 2 (Nrf2) and the expression of antioxidant enzymes regulated by Nrf2, including SOD, HO-1, and NQO-1. Conclusions: GYY4137 alleviates ischaemia reperfusion-induced renal injury through activating the antioxidant effect mediated by Nrf2 signalling.

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Indoxyl-Sulfate-Induced Redox Imbalance in Chronic Kidney Disease

Antioxidants ◽

10.3390/antiox10060936 ◽

2021 ◽

Vol 10 (6) ◽

pp. 936

Author(s):

Chien-Lin Lu ◽

Cai-Mei Zheng ◽

Kuo-Cheng Lu ◽

Min-Tser Liao ◽

Kun-Lin Wu ◽

...

Keyword(s):

Oxidative Stress ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Muscle Wasting ◽

Mesangial Cells ◽

Target Organ Damage ◽

Organ Damage ◽

Indoxyl Sulfate ◽

Uremic Toxin ◽

Tubulointerstitial Injury

The accumulation of the uremic toxin indoxyl sulfate (IS) induces target organ damage in chronic kidney disease (CKD) patients, and causes complications including cardiovascular diseases, renal osteodystrophy, muscle wasting, and anemia. IS stimulates reactive oxygen species (ROS) production in CKD, which impairs glomerular filtration by a direct cytotoxic effect on the mesangial cells. IS further reduces antioxidant capacity in renal proximal tubular cells and contributes to tubulointerstitial injury. IS-induced ROS formation triggers the switching of vascular smooth muscular cells to the osteoblastic phenotype, which induces cardiovascular risk. Low-turnover bone disease seen in early CKD relies on the inhibitory effects of IS on osteoblast viability and differentiation, and osteoblastic signaling via the parathyroid hormone. Excessive ROS and inflammatory cytokine releases caused by IS directly inhibit myocyte growth in muscle wasting via myokines’ effects. Moreover, IS triggers eryptosis via ROS-mediated oxidative stress, and elevates hepcidin levels in order to prevent iron flux in circulation in renal anemia. Thus, IS-induced oxidative stress underlies the mechanisms in CKD-related complications. This review summarizes the underlying mechanisms of how IS mediates oxidative stress in the pathogenesis of CKD’s complications. Furthermore, we also discuss the potential role of oral AST-120 in attenuating IS-mediated oxidative stress after gastrointestinal adsorption of the IS precursor indole.

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Sickle Cell Disease: Role of Oxidative Stress and Antioxidant Therapy

Antioxidants ◽

10.3390/antiox10020296 ◽

2021 ◽

Vol 10 (2) ◽

pp. 296

Author(s):

Rosa Vona ◽

Nadia Maria Sposi ◽

Lorenza Mattia ◽

Lucrezia Gambardella ◽

Elisabetta Straface ◽

...

Keyword(s):

Oxidative Stress ◽

Sickle Cell Disease ◽

Sickle Cell ◽

Globin Gene ◽

Organ Damage ◽

Cell Disease ◽

Vessel Occlusion ◽

Antioxidant Agents ◽

Oxidant Status

Sickle cell disease (SCD) is the most common hereditary disorder of hemoglobin (Hb), which affects approximately a million people worldwide. It is characterized by a single nucleotide substitution in the β-globin gene, leading to the production of abnormal sickle hemoglobin (HbS) with multi-system consequences. HbS polymerization is the primary event in SCD. Repeated polymerization and depolymerization of Hb causes oxidative stress that plays a key role in the pathophysiology of hemolysis, vessel occlusion and the following organ damage in sickle cell patients. For this reason, reactive oxidizing species and the (end)-products of their oxidative reactions have been proposed as markers of both tissue pro-oxidant status and disease severity. Although more studies are needed to clarify their role, antioxidant agents have been shown to be effective in reducing pathological consequences of the disease by preventing oxidative damage in SCD, i.e., by decreasing the oxidant formation or repairing the induced damage. An improved understanding of oxidative stress will lead to targeted antioxidant therapies that should prevent or delay the development of organ complications in this patient population.

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The Colonic Microbiome and Epithelial Transcriptome Are Altered in Rats Fed a High-Protein Diet Compared with a Normal-Protein Diet

Journal of Nutrition ◽

10.3945/jn.115.223990 ◽

2016 ◽

Vol 146 (3) ◽

pp. 474-483 ◽

Cited By ~ 49

Author(s):

Chunlong Mu ◽

Yuxiang Yang ◽

Zhen Luo ◽

Leluo Guan ◽

Weiyun Zhu

Keyword(s):

High Protein Diet ◽

High Protein ◽

Protein Diet ◽

Normal Protein Diet

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Role of antioxidant therapy in patients with moderate and severe COVID-19

Infekcionnye bolezni ◽

10.20953/1729-9225-2021-1-159-164 ◽

2021 ◽

Vol 19 (1) ◽

pp. 159-164

Author(s):

E.K. Shavarova ◽

◽

E.R. Cazakhmedov ◽

M.V. Alekseeva ◽

L.G. Ezhova ◽

...

Keyword(s):

Oxidative Stress ◽

Intervention Group ◽

Clinical Manifestations ◽

Organ Damage ◽

Control Group ◽

Reactive Protein ◽

Virus Rna ◽

Active Intervention Group ◽

Group 2 ◽

Novel Coronavirus

The coronavirus disease COVID-19 is characterized by high mortality and the lack of effective etiotropic therapy. Activation of oxidative stress may be one of the links in the pathogenesis of organ damage of this infection. Objective. To assess the ability of Mexidol® to influence the rate of clinical improvement in pneumonia caused by the SARSCoV-2 virus in hospitalized patients with the novel coronavirus disease COVID-19 and concomitant discirculatory encephalopathy. 62 patients over the age of 18 years with confirmed new coronavirus disease COVID-19 according to computed tomography (CT) of the lungs (stages CT1, CT2, CT3) and PCR of a swab from the nasopharynx and oropharynx for SARS-CoV-2 virus RNA were included. After randomization patients of group 1 received an infusion of Mexidol® at a dose of 1000 mg/day, patients of group 2 – an infusion of isotonic sodium chloride solution for 7 days. Compared with the control group, the patients receiving Mexidol® therapy showed a significantly more pronounced decrease in body temperature, a tendency towards a decrease in the severity of shortness of breath. In the Mexidol® group, the concentration of superoxidedismutase did not change, while in the control group there was a tendency to its decrease, C-reactive protein decreased 2.2 times more than in the control group (p = 0.09). There was a tendency for a more rapid decrease in ferritin in the active intervention group. Mexidol® therapy can have a positive effect on the clinical manifestations and severity of laboratory-inflammatory syndrome in patients with the new coronavirus disease COVID-19. Key words: coronavirus disease COVID-19, oxidative stress, Mexidol

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Recurrent insulin-induced hypoglycemia induces AngII and COX2 leading to renal (pro)renin receptor expression and oxidative stress

International Journal of Medicine ◽

10.14419/ijm.v5i1.6858 ◽

2017 ◽

Vol 5 (1) ◽

pp. 71 ◽

Cited By ~ 1

Author(s):

Wael Alanazi ◽

Mohammad Uddin ◽

Selim Fakhruddin ◽

Keith Jackson

Keyword(s):

Oxidative Stress ◽

Nadph Oxidase ◽

Kidney Injury ◽

Organ Damage ◽

Day Surgery ◽

Receptor Expression ◽

Sprague Dawley ◽

Subunit Expression ◽

Renal Biomarker ◽

And Oxidative Stress

Background: Recurrent insulin-induced hypoglycemia (RIIH) is an avoidable consequence in the therapeutic management of diabetes mellitus. RIIH has been implicated in causing hypertension through an increase in renal and systemic AngII production.Objective: The present study was performed to assess the hypothesis that chronic insulin treatment enhances AngII and COX2 formation which in turn increases (pro) renin receptor (PRR) expression and NADPH oxidase-mediated oxidative stress, leading to renal and cardiac injury.Methods: The present studies were conducted in Male Sprague Dawley rats treated with daily subcutaneous injections of 7u/kg insulin or saline for 14 days. On the 14th day, surgery was performed for treatment infusion (captopril 12mg/kg, NS398 0.3mg/kg or vehicle), and renal interstitial fluid sample and urine collections for biomarker measurements. At the end of the experiments, kidneys and hearts were harvested to evaluate PRR and NOX2 (NADPH oxidase subunit) expression and oxidative stress.Results: We found that RIIH enhanced AngII and COX2 activity, leading to renal PRR expression and NADPH oxidase-induced oxidative stress in the heart and kidney. 8-isoprostane was evaluated as a renal biomarker of oxidative stress, which was induced in insulin treated animals and modulated by captopril and NS398. In addition, there was a slight increase in NGAL, a urinary biomarker of acute kidney injury (AKI), in insulin treated animals when compared to control.Conclusion: These results demonstrate that RIIH induces renal PRR expression and oxidative stress through increasing AngII and COX2 in the heart and kidney, leading to end-organ damage.

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THE CHANGES IN DYNAMICS OF ORNITHINE CYCLE COMPONENTS LEVELS DURING THE ACUTE PERIOD OF POLYTRAUMA

Wiadomości Lekarskie ◽

10.36740/wlek201909214 ◽

2019 ◽

Vol 72 (9) ◽

pp. 1781-1785

Author(s):

Nataliya Matolinets

Keyword(s):

Oxidative Stress ◽

Intensive Care ◽

Serum Levels ◽

Organ Damage ◽

Multiple Organ ◽

Oxidation Products ◽

Acute Period ◽

Proinflammatory Mediators ◽

Biomechanical Parameters ◽

Injury Causes

Introduction: Polytrauma or multiple organ damage is associated with shock and lead to systemic inflammation, oxidative stress and endothelial dysfunction. A severe mechanical injury causes an increased proinflammatory mediators and cytokines levels. Among them, the overproduction of nitric oxide and its oxidation products play a key role in tissue damage. The aim: To evaluate the changes in dynamics of some ornithine cycle components levels during acute period of polytrauma. Materials and methods: We measured standard biomechanical parameters and serum levels of NO, sum of nitrite and nitrate (NOx), L-arginine, arginase, and peroxynitrite. According to the ISS, the study included patients with moderate (n=15) to severe (n=15) polytrauma. Results: In 24 hours after polytrauma on the background of intensive care, it was observed significant increasing of NO, NOx, and arginase levels (severe cases) with decreasing of L-arginine and peroxynitrite levels. Conclusions: Elevated NO and NOx serum levels in patients with polytrauma is associated with increasing of arginase activity with decreasing of L-arginine and peroxynitrite levels on the background of intensive care.

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Ghrelin Pre-treatment Attenuates Local Oxidative Stress and End Organ Damage During Cardiopulmonary Bypass in Anesthetized Rats

Frontiers in Physiology ◽

10.3389/fphys.2018.00196 ◽

2018 ◽

Vol 9 ◽

Cited By ~ 6

Author(s):

Vijayakumar Sukumaran ◽

Hirotsugu Tsuchimochi ◽

Yutaka Fujii ◽

Hiroshi Hosoda ◽

Kenji Kangawa ◽

...

Keyword(s):

Oxidative Stress ◽

Cardiopulmonary Bypass ◽

Organ Damage ◽

End Organ Damage ◽

Anesthetized Rats ◽

Pre Treatment

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Pathophysiology of Hypertension

Circulation Research ◽

10.1161/circresaha.121.318082 ◽

2021 ◽

Vol 128 (7) ◽

pp. 847-863 ◽

Cited By ~ 1

Author(s):

David G. Harrison ◽

Thomas M. Coffman ◽

Christopher S. Wilcox

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Organ Damage ◽

Experimental Models ◽

Sodium Homeostasis ◽

Circulation Research ◽

Raise Blood Pressure ◽

New Concepts ◽

Constant Feature ◽

Mosaic Theory

Dr Irvine Page proposed the Mosaic Theory of Hypertension in the 1940s advocating that hypertension is the result of many factors that interact to raise blood pressure and cause end-organ damage. Over the years, Dr Page modified his paradigm, and new concepts regarding oxidative stress, inflammation, genetics, sodium homeostasis, and the microbiome have arisen that allow further refinements of the Mosaic Theory. A constant feature of this approach to understanding hypertension is that the various nodes are interdependent and that these almost certainly vary between experimental models and between individuals with hypertension. This review discusses these new concepts and provides an introduction to other reviews in this compendium of Circulation Research .

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