scholarly journals Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats

Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 485 ◽  
Author(s):  
Pereira-Maróstica ◽  
Castro ◽  
Gonçalves ◽  
Silva ◽  
Bracht ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Methyl Jasmonate ◽  
Lipid Peroxides ◽  
Mitochondrial Respiratory Chain ◽  
Antioxidant Defenses ◽  
Protein Carbonyls ◽  
Partial Recovery ◽  
Negative Effects ◽  
The Brain ◽  
And Oxidative Stress

Methyl jasmonate (MeJA), common in the plant kingdom, is capable of reducing articular and hepatic inflammation and oxidative stress in adjuvant-induced arthritic rats. This study investigated the actions of orally administered MeJA (75–300 mg/kg) on inflammation, oxidative stress and selected enzyme activities in the brain of Holtzman rats with adjuvant-induced arthritis. MeJA prevented the arthritis-induced increased levels of nitrites, nitrates, lipid peroxides, protein carbonyls and reactive oxygen species (ROS). It also prevented the enhanced activities of myeloperoxidase and xanthine oxidase. Conversely, the diminished catalase and superoxide dismutase activities and glutathione (GSH) levels caused by arthritis were totally or partially prevented. Furthermore, MeJA increased the activity of the mitochondrial isocitrate dehydrogenase, which helps to supply NADPH for the mitochondrial glutathione cycle, possibly contributing to the partial recovery of the GSH/oxidized glutathione (GSSG) ratio. These positive actions on the antioxidant defenses may counterbalance the effects of MeJA as enhancer of ROS production in the mitochondrial respiratory chain. A negative effect of MeJA is the detachment of hexokinase from the mitochondria, which can potentially impair glucose phosphorylation and metabolism. In overall terms, however, it can be concluded that MeJA attenuates to a considerable extent the negative effects caused by arthritis in terms of inflammation and oxidative stress.

Anaerobic Exercise and Oxidative Stress: A Review

2004 ◽  
Vol 29 (3) ◽  
pp. 245-263 ◽  
Author(s):  
Richard J. Bloomer ◽  
Allan H. Goldfarb
Keyword(s):  
Oxidative Stress ◽  
Exercise Training ◽  
Exercise Bout ◽  
Oxidative Modification ◽  
Anaerobic Exercise ◽  
Antioxidant Defenses ◽  
Protein Carbonyls ◽  
Anaerobic Work ◽  
Exercise Induced ◽  
And Oxidative Stress

Oxidative stress and subsequent damage to cellular proteins, lipids, and nucleic acids, as well as changes to the glutathione system, are well documented in response to aerobic exercise. However, far less information is available on anaerobic exercise-induced oxidative modifications. Recent evidence indicates that high intensity anaerobic work does result in oxidative modification to the above-mentioned macromolecules in both skeletal muscle and blood. Also, it appears that chronic anaerobic exercise training can induce adaptations that act to attenuate the exercise-induced oxidative stress. These may be specific to increased antioxidant defenses and/or may act to reduce the generation of pro-oxidants during and after exercise. However, a wide variety of exercise protocols and assay procedures have been used to study oxidative stress pertaining to anaerobic work. Therefore, precise conclusions about the exact extent and location of oxidative macromolecule damage, in addition to the adaptations resulting from chronic anaerobic exercise training, are difficult to indicate. This manuscript provides a review of anaerobic exercise and oxidative stress, presenting both the acute effects of a single exercise bout and the potential for adaptations resulting from chronic anaerobic training. Key words: antioxidants, free radicals, training, lipid peroxidation, protein carbonyls

Methyl jasmonate delays the latency to anoxic convulsions by normalizing the brain levels of oxidative stress biomarkers and serum corticosterone contents in mice with repeated anoxic stress

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Abayomi Ololade Adelaja ◽  
Oluwafemi Gabriel Oluwole ◽  
Oritoke Modupe. Aluko ◽  
Solomon Umukoro
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Methyl Jasmonate ◽  
Brain Injuries ◽  
Antioxidant Property ◽  
Oxidative Stress Biomarkers ◽  
Serum Corticosterone ◽  
Stress Agent ◽  
Cellular Antioxidants ◽  
The Brain

AbstractObjectivesRepeated exposure to anoxic stress damages the brain through cortisol-mediated increases in oxidative stress and cellular-antioxidants depletion. Thus, compounds with antioxidant property might confer protection against anoxic stress-induced brain injuries. In this study, we further examined the protective effect of methyl jasmonate (MJ), a potent anti-stress agent against anoxic stress-induced convulsions in mice.MethodsThirty-six male Swiss mice randomized into six groups (n=6) were given MJ (25, 50 and 100 mg/kg, i.p.) or vehicle (10 mL/kg, i.p.) 30 min before 15 min daily exposure to anoxic stress for 7 days. The latency(s) to anoxic convulsion was recorded on day 7. The blood glucose and serum corticosterone levels were measured afterwards. The brains were also processed for the determination of malondialdehyde, nitrite, and glutathione levels.ResultsMethyl jasmonate (MJ) delayed the latency to anoxic convulsion and reduced the blood glucose and serum corticosterone levels. The increased malondialdehyde and nitrite contents accompanied by decreased glutathione concentrations in mice with anoxic stress were significantly attenuated by MJ.ConclusionsThese findings further showed that MJ possesses anti-stress property via mechanisms relating to the reduction of serum contents of corticosterone and normalization of brain biomarker levels of oxidative stress in mice with anoxic stress.

scholarly journals SHR/NCrl rats as a model of ADHD can be discriminated from controls based on their brain, blood, or urine metabolomes

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Camille Dupuy ◽  
Pierre Castelnau ◽  
Sylvie Mavel ◽  
Antoine Lefevre ◽  
Lydie Nadal-Desbarats ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Attention Deficit Hyperactivity Disorder ◽  
Animal Model ◽  
Metabolic Pathways ◽  
Neurodevelopmental Disorder ◽  
Hyperactivity Disorder ◽  
Pathophysiological Condition ◽  
The Brain ◽  
And Oxidative Stress ◽  
Peripheral Samples

AbstractAttention-Deficit Hyperactivity Disorder (ADHD) is one of the most common neurodevelopmental disorder characterized by inattention, impulsivity, and hyperactivity. The neurobiological mechanisms underlying ADHD are still poorly understood, and its diagnosis remains difficult due to its heterogeneity. Metabolomics is a recent strategy for the holistic exploration of metabolism and is well suited for investigating the pathophysiology of diseases and finding molecular biomarkers. A few clinical metabolomic studies have been performed on peripheral samples from ADHD patients but are limited by their access to the brain. Here, we investigated the brain, blood, and urine metabolomes of SHR/NCrl vs WKY/NHsd rats to better understand the neurobiology and to find potential peripheral biomarkers underlying the ADHD-like phenotype of this animal model. We showed that SHR/NCrl rats can be differentiated from controls based on their brain, blood, and urine metabolomes. In the brain, SHR/NCrl rats displayed modifications in metabolic pathways related to energy metabolism and oxidative stress further supporting their importance in the pathophysiology of ADHD bringing news arguments in favor of the Neuroenergetic theory of ADHD. Besides, the peripheral metabolome of SHR/NCrl rats also shared more than half of these differences further supporting the importance of looking at multiple matrices to characterize a pathophysiological condition of an individual. This also stresses out the importance of investigating the peripheral energy and oxidative stress metabolic pathways in the search of biomarkers of ADHD.

scholarly journals Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 229
Author(s):  
JunHyuk Woo ◽  
Hyesun Cho ◽  
YunHee Seol ◽  
Soon Ho Kim ◽  
Chanhyeok Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Computational Models ◽  
Neuronal Damage ◽  
Living Organism ◽  
The Body ◽  
Mitochondrial Functions ◽  
A Cell ◽  
The Brain ◽  
And Oxidative Stress

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5′-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

Exposure to aluminium causes behavioural alterations and oxidative stress in the brain of adult zebrafish

2021 ◽  
Vol 85 ◽  
pp. 103636
Author(s):  
Teresa Capriello ◽  
Luis M. Félix ◽  
Sandra M. Monteiro ◽  
Dércia Santos ◽  
Rita Cofone ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adult Zebrafish ◽  
The Brain ◽  
And Oxidative Stress

Abstract 305: Nebivolol Confers Mitochondria-Targeted Cardioprotection in Isoproterenol-Induced Acute Stressor State

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Sumeet S Vaikunth ◽  
Karl T Weber ◽  
Syamal K Bhattacharya
Keyword(s):  
Oxidative Stress ◽  
Cardiac Tissue ◽  
Mitochondrial Permeability Transition ◽  
Therapeutic Potential ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Antioxidant Defenses ◽  
Sprague Dawley ◽  
Acute Stressor ◽  
And Oxidative Stress

Introduction: Isoproterenol-induced acute stressor state simulates injury from burns or trauma, and results in Ca 2+ overloading and oxidative stress in diverse tissues, including cardiac myocytes and their subsarcolemmal mitochondria (SSM), overwhelming endogenous Zn 2+ -based antioxidant defenses. We hypothesized that pretreatment with nebivolol (Nebi), having dual beta-1 antagonistic and novel beta-3 receptor agonistic properties, would prevent Ca 2+ overloading and oxidative stress and upregulate Zn 2+ -based antioxidant defenses, thus enhancing its overall cardioprotective potential in acute stressor state. Methods: Eight-week-old male Sprague-Dawley rats received a single subcutaneous dose of isoproterenol (1 mg/kg) and compared to those treated with Nebi (10 mg/kg by gavage) for 10 days prior to isoproterenol. SSM were harvested from cardiac tissue at sacrifice. Total Ca 2+ , Zn 2+ and 8-isoprostane levels in tissue, and mitochondrial permeability transition pore (mPTP) opening, free [Ca 2+ ] m and H 2 O 2 production in SSM were monitored. Untreated, age-/sex-matched rats served as controls; each group had six rats and data shown as mean±SEM. Results: Compared to controls, isoproterenol rats revealed: (1) Significantly (*p<0.05) increased cardiac tissue Ca 2+ (8.2±0.8 vs. 13.7±1.0*, nEq/mg fat-free dry tissue (FFDT)), which was abrogated ( # p<0.05) by Nebi (8.9±0.4 # ); (2) Reduced cardiac Zn 2+ (82.8±2.4 vs. 78.5±1.0*, ng/mg FFDT), but restored by Nebi (82.4±0.6 # ); (3) Two-fold rise in cardiac 8-isoprostane (111.4±13.7 vs. 232.1±17.2*, pmoles/mg protein), and negated by Nebi (122.3+14.5 # ); (4) Greater opening propensity for mPTP that diminished by Nebi; (5) Elevated [Ca 2+ ] m (88.8±2.5 vs. 161.5±1.0*, nM), but normalized by Nebi (93.3±2.7 # ); and (6) Increased H 2 O 2 production by SSM (97.4±5.3 vs. 142.8±7.0*, pmoles/mg protein/min), and nullified by Nebi (106.8±9.0 # ). Conclusions : Cardioprotection conferred by Nebi, a unique beta-blocker, prevented Ca 2+ overloading and oxidative stress in cardiac tissue and SSM, while simultaneously augmenting antioxidant capacity and promoting mPTP stability. Therapeutic potential of Nebi in patients with acute stressor states remains a provocative possibility that deserves to be explored.

246 Effects of Feeding Thermally Processed Spray-dried Egg Whites on Growth Performance, Apparent Digestibility, and Oxidative Stress in Nursery Pigs

2021 ◽  
Vol 99 (Supplement_1) ◽  
pp. 91-92
Author(s):  
Victoria C Wilson ◽  
Brian J Kerr
Keyword(s):  
Oxidative Stress ◽  
Growth Performance ◽  
Liver Tissue ◽  
Protein Carbonyls ◽  
Nursery Pigs ◽  
Thermally Processed ◽  
Markers Of Oxidative Stress ◽  
Dietary Treatments ◽  
And Oxidative Stress ◽  
Spray Dried

Abstract The objectives of this study were to determine if feeding thermally processed (TP, heated at 100°C for 120 h) spray-dried egg whites (SDEW) to nursery pigs would impact growth performance, apparent total tract digestibility (ATTD) of GE, N, and S, and oxidative stress. Thirty-two barrows, (initial BW 7.1 kg) were randomly assigned to dietary treatments with 1 pig per pen. In a preliminary study, thermally processing SDEW at 100°C for 120 h increased protein carbonyls (PC) from 6 µmol/g to 19.4 µmol/g (P ≤ 0.01). Diets included either 12% SDEW, 6% TP-SDEW plus 6% SDEW, or 12% TP-SDEW. The experiment lasted 24 d for collection of growth performance data, while plasma was collected on d 21 and liver tissue harvested on d 24 to analyze for markers of oxidative stress. Feces were collected on d 22 for measures of ATTD. Daily gain, daily feed intake, feed efficiency, and ATTD of GE were not found to be different among dietary treatments (P ≥ 0.57). In contrast, ATTD of N (P = 0.11) and S (P = 0.03) were found to increase with increasing protein oxidation in the diet. There was no change in the plasma or liver F2-isoprostanes and 8-hydroxy-2’-deoxyguanosine among dietary treatments (P ≥ 0.28). An increase in plasma PC (P = 0.02) was observed in pigs fed 12% TP-SDEW compared to pigs fed 12% SDEW and pigs fed 6% TP-SDEW. In contrast, a decrease in liver tissue PC (P = 0.04) was observed in pigs fed 6% TP-SDEW compared to pigs fed 12% SDEW and 12% TP-SDEW. These results indicate that feeding TP-SDEW does not affect growth performance, ATTD of GE, and oxidative stress as indicated by F2-isoprostanes or 8-hydroxy-2’-deoxyguanosine; but appeared to have variable effects on oxidative stress as measured by PC.

scholarly journals The Effect of Herniarin on Spatial Working Memory, Pain Threshold, and Oxidative Stress in Ischemic Hypoperfusion Model in Rats

2021 ◽  
Vol 7 (1) ◽  
pp. 42-50
Author(s):  
Zahra Nazari Barchestani ◽  
◽  
Maryam Rafieirad ◽  
Keyword(s):  
Oxidative Stress ◽  
Pain Threshold ◽  
Male Rats ◽  
Control Group ◽  
Tail Flick ◽  
Pain Thresholds ◽  
Ischemic Group ◽  
Significant Difference ◽  
The Brain ◽  
And Oxidative Stress

Background: Ischemia causes severe neuronal damage and induces oxidative stress, memory impairment, and reduces pain threshold. Herniarin is a powerful antioxidant. Objectives: This study aimed to evaluate the effect of herniarin on memory, pain, and oxidative stress in an ischemia model in male rats. Materials & Methods: In this study, 50 male rats were divided into 5 groups of control, sham, ischemic, and two other ischemic groups, which received herniarin at doses of 150 and 300 mg/kg by gavage for 14 days. Behavioral tests were performed by shuttle box, and Y-maze and pain tests were performed by Tail-Flick test. Then, the rats’ brains were extracted to evaluate lipid peroxidation and measure the levels of thiol and Glutathione Peroxidase (GPX) in the hippocampus and striatum tissues. The results were expressed as Mean±SEM and then analyzed using suitable statistical methods of ANOVA and least significant difference post-hoc test in SPSS V. 20. Results: Herniarin significantly increased the avoidance memory, spatial memory, and pain thresholds of ischemic rats at different concentrations (P<0.001). Besides, the amount of malondialdehyde (MDA) and thiol in the ischemic group increased significantly in comparison to the control group (P<0.001). Also, in the ischemic group, GPX (P<0.001) significantly decreased. Decreased MDA (P<0.001) and thiol (P<0.001) and increased GPX levels were observed with herniarin administration (P<0.01). Conclusion: According to this study’s results, herniarin can remove free radicals and oxidant substances from the brain. Thus, it improves memory and pain thresholds in the brain hypoperfusion ischemia model.

Sign in / Sign up

Export Citation Format

Share Document