scholarly journals Selenium and alpha-tocopherol reduces ϑluoride induced oxidative stress in brain and muscle of mice

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 1794-1799
Author(s):  
Chandra Shakar Reddy N ◽  
Pratap Reddy K
Keyword(s):  
Oxidative Stress ◽  
Environmental Pollutants ◽  
Treated Group ◽  
Alpha Tocopherol ◽  
Control Group ◽  
Protective Effects ◽  
Stress Prevention ◽  
Wide Availability ◽  
Markers Of Oxidative Stress ◽  
Ros Formation

Fluoride is one of the common environmental pollutants. Its excessive exposure results in a wide array of toxicity phenotypes including oxidative stress, skeletal and soft tissue damage etc. Antioxidants such as Selenium (Se) and α-tocopherol are attractive agents for oxidative stress prevention because of their safety profile and wide availability. It is known that in combination, Se and alpha-tocopherol act synergistically against ROS formation. This study investigated the protective effects of selenium (05 µg/kg BW) and Alpha-tocopherol (2 mg/kg BW) on markers of oxidative stress in brain and muscle of mice exposed to sodium fluoride (20mg/kg BW) for 15 days. The results showed significant (p<0.05) alterations in markers of oxidative stress includes; an increase in xanthine oxidase activity and lipid peroxidation, a decline in SOD, CAT, GST and GPx activities in fluoride exposure group in comparison with control group indicates oxidative stress induced by fluoride. These changes were reversed modestly in Se and alpha-tocopherol alone treated groups and significantly  (p<0.05) in the combinedly treated group indicating synergistic action in mitigation of fluoride effect.

scholarly journals D-Limonene Alleviates Acute Kidney Injury Following Gentamicin Administration in Rats: Role of NF-κB Pathway, Mitochondrial Apoptosis, Oxidative Stress, and PCNA

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Esmaeel Babaeenezhad ◽  
Forouzan Hadipour Moradi ◽  
Sobhan Rahimi Monfared ◽  
Mohammad Davood Fattahi ◽  
Maryam Nasri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Treated Group ◽  
Control Group ◽  
Myeloperoxidase Activity ◽  
Protective Effects ◽  
Mitochondrial Apoptosis ◽  
Protein Expressions ◽  
Apoptosis And Inflammation

Clinical application of gentamicin (GM) is well known to be associated with the development of acute kidney injury (AKI). This study was the first to investigate the possible protective effects of D-limonene (D-lim) on AKI following GM administration in rats. 32 rats arranged in four groups ( n = 8 ): (1) the control group received saline intraperitoneally (0.5 ml/day) and orally (0.5 ml/day), (2) the D-lim group received D-lim (100 mg/kg) orally and saline (0.5 ml/day) intraperitoneally, (3) the GM group received GM (100 mg/kg/day) intraperitoneally and saline (0.5 ml/day) orally, and (4) the treated group received intraperitoneal GM (100 mg/kg) and oral D-lim (100 mg/kg). All treatments were performed daily for 12 consecutive days. Results revealed that D-lim ameliorated GM-induced AKI, oxidative stress, mitochondrial apoptosis, and inflammation. D-lim showed nephroprotective effects as reflected by the decrease in serum urea and creatinine and improvement of renal histopathological changes. D-lim alleviated GM-induced oxidative stress by increasing the activities of renal catalase, serum and renal glutathione peroxidase, and renal superoxide dismutase and decreasing renal malondialdehyde and serum nitric oxide levels. Intriguingly, D-lim suppressed mitochondrial apoptosis by considerably downregulating Bax and caspase-3 (Casp-3) mRNA and protein expressions and markedly enhancing Bcl2 mRNA and protein expressions. Furthermore, D-lim significantly decreases GM-induced inflammatory response through downregulation of NF-κB, IL-6, and TNF-α mRNA and/or protein expressions and decrease in renal myeloperoxidase activity. Finally, D-lim remarkably downregulated PCNA protein expression in the treated group compared with the GM group. In brief, this study showed that D-lim alleviated AKI following GM administration in rats, partially through its antioxidant, anti-inflammatory, and antiapoptotic activities as well as downregulation of PCNA expression.

scholarly journals Effect of caraway on gentamicin-induced oxidative stress, inflammation and nephrotoxicity in rats

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Hoda Erjaee ◽  
Fatemeh Azma ◽  
Saeed Nazifi
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Group Treatment ◽  
Structural Damage ◽  
Seed Oil ◽  
Treated Group ◽  
Control Group ◽  
Protective Effects ◽  
Simultaneous Treatment ◽  
Tnf Α

Different potentially therapeutic approaches to prevent or attenuate gentamicin (GEM) induced nephrotoxicity have been proposed. The aim of the present study was to investigate the possible protective effects of caraway seed oil against GEM-induced nephrotoxicity in rats. Rats (24) were randomly assigned into four equal groups: i) normal control group, ii) treated with GEM, iii) pretreated with orally caraway seed oil 10 (mg kg−1) plus GEM and iv) treated with GEM and caraway seed oil 10 mg kg−1. Biochemical examinations were utilized for evaluation of the oxidative stress and renal nephrotoxicity. Creatinine, blood urea nitrogen (BUN), plasma malondialdehyde (MDA) levels, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined. Administration of gentamicin to rats induced a marked renal failure, characterized by a significant increase in plasma creatinine and BUN concentrations. The animals treated with gentamicin alone showed a significantly higher plasma MDA level andlower SOD, GSH-Px and CAT activities when compared with the control group. Treatment and simultaneous treatment with caraway seed oil produced amelioration in MDA and increased the activity of antioxidant enzymes SOD, GSH-Px and CAT when compared with the gentamicin treated group. In addition, GEM nephrotoxicity increased renal inflammatory cytokines (TNF-α, IL-6 and IFN-γ). Pro-inflammatory cytokines were significantly decreased (P&lt;0.05) in the test groups administered caraway seed oil. These findings suggest that caraway seed oil treatment attenuates renal dysfunction and structural damage through the reduction of oxidative stress and inflammation in rats.

scholarly journals Protective Effects of Sal B on Oxidative Stress-Induced Aging by Regulating the Keap1/Nrf2 Signaling Pathway in Zebrafish

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5239
Author(s):  
Erzhuo Li ◽  
Yunhao Wang ◽  
Qiao Li ◽  
Li Li ◽  
Lijun Wei
Keyword(s):  
Oxidative Stress ◽  
Morphological Changes ◽  
Treated Group ◽  
Spinal Curvature ◽  
Control Group ◽  
Protective Effects ◽  
Related Factors ◽  
Nrf2 Signaling Pathway ◽  
Pericardial Edema ◽  
6 Hydroxydopamine

The models of oxidative damage-induced aging were established by adding ethanol (C2H5OH), hydrogen peroxide (H2O2) and 6-hydroxydopamine (6-OHDA) to zebrafish embryos in this research. To find effective protective drugs/foods, Salvianolic acid B (Sal B) was added after the embryos were treated by these oxidative reagents. After being treated with ethanol, H2O2 and 6-OHDA, the morphological changes were obvious and the deformities included spinal curvature, heart bleeding, liver bleeding, yolk sac deformity and pericardial edema, and the expression of oxidative stress-related genes Nrf2b, sod1 and sod2 and aging-related genes myl2a and selenbp1 were significantly up-regulated compared to the control group. While after adding 0.05 μg/mL and 0.5 μg/mL Sal B to the ethanol-treated group, death rates and MDA levels decreased, the activity of antioxidant enzyme (SOD, CAT and GSH-Px) changed and Nrf2b, sod1, sod2, myl2a, selenbp1, p53 and p21 were down-regulated compared to the ethanol-treated group. The bioinformatics analysis also showed that oxidative stress-related factors were associated with a variety of cellular functions and physiological pathways. In conclusion, Sal B can protect against aging through regulating the Keap1/Nrf2 pathway as well as antioxidative genes and enzyme activity.

scholarly journals Strategies for Reducing or Preventing the Generation of Oxidative Stress

2011 ◽  
Vol 2011 ◽  
pp. 1-15 ◽  
Author(s):  
B. Poljsak
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Environmental Pollutants ◽  
Psychosocial Interventions ◽  
Epidemiological Studies ◽  
Stress Prevention ◽  
Future Success ◽  
Ros Formation ◽  
Stress Oxidative ◽  
Antioxidant Supplements

The reduction of oxidative stress could be achieved in three levels: by lowering exposure to environmental pollutants with oxidizing properties, by increasing levels of endogenous and exogenous antioxidants, or by lowering the generation of oxidative stress by stabilizing mitochondrial energy production and efficiency. Endogenous oxidative stress could be influenced in two ways: by prevention of ROS formation or by quenching of ROS with antioxidants. However, the results of epidemiological studies where people were treated with synthetic antioxidants are inconclusive and contradictory. Recent evidence suggests that antioxidant supplements (although highly recommended by the pharmaceutical industry and taken by many individuals) do not offer sufficient protection against oxidative stress, oxidative damage or increase the lifespan. The key to the future success of decreasing oxidative-stress-induced damage should thus be the suppression of oxidative damage without disrupting the wellintegrated antioxidant defense network. Approach to neutralize free radicals with antioxidants should be changed into prevention of free radical formation. Thus, this paper addresses oxidative stress and strategies to reduce it with the focus on nutritional and psychosocial interventions of oxidative stress prevention, that is, methods to stabilize mitochondria structure and energy efficiency, or approaches which would increase endogenous antioxidative protection and repair systems.

Effects of Polysaccharides from Radix astragali on Oxidative Stress Induced by Exhaustive Swimming Exercise in Liver and Muscle of Mice

2014 ◽  
Vol 633-634 ◽  
pp. 558-561
Author(s):  
Ming Wu ◽  
Dan Han ◽  
Chuan Fu Ma ◽  
Zhen Wei Wei ◽  
Jun Hong Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Treated Group ◽  
Swimming Exercise ◽  
Control Group ◽  
High Dose ◽  
Protective Effects ◽  
Radix Astragali ◽  
Final Treatment ◽  
Exercise Induced ◽  
Different Doses

Polysaccharides, the mainly bioactive ingredient ofRadix Astragali, were evaluated for its effects on the oxidative stress induced by exhaustive swimming exercise of mice. A total of 48 mice were randomly divided into four groups: control group, low-dose polysaccharide fromAstragali radix(RAP) treated group, medium-dose RAP treated group, and high-dose RAP treated group. The control group received only distilled water ig, and the RAP treated groups received different doses of RAP (50, 100, and 200 mg/kg, ig) for 28 days. After the final treatment with RAP, the mice were subjected to swimming to exhaustion and the superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) were measured. The data showed that RAP promote increases in the activities of SOD, GPX and CAT in liver and muscle of mice, and the high-dose RAP (200 mg/kg) presented the best effect. These results indicated that RAP possessed protective effects against exercise-induced oxidative stress.

Glycine and L-Arginine supplementation ameliorates gastro-duodenal toxicity in a rat model of NSAID (Diclofenac)-gastroenteropathy via inhibition of oxidative stress

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Akinleye Stephen Akinrinde ◽  
Halimot Olawalarami Hameed
Keyword(s):  
Oxidative Stress ◽  
Total Protein ◽  
Therapeutic Index ◽  
Control Treatment ◽  
Control Group ◽  
Protective Effects ◽  
Serum Total Protein ◽  
Significant Amelioration ◽  
Group A ◽  
Group B

Abstract Objectives This study examined the possible protective roles of exogenous glycine (Gly) and L-Arginine (l-Arg) against Diclofenac (DIC)-induced gastro-duodenal damage in rats. Methods Rats were divided into Group A (control), Group B (DIC group) and Groups C–F which were pre-treated for five days with Gly1 (250 mg/kg), Gly2 (500 mg/kg), l-Arg1 (200 mg/kg) and l-Arg2 (400 mg/kg), respectively, before co-treatment with DIC for another three days. Hematological, biochemical and histopathological analyses were then carried out. Results DIC produced significant (p<0.05) reduction in PCV (13.82%), Hb (46.58%), RBC (30.53%), serum total protein (32.72%), albumin (28.44%) and globulin (38.01%) along with significant (p<0.05) elevation of serum MPO activity (83.30%), when compared with control. In addition, DIC increased gastric H2O2 and MDA levels by 33.93 and 48.59%, respectively, while the duodenal levels of the same parameters increased by 19.43 and 85.56%, respectively. Moreover, SOD, GPx and GST activities in the DIC group were significantly (p<0.05) reduced in the stomach (21.12, 24.35 and 51.28%, respectively) and duodenum (30.59, 16.35 and 37.90%, respectively), compared to control. Treatment with Gly and l-Arg resulted in significant amelioration of the DIC-induced alterations although l-Arg produced better amelioration of RBC (29.78%), total protein (10.12%), albumin (9.93%) and MPO (65.01%), compared to the DIC group. The protective effects of both amino acids against oxidative stress parameters and histological lesions were largely similar. Conclusions The data from this study suggest that Gly or l-Arg prevented DIC-induced gastro-duodenal toxicity and might, therefore be useful in improving the therapeutic index of DIC.

scholarly journals Neurological Alterations and Testicular Damages in Aging Induced by D-Galactose and Neuro and Testicular Protective Effects of Combinations of Chitosan Nanoparticles, Resveratrol and Quercetin in Male Mice

Coatings ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 435
Author(s):  
Reham Z. Hamza ◽  
Mohammad S. Al-Harbi ◽  
Munirah A. Al-Hazaa
Keyword(s):  
Oxidative Stress ◽  
Chitosan Nanoparticles ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Enzymatic Antioxidants ◽  
Protective Effects ◽  
Biochemical Alterations ◽  
Wide Range ◽  
Neurological Alterations

Aging is a neurological disease that is afforded by incidence of oxidative stress. Chitosan has received global interests due to its wide medical uses. Quercetin (Q) is a bioflavonoid and widely distributed in vegetables and fruits. Resveratrol is considered as a potent antioxidant and is a component of a wide range of foods. The using of either chitosan nanopartciles (CH-NPs), querectin (Q), and resveratrol (RV) to reduce the oxidative stress and biochemical alterations on brain and testicular tissues induced by D-galactose (DG) (100 mg/Kg) were the aim of the present study. This study investigated the probable protective effects of CH-NPs in two doses (140,280 mg/Kg), Q (20 mg/Kg) and RV (20 mg/Kg), against DG induced aging and neurological alterations. Brain antioxidant capacity as malonaldehyde (MDA), catalase (CAT), and glutathione reductase (GRx), as well as histopathological damages of the brain and testicular tissues were measured. The DG treated group had significantly elevated the oxidative stress markers by 96% and 91.4% in brain and testicular tissues respectively and lower significantly the antioxidant enzyme activities of both brain and testicular tissues than those of the control group by 86.95%, 69.27%, 83.07%, and 69.43%. Groups of DG that treated with a combination of CH-NPs in two doses, Q and RV, the levels of oxidative stress marker declined significantly by 68.70%, 76.64% in brain tissues and by 74.07% and 76.61% in testicular tissues, and the enzymatic antioxidants increased significantly by 75.55%, 79.24%, 62.32%, and 61.97% as compared to the DG group. The present results indicate that CH-NPs, Q, and RV have protective effects against DG-induced brain and testis tissue damage at the biochemical and histopathological levels. Mechanisms of this protective effect of used compounds against neurological and testicular toxicity may be due to the enhanced brain and testis antioxidant capacities.

Protective effects of histamine on Gq-mediated relaxation in regenerated endothelium

2014 ◽  
Vol 306 (2) ◽  
pp. H286-H290 ◽  
Author(s):  
Calvin K. Chan ◽  
Song Yan Liao ◽  
Yue Lin Zhang ◽  
Aimin Xu ◽  
Hung Fat Tse ◽  
...  
Keyword(s):  
Area Under The Curve ◽  
Treated Group ◽  
Control Group ◽  
Protective Effects ◽  
Treatment Control ◽  
Porcine Coronary Artery ◽  
Endogenous Histamine ◽  
Coronary Endothelium ◽  
Treatment Control Group

In the porcine coronary artery, regenerated endothelium is dysfunctional as regards the responses to endothelium-dependent agonists. The current study aimed to determine the possible involvement of histamine in such dysfunction. Pigs were treated chronically with pyrilamine (H1 receptor inhibitor, 2 mg·kg−1·day−1) with part of their coronary endothelium and allowed to regenerate for 28 days after balloon denudation. The results showed a reduction in relaxation to bradykinin (Gq protein dependent) only in the pyrilamine-treated group (area under the curve, 269.7 ± 13.4 vs. 142.0 ± 31.0, native endothelium vs. regenerated endothelium) but not in the control group (253.0 ± 22.1 vs. 231.9 ± 29.5, native endothelium vs. regenerated endothelium). The differences in the relaxation to serotonin (Gi protein dependent) between native and regenerated endothelium were not affected by the pyrilamine treatment (control group, 106.3 ± 17.0 vs. 55.61 ± 12.7; and pyrilamine group, 106.0 ± 8.20 vs. 49.30 ± 6.31, native endothelium vs. regenerated endothelium). These findings indicate that during regeneration of the endothelium, the activation of H1 receptors by endogenous histamine may be required to maintain the endothelium-dependent Gq protein-mediated relaxation to bradykinin, suggesting a beneficial role of the monoamine in the process of endothelial regeneration.

scholarly journals Comparison of Effects of Different Statins on Contrast-Induced Acute Kidney Injury in Rats: Histopathological and Biochemical Findings

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Xiao-lei Wang ◽  
Tuo Zhang ◽  
Liu-hua Hu ◽  
Shi-qun Sun ◽  
Wei-feng Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Lipid Lowering ◽  
Control Group ◽  
Sprague Dawley ◽  
Atorvastatin Group ◽  
New Strategy ◽  
Ameliorative Effect ◽  
Markers Of Oxidative Stress

Statins are a promising new strategy to prevent contrast-induced acute kidney injury (CI-AKI). In this study we compared the ameliorative effect of different statins in a rat model of CI-AKI. Sprague-Dawley rats were divided into five groups: control group; CI-AKI group; CI-AKI + rosuvastatin group (10 mg/kg/day); CI-AKI + simvastatin group (80 mg/kg/day); and CI-AKI + atorvastatin group (20 mg/kg/day). CI-AKI was induced by dehydration for 72 hours, followed by furosemide intramuscular injection 20 minutes before low-osmolar contrast media (CM) intravenous injection. Statins were administered by oral gavage once daily for 3 consecutive days before CM injection and once 4 hours after CM injection. Rats were sacrificed 24 hours after CM injection, and renal function, kidney histopathology, nitric oxide (NO) metabolites, and markers of oxidative stress, inflammation, and apoptosis were evaluated. The results showed that atorvastatin and rosuvastatin but not simvastatin ameliorated CM-induced serum creatinine elevation and histopathological alterations. Atorvastatin and rosuvastatin showed similar effectiveness against CM-induced oxidative stress, but simvastatin was less effective. Atorvastatin was most effective against NO system dysfunction and cell apoptosis, whereas rosuvastatin was most effective against inflammation. Our findings indicate that statins exhibit differential effects in preventing CI-AKI when given at equivalent lipid-lowering doses.

Abstract P211: Single High Na + Ingestion Leads To An Increase In Oxidative Stress And Triggers Inflammation.

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Ginette Bordcoch ◽  
Ivan Tavera Busso ◽  
Juan Masjoan Juncos ◽  
Luis I Juncos
Keyword(s):  
Oxidative Stress ◽  
The United States ◽  
Male Rats ◽  
Control Group ◽  
Aortic Tissue ◽  
Tissue Samples ◽  
Extracellular Signal ◽  
High Prevalence ◽  
Markers Of Oxidative Stress ◽  
The Difference

Hypertension has been linked to a progressive increased in oxidative stress and inflammation. The high prevalence of hypertension poses a great risk to public health as 108 million adults in the United States have the condition. For that reason, a better understanding of the link between a high Na+ intake and the development of hypertension is of crucial importance. We hypothesize that a single ingestion of a high Na+ solution leads to increased oxidative stress and triggers an inflammatory response. Wistar 200-250 g male rats had gastric infusions through the esophagus. Groups were infused with 8 mL liquid Vaseline (Control), 8 mL of NaCl 0.684 M (4% m/v), and 8 mL of NaCl 1.368 M (8% m/v). After infusion, blood was collected at different time points during the first hour. Tissue samples were obtained from the aorta, heart, and kidney. Electron Microscopy (EM) was performed on all tissues, which were also analyzed for molecular markers of oxidative stress: Superoxide Dismutase (SOD) and Malondialdehyde (MDA), and an inflammation marker: Extracellular Signal-Regulated Kinase (ERK). At 2 and a half minutes, serum Na+ concentration was unchanged in the control group compared to an increase observed in animals receiving 4% and 8% Na+ with concentrations of 135±1.4 mEq/L, 141±2.0 mEq/L, and 140±1.2 mEq/L respectively. At the 1-hour time point after infusion, the difference was further increased in the 8% group with serum concentrations of 135±1.8 mEq/L, 140±1.5 mEq/L, and 152±1mEq/L respectively (p<0.05). There was an increase in oxidative stress in the aorta from values of 36.22±4.64 mU/mg SOD and 0.131±0.013 pg/mL MDA in the control group, to 47.11±4.89 mU/mg SOD and 0.291±0.022 pg/mL MDA in the 8% group (p<0.05 in both cases). The same was observed in the heart, where values were: 174.6125.26 mU/mg SOD, 0.026±0.007 pg/mL MDA in controls, and 259.22±21.98 mU/mg SOD, 0.215±0.073 pg/mL MDA in 8% group (p<0.05 both cases). Increased ERK in aortic tissue, values of 0.29±0.03 pg/mL in controls, 2.68±0.18 pg/mL in 4% group and 3.97±0.68pg/mL in 8% group (p<0.05) suggest increased inflammation. We conclude that the elevation in serum Na+ concentration that follows Na+ ingestion leads to increased oxidative stress and inflammation.

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