scholarly journals The effect of exogenous melatonin on behavior and oxidative stress indicators in the brain of aging mice with experimental models of nervous system pathology

2021 ◽  
Vol 17 (2) ◽  
pp. 37-43
Author(s):  
I.F. Labunets ◽  
N.A. Utko ◽  
T.N. Panteleymonova ◽  
G.M. Butenko
Keyword(s):  
Oxidative Stress ◽  
Nervous System ◽  
Antioxidant Properties ◽  
Step Length ◽  
Experimental Models ◽  
Antioxidant Protection ◽  
Exogenous Melatonin ◽  
Positive Effects ◽  
The Brain ◽  
And Oxidative Stress

Background. There is a connection between impaired functioning of the nervous system and oxidative stress in Parkinson’s disease and multiple sclerosis. The influence of age on the development of these pathologies was shown, as well as the antioxidant properties of the hormone melatonin. The purpose was to investigate the effect of melatonin administration on the behavior, factors of oxidative stress and antioxidant protection in the brain of aging mice with experimental models of parkinsonism and demyelination. Materials and methods. 129/Sv mice aged 15–16 months received neurotoxins 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at a dose of 30 mg/kg once, or cuprizone daily with food for 3 weeks. Melatonin was administered at a dose of 1 mg/kg daily at 6 p.m. starting from day 7–8 of toxin exposure. The content of malondialdehyde, the activity of antioxidant enzymes in the brain and behavior parameters were assessed in the open field tests for rigidity and in the rotarod test. Results. The locomotor, emotional and exploratory activities in mice with parkinsonism and demyelination models are lower than those in intact animals. Muscle tone decreases under the influence of cuprizone and increases after MPTP injection; the step length decreases in parkinsonism. Melatonin treatment resulted in increasing the number of squares, step length, and decreasing the retention time on a rotating cylinder in mice with parkinsonism and increasing the number of squares, rea-ring and number of boluses in cuprizone-treated mice. Exogenous melatonin reduces the level of brain malondialdehyde increased by neurotoxins and increases the reduced activity of superoxide dismutase and catalase in mice with parkinsonism, catalase and glutathione peroxidase in mice with demyelination. Conclusions. The positive effects of melatonin on the behavior of aging mice with the MPTP parkinsonism model and the cuprizone model of demyeli-nation are mediated by increased antioxidant protection in the brain.

scholarly journals Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Genaro G. Ortiz ◽  
Fermín P. Pacheco-Moisés ◽  
Oscar K. Bitzer-Quintero ◽  
Ana C. Ramírez-Anguiano ◽  
Luis J. Flores-Alvarado ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Tissue Injury ◽  
Autoimmune Disorder ◽  
Demyelinating Lesions ◽  
The Central Nervous System ◽  
The Brain ◽  
And Oxidative Stress

Multiple sclerosis (MS) exhibits many of the hallmarks of an inflammatory autoimmune disorder including breakdown of the blood-brain barrier (BBB), the recruitment of lymphocytes, microglia, and macrophages to lesion sites, the presence of multiple lesions, generally being more pronounced in the brain stem and spinal cord, the predominantly perivascular location of lesions, the temporal maturation of lesions from inflammation through demyelination, to gliosis and partial remyelination, and the presence of immunoglobulin in the central nervous system and cerebrospinal fluid. Lymphocytes activated in the periphery infiltrate the central nervous system to trigger a local immune response that ultimately damages myelin and axons. Pro-inflammatory cytokines amplify the inflammatory cascade by compromising the BBB, recruiting immune cells from the periphery, and activating resident microglia. inflammation-associated oxidative burst in activated microglia and macrophages plays an important role in the demyelination and free radical-mediated tissue injury in the pathogenesis of MS. The inflammatory environment in demyelinating lesions leads to the generation of oxygen- and nitrogen-free radicals as well as proinflammatory cytokines which contribute to the development and progression of the disease. Inflammation can lead to oxidative stress and vice versa. Thus, oxidative stress and inflammation are involved in a self-perpetuating cycle.

Toxic Effects of Methamphetamine on Perivascular Health: Co-morbid Effects of Stress and Alcohol Use Disorders

2021 ◽  
Vol 19 ◽  
Author(s):  
Eric A. Rodriguez ◽  
Bryan K. Yamamoto
Keyword(s):  
Oxidative Stress ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Alcohol Use ◽  
Alcohol Abuse ◽  
Chronic Stress ◽  
Alcohol Use Disorders ◽  
Vascular Health ◽  
The Brain ◽  
And Oxidative Stress

: Methamphetamine (Meth) abuse presents a worldwide problem and commonly occurs with stress and/or alcohol use disorders. Regardless, the biological causes and consequences of these co-morbidities are unclear. Whereas the mechanisms of Meth, stress and alcohol abuse have been examined individually and well-characterized, these processes overlap significantly and can impact the neural and peripheral consequences of Meth. This review focuses on the deleterious cardio- and cerebrovascular effects of Meth, stress, alcohol abuse and their comorbid effects on the brain and periphery. Points of emphasis are on the composition of the blood brain barrier and their effects on the heart and vasculature. The autonomic nervous system, inflammation, and oxidative stress are specifically highlighted as common mediators of the toxic consequences to vascular and perivascular health. Given that a significant portion of the Meth abusing population also presents with stress and alcohol use disorders prompts a need to understand the mechanisms underlying their comorbidities. Little is known about their possible convergent effects and therefore, the purpose of this critical review is to identify shared mechanisms of Meth, chronic stress and alcohol abuse that contribute to the dysfunction of vascular health and underscore the need for studies that directly address their interactions.

scholarly journals Thioredoxin System Regulation in the Central Nervous System: Experimental Models and Clinical Evidence

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Daniela Silva-Adaya ◽  
María E. Gonsebatt ◽  
Jorge Guevara
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Thioredoxin Reductase ◽  
Brain Regions ◽  
Experimental Models ◽  
Thioredoxin System ◽  
The Central Nervous System ◽  
Postmortem Brains ◽  
The Brain

The reactive oxygen species produced continuously during oxidative metabolism are generated at very high rates in the brain. Therefore, defending against oxidative stress is an essential task within the brain. An important cellular system against oxidative stress is the thioredoxin system (TS). TS is composed of thioredoxin, thioredoxin reductase, and NADPH. This review focuses on the evidence gathered in recent investigations into the central nervous system, specifically the different brain regions in which the TS is expressed. Furthermore, we address the conditions that modulate the thioredoxin system in both, animal models and the postmortem brains of human patients associated with the most common neurodegenerative disorders, in which the thioredoxin system could play an important part.

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

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.

Ozone Therapy Ameliorates Nervous System Disorders and Oxidative Stress in Patients During Ethanol Withdrawal—A Pilot Study

2012 ◽  
Vol 34 (6) ◽  
pp. 432-437
Author(s):  
María Teresa Díaz-Soto ◽  
Angela Fraga Pérez ◽  
Jaqueline Dranguet Vaillant ◽  
A. Mallok ◽  
Renate Viebahn-Hänsler ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nervous System ◽  
Pilot Study ◽  
Ethanol Withdrawal ◽  
Ozone Therapy ◽  
And Oxidative Stress
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