scholarly journals Static Magnetic Fields Modulate the Response of Different Oxidative Stress Markers in a Restraint Stress Model Animal

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
E. Coballase-Urrutia ◽  
L. Navarro ◽  
J. L. Ortiz ◽  
L. Verdugo-Díaz ◽  
J. M. Gallardo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Magnetic Fields ◽  
Oxidative Damage ◽  
Restraint Stress ◽  
Complementary Therapy ◽  
Stress Model ◽  
Static Magnetic Fields ◽  
Stress Markers ◽  
Model Animal ◽  
New Perspective

Stress is a state of vulnerable homeostasis that alters the physiological and behavioral responses. Stress induces oxidative damage in several organs including the brain, liver, kidney, stomach, and heart. Preliminary findings suggested that the magnetic stimulation could accelerate the healing processes and has been an effective complementary therapy in different pathologies. However, the mechanism of action of static magnetic fields (SMFs) is not well understood. In this study, we demonstrated the effects of static magnetic fields (0.8 mT) in a restraint stressed animal model, focusing on changes in different markers of oxidative damage. A significant increase in the plasma levels of nitric oxide (NO), malondialdehyde (MDA), and advanced oxidation protein products (AOPP), and a decrease in superoxide dismutase (SOD), glutathione (GSH), and glycation end products (AGEs) were observed in restraint stress model. Exposure to SMFs over 5 days (30, 60, and 240 min/day) caused a decrease in the NO, MDA, AGEs, and AOPP levels; in contrast, the SOD and GSH levels increased. The response to SMFs was time-dependent. Thus, we proposed that exposure to weak-intensity SMFs could offer a complementary therapy by attenuating oxidative stress. Our results provided a new perspective in health studies, particularly in the context of oxidative stress.

Evaluation of oxidative stress and its modulation by L-Arginine and L-Ascorbic acid in repetitive restraint stress model in Wistar rats

2020 ◽  
Vol 17 ◽  
pp. 100172
Author(s):  
Giridhari Pal ◽  
Tapan Behl ◽  
Vishwajeet Rohil ◽  
Mimansa Khandelwal ◽  
Garima Gupta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Restraint Stress ◽  
Wistar Rats ◽  
Stress Model

scholarly journals Curcumin Reduce Sodium Fluoride-Induced Oxidative Stress in Rat Brain

2018 ◽  
Vol 15 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Nagapuri Kiran Kumar ◽  
Mesram Nageshwar ◽  
Karnati Pratap Reddy
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Oral Administration ◽  
Rat Brain ◽  
Sodium Fluoride ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
The Brain

This study reports the ameliorative role of curcumin against sodium fluoride (NaF) induced oxidative stress in the brain of rats. The rats were divided into control, NaF (20 mg/kg), NaF+Curcumin (20mg/kg) and Curcumin (20mg/kg) groups respectively and treated at everyday interval for 60 consecutive days. Oxidative stress markers in the brain were measured at 60th day. NaF treatment significantly increased LPO content, but decreased the level of GSH and activities of SOD, GPx, and CAT the brain of rats in comparison to the control rats. Oral administration of curcumin to fluoride exposed rats significantly reversed the content of lipid peroxidation, as well as enhanced the level of GSH and SOD, GPx and CAT activities to normal compared to NaF exposed rats. Thus, curcumin showed the potential to prevent sodium fluoride induced oxidative damage in the brain of rats and curcumin may be useful agents against neurodegeneration in the brain.

scholarly journals Oxidative Stress Markers (8-Isoprostane and 8-Hydroxy-2-Deoxyguanosine) in Major Depression: A Case-control Study

2021 ◽  
Author(s):  
Parul Chopra ◽  
Rajesh Sagar ◽  
Asok Kumar Mukhopadhyay
Keyword(s):  
Oxidative Stress ◽  
Major Depression ◽  
Oxidative Damage ◽  
Case Control Study ◽  
Case Control ◽  
Clinical Severity ◽  
Healthy Controls ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Control Study

Introduction: Depression is associated with activation of innate immune response leading to oxidative damage. The 8-isoprostanes and 8-hydroxy-2-deoxyguanosine (8-OHdG) are biomarkers of oxidative damage to lipids and Deoxyribonucleic Acid (DNA), respectively. They have been independently linked to depression. Aim: To study the oxidative stress markers (8-Isoprostanes and 8-OHdG) in subjects with major depression. Materials and Methods: In this observational case-control study 42 cases of depression, 13-25 years of age were recruited from Psychiatry Out Patient Department (OPD) at a tertiary-care hospital in Delhi, India, along with 42 healthy controls. They were assessed clinically and using psychometric evaluation scores, Beck’s Depression Inventory-II (BDI-II) and Hamilton Depression Rating Scale (HAM-D). All 42 subjects were on medication with antidepressants {33/42 with Selective Serotonin Reuptake Inhibitors (SSRI) 8/42 with Tricyclic Antidepressants (TCA) and 1/42 on a combination of both}. Routine laboratory investigations were done. Plasma 8-Isoprostane and serum 8-OHdG concentrations were measured in both cases and controls. The results obtained were analysed using relevant statistical tests on STATA version 11 (StataCorp, 2009). Results: Clinically, all patients had moderate to severe depression. BDI-II and HAM-D scores were raised in all cases as compared to the controls (28.81±5.60 vs 1.62±1.59 for BDI and 20.88±4.67 vs 1.33±1.43 for HAM-D, respectively). The concentration (in depressed vs controls) of plasma 8-Isoprostane (107.70±54.48 pg/mL vs 77.78±60.15 pg/mL) and serum 8-OHdG (2103.03±154 pg/mL vs 2017±164.69 pg/mL) were significantly elevated (p-value <0.05). Though elevated in patients belonging to both genders, showed significant increase of 8-Isoprostane only in females and 8-OHdG only in males as compared to their healthy controls. No correlation of the levels of any of two markers was seen with clinical severity of depression of patients as assessed by BDI. Conclusion: Evidence of oxidative stress to lipids and DNA are present in the peripheral blood. These can be explored further in establishing the biomarkers for diagnosis and prognosis of depression.

The Effects of Moderate, Strenuous, and Overtraining on Oxidative Stress Markers and DNA Repair in Rat Liver

2005 ◽  
Vol 30 (2) ◽  
pp. 186-195 ◽  
Author(s):  
Helga Ogonovszky ◽  
Maria Sasvári ◽  
Agoston Dosek ◽  
István Berkes ◽  
Takao Kaneko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Rat Liver ◽  
Nuclear Dna ◽  
Activity Levels ◽  
Carbonyl Derivative ◽  
Stress Markers ◽  
Cell Extracts

Physical exercise above a certain load has been suggested as being a cause of oxidative stress. We have tested whether training with moderate (MT), strenuous (ST), or over (OT) load can cause alterations in the activities of antioxidant enzymes, lipid peroxidation, protein oxidation, DNA damage, or activity of 8-oxoG-DNA glycosylase (OGG1) in rat liver. The levels of corticosterone decreased in all exercising groups but the differences were not significant. Adrenocorticotrophin hormone (ACTH) levels decreased, not significantly, in MT and OT compared to C. Activity levels of antioxidant enzymes did not change significantly in the liver. The levels of reactive carbonyl derivative (RCD) content decreased in the liver of exercising animals, and the differences reached significance between control and moderately trained groups. The changes in the levels of lipid peroxidation (LIPOX) were not significant, but were lower in the exercised groups. The 8-hydroxydeoxyguanosine (8-OHdG) levels increased in the OT group, and the activity of OGG1 measured from crude cell extracts tended to increase in MT and ST. The findings of this study imply that overtraining induces oxidative damage to nuclear DNA, but not to liver lipids and proteins. Key words: exercise, oxidative damage, adaptation, OGG1

scholarly journals Physiopathological Bases of the Disease Caused by HACE1 Mutations: Alterations in Autophagy, Mitophagy and Oxidative Stress Response

2020 ◽  
Vol 9 (4) ◽  
pp. 913
Author(s):  
Olatz Ugarteburu ◽  
Marta Sánchez-Vilés ◽  
Julio Ramos ◽  
Tamara Barcos-Rodríguez ◽  
Gloria Garrabou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Damage ◽  
Neurodevelopmental Disorder ◽  
Psychomotor Retardation ◽  
Oxidative Stress Response ◽  
Autophagic Flux ◽  
Mrna Levels ◽  
Mitochondrial Oxidative Stress ◽  
Stress Markers

Recessive HACE1 mutations are associated with a severe neurodevelopmental disorder (OMIM: 616756). However, the physiopathologycal bases of the disease are yet to be completely clarified. Whole-exome sequencing identified homozygous HACE1 mutations (c.240C>A, p.Cys80Ter) in a patient with brain atrophy, psychomotor retardation and 3-methylglutaconic aciduria, a biomarker of mitochondrial dysfunction. To elucidate the pathomechanisms underlying HACE1 deficiency, a comprehensive molecular analysis was performed in patient fibroblasts. Western Blot demonstrated the deleterious effect of the mutation, as the complete absence of HACE1 protein was observed. Immunofluorescence studies showed an increased number of LC3 puncta together with the normal initiation of the autophagic cascade, indicating a reduction in the autophagic flux. Oxidative stress response was also impaired in HACE1 fibroblasts, as shown by the reduced NQO1 and Hmox1 mRNA levels observed in H2O2-treated cells. High levels of lipid peroxidation, consistent with accumulated oxidative damage, were also detected. Although the patient phenotype could resemble a mitochondrial defect, the analysis of the mitochondrial function showed no major abnormalities. However, an important increase in mitochondrial oxidative stress markers and a strong reduction in the mitophagic flux were observed, suggesting that the recycling of damaged mitochondria might be targeted in HACE1 cells. In summary, we demonstrate for the first time that the impairment of autophagy, mitophagy and oxidative damage response might be involved in the pathogenesis of HACE1 deficiency.

scholarly journals Bioeffects of Static Magnetic Fields: Oxidative Stress, Genotoxic Effects, and Cancer Studies

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Soumaya Ghodbane ◽  
Aida Lahbib ◽  
Mohsen Sakly ◽  
Hafedh Abdelmelek
Keyword(s):  
Oxidative Stress ◽  
Magnetic Fields ◽  
Life Time ◽  
Genetic Mutation ◽  
Current Evidence ◽  
Static Magnetic Fields ◽  
New Strategy ◽  
Radical Generation ◽  
Living Organisms ◽  
And Oxidative Stress

The interaction of static magnetic fields (SMFs) with living organisms is a rapidly growing field of investigation. The magnetic fields (MFs) effect observed with radical pair recombination is one of the well-known mechanisms by which MFs interact with biological systems. Exposure to SMF can increase the activity, concentration, and life time of paramagnetic free radicals, which might cause oxidative stress, genetic mutation, and/or apoptosis. Current evidence suggests that cell proliferation can be influenced by a treatment with both SMFs and anticancer drugs. It has been recently found that SMFs can enhance the anticancer effect of chemotherapeutic drugs; this may provide a new strategy for cancer therapy. This review focuses on our own data and other data from the literature of SMFs bioeffects. Three main areas of investigation have been covered: free radical generation and oxidative stress, apoptosis and genotoxicity, and cancer. After an introduction on SMF classification and medical applications, the basic phenomena to understand the bioeffects are described. The scientific literature is summarized, integrated, and critically analyzed with the help of authoritative reviews by recognized experts; international safety guidelines are also cited.

scholarly journals Prenatal exposure to testosterone impairs oxidative damage repair efficiency in the domestic chicken ( Gallus gallus )

2013 ◽  
Vol 9 (5) ◽  
pp. 20130684 ◽  
Author(s):  
L. A. Treidel ◽  
B. N. Whitley ◽  
Z M. Benowitz-Fredericks ◽  
M. F. Haussmann
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Gallus Gallus ◽  
Yolk Androgens ◽  
Stress Markers ◽  
Damage Repair ◽  
Before And After ◽  
Total Antioxidant ◽  
Oxidative Challenge ◽  
Acute Stressor

Elevated levels of maternal androgens in avian eggs affect numerous traits, including oxidative stress. However, current studies disagree as to whether prenatal androgen exposure enhances or ameliorates oxidative stress. Here, we tested how prenatal testosterone exposure affects oxidative stress in female domestic chickens ( Gallus gallus ) during the known oxidative challenge of an acute stressor. Prior to incubation, eggs were either injected with an oil vehicle or 5 ng testosterone. At either 17 or 18 days post-hatch, several oxidative stress markers were assessed from blood taken before and after a 20 min acute stressor, as well as following a 25 min recovery from the stressor. We found that, regardless of yolk treatment, during both stress and recovery all individuals were in a state of oxidative stress, with elevated levels of oxidative damage markers accompanied by a reduced total antioxidant capacity. In addition, testosterone-exposed individuals exhibited poorer DNA damage repair efficiencies in comparison with control individuals. Our work suggests that while yolk androgens do not alter oxidative stress directly, they may impair mechanisms of oxidative damage repair.

scholarly journals Oxidative Damage in the Aging Heart: an Experimental Rat Model

2015 ◽  
Vol 9 (1) ◽  
pp. 78-82 ◽  
Author(s):  
Gustavo Lenci Marques ◽  
Francisco Filipak Neto ◽  
Ciro Alberto de Oliveira Ribeiro ◽  
Samuel Liebel ◽  
Rogério de Fraga ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Oxidative Damage ◽  
Catalase Activity ◽  
Protein Carbonylation ◽  
Antioxidant Defenses ◽  
Stress Markers ◽  
Complex Process ◽  
Protein Thiols

Introduction: Several theories have been proposed to explain the cause of ‘aging’; however, the factors that affect this complex process are still poorly understood. Of these theories, the accumulation of oxidative damage over time is among the most accepted. Particularly, the heart is one of the most affected organs by oxidative stress. The current study, therefore, aimed to investigate oxidative stress markers in myocardial tissue of rats at different ages.Methods: Seventy-two rats were distributed into 6 groups of 12 animals each and maintained for 3, 6, 9, 12, 18 and 24 months. After euthanasia, the heart was removed and the levels of non-protein thiols, lipid peroxidation, and protein carbonylation, as well as superoxide dismutase and catalase activities were determined.Results:Superoxide dismutase, catalase activity and lipid peroxidation were reduced in the older groups of animals, when compared with the younger group. However, protein carbonylation showed an increase in the 12-month group followed by a decrease in the older groups. In addition, the levels of non-protein thiols were increased in the 12-month group and not detected in the older groups.Conclusion:Our data showed that oxidative stress is not associated with aging in the heart. However, an increase in non-protein thiols may be an important factor that compensates for the decrease of superoxide dismutase and catalase activity in the oldest rats, to maintain appropriate antioxidant defenses against oxidative insults.

Sign in / Sign up

Export Citation Format

Share Document