scholarly journals Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 818
Author(s):  
D. Allan Butterfield ◽  
Debra Boyd-Kimball
Keyword(s):  
Alzheimer Disease ◽  
Nitrosative Stress ◽  
Review Paper ◽  
Amnestic Mild Cognitive Impairment ◽  
Review Article ◽  
Critical Factors ◽  
Imaging Studies ◽  
Oxidative And Nitrosative Stress ◽  
Mitochondrial Alterations ◽  
The Brain

Oxidative and nitrosative stress are widely recognized as critical factors in the pathogenesis and progression of Alzheimer disease (AD) and its earlier stage, amnestic mild cognitive impairment (MCI). A major source of free radicals that lead to oxidative and nitrosative damage is mitochondria. This review paper discusses oxidative and nitrosative stress and markers thereof in the brain, along with redox proteomics, which are techniques that have been pioneered in the Butterfield laboratory. Selected biological alterations in—and oxidative and nitrosative modifications of—mitochondria in AD and MCI and systems of relevance thereof also are presented. The review article concludes with a section on the implications of mitochondrial oxidative and nitrosative stress in MCI and AD with respect to imaging studies in and targeted therapies toward these disorders. Taken together, this review provides support for the notion that brain mitochondrial alterations in AD and MCI are key components of oxidative and nitrosative stress observed in these two disorders, and as such, they provide potentially promising therapeutic targets to slow—and hopefully one day stop—the progression of AD, which is a devastating dementing disorder.

scholarly journals The Changes of Expression and Methylation of Genes Involved in Oxidative Stress in Course of Chronic Mild Stress and Antidepressant Therapy with Agomelatine

Genes ◽  
2020 ◽  
Vol 11 (6) ◽  
pp. 644
Author(s):  
Paulina Wigner ◽  
Ewelina Synowiec ◽  
Paweł Jóźwiak ◽  
Piotr Czarny ◽  
Michał Bijak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitrosative Stress ◽  
Mononuclear Cells ◽  
Methylation Status ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Oxidative And Nitrosative Stress ◽  
Peripheral Blood Mononuclear ◽  
Taqman Gene Expression Assay ◽  
The Brain

Preclinical studies conducted so far suggest that oxidative stress processes may be associated with the mechanism of depression development. This study shows the effects of chronic administration of agomelatine on expression and the methylation status of Sod1, Sod2, Gpx1, Gpx4, Cat, Nos1, and Nos2 in the brain stricture and blood in the chronic mild stress (CMS) animal model of depression. The animals were exposed to the CMS procedure and treatment with agomelatine (10 mg/kg/day, IP) for five weeks and then were sacrificed. TaqMan Gene Expression Assay, Western blot, and methylation-sensitive high-resolution melting techniques were used to evaluate mRNA and protein expression of the genes, and the methylation status of their promoters. Gpx1, Gpx4, and Sod2 expression in the PBMCs and Sod1 and Sod2 expression in the brain were reduced in the stressed group after agomelatine administration. CMS caused an increase in the methylation of the third Gpx4 promoter in peripheral blood mononuclear cells and Gpx1 promoter in the cerebral cortex. Additionally, stressed rats treated with agomelatine displayed a significantly lower Gpx4 level in the hypothalamus. The results confirm the hypothesis that the CMS procedure and agomelatine administration change the expression level and methylation status of the promoter region of genes involved in oxidative and nitrosative stress.

scholarly journals MicroRNAs, Multiple Sclerosis and Depression

2021 ◽  
Vol 22 (15) ◽  
pp. 7802
Author(s):  
Hsiuying Wang
Keyword(s):  
Multiple Sclerosis ◽  
Depressive Disorders ◽  
Nitrosative Stress ◽  
Mirna Regulation ◽  
Oxidative And Nitrosative Stress ◽  
Relapsing Remitting ◽  
The Central Nervous System ◽  
Patients Experience ◽  
Brain And Spinal Cord ◽  
The Brain

Multiple sclerosis (MS) is a chronic disease of the central nervous system that affects the brain and spinal cord. There are several disease courses in MS including relapsing–remitting MS (RRMS), primary progressive MS (PPMS), and secondary progressive MS (SPMS). Up to 50% of MS patients experience depressive disorders. Major depression (MD) is a serious comorbidity of MS. Many dysfunctions including neuroinflammation, peripheral inflammation, gut dysbiosis, chronic oxidative and nitrosative stress, and neuroendocrine and mitochondrial abnormalities may contribute to the comorbidity between MS and MD. In addition to these actions, medical treatment and microRNA (miRNA) regulation may also be involved in the mechanisms of the comorbidity between MS and MD. In the study, I review many common miRNA biomarkers for both diseases. These common miRNA biomarkers may help further explore the association between MS and MD.

Malfunctions of the conjugated system “Restoring thiols – Nitrogen oxide” with acute cerebrovascular accident and possible correction

2015 ◽  
Vol 17 (4) ◽  
Author(s):  
S. V. Horbachova ◽  
I. F. Bielenichev ◽  
L. I. Kucherenko
Keyword(s):  
Brain Tissue ◽  
Nitrosative Stress ◽  
Free Radical Oxidation ◽  
Thiol Group ◽  
Oxidative And Nitrosative Stress ◽  
Radical Oxidation ◽  
Active Mobilization ◽  
Common Carotid Arteries ◽  
The Brain ◽  
Stress Simulation

<p>Experimental acute ischemic stroke was modeled by bilateral occlusion of the common carotid arteries in rats. Antioxidant system in the brain tissue was evaluated by the activity of key enzymes of thiol and disulfide indicators<br />nitrosative stress. Simulation of acute ischemic accompanied by violation of the thiol-disulfide balance and increased nitrotyrosine levels, indicating that the development of oxidative and nitrosative stress in brain tissue. It is established<br />that the use of thiol-containing antioxidants – Thiotriazoline and Angiolin set the highest possible ratio between the levels of reduced and oxidized thiol groups and glutathione, which indicates that the active mobilization of thioldisulfide<br />system in the neutralization products of free-radical oxidation. Identified effects of the drugs used due to the presence in their structure of the thiol group, which contributes to the normalization of the glutathione system in conditions of oxidative stress.</p>

scholarly journals Immunohistochemical Study of Antioxidant Enzymes Regulated by Nrf2 in the Models of Epileptic Seizures (KA and PTZ)

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
María Fernanda Munguía-Martínez ◽  
Concepción Nava-Ruíz ◽  
Amairani Ruíz-Díaz ◽  
Araceli Díaz-Ruíz ◽  
Petra Yescas-Gómez ◽  
...  
Keyword(s):  
Antioxidant Enzymes ◽  
Nitrosative Stress ◽  
Epileptic Seizures ◽  
Experimental Models ◽  
Immunohistochemical Expression ◽  
Oxidative And Nitrosative Stress ◽  
Stress Effects ◽  
Spontaneous Seizures ◽  
The Brain

Epilepsy is a neurological disorder characterized by recurrent spontaneous seizures due to an imbalance between cerebral excitability and inhibition, with a tendency towards uncontrolled excitability. Epilepsy has been associated with oxidative and nitrosative stress due to prolonged neuronal hyperexcitation and loss neurons during seizures. The experimental animal models report level of ATP diminished and increase in lipid peroxidation, catalase, and glutathione altered activity in the brain. We studied the immunohistochemical expression and localization of antioxidant enzymes GPx, SOD, and CAT in the rat brains treated with KA and PTZ. A significant decrease was observed in the number of immunoreactive cells to GPx, without significant changes for SOD and CAT in KA-treated rats, and decrease in the number of immunoreactive cells to SOD, without significant changes for GPx and only CAT in PTZ-treated rats. Evident immunoreactivity of GPx, SOD, and CAT was observed mainly in astrocytes and neurons of the hippocampal brain region in rats exposed at KA; similar results were observed in rats treated with PTZ at the first hours. These results provide evidence supporting the role of activation of the Nrf2 antioxidant system pathway against oxidative stress effects in the experimental models of epileptic seizures.

scholarly journals Oxidative stress and post-stroke depression

2018 ◽  
Vol 16 (3) ◽  
pp. 249-253 ◽  
Author(s):  
D. Komsiyska
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Nitrosative Stress ◽  
Multifactorial Disease ◽  
Oxygen Utilization ◽  
Oxidative And Nitrosative Stress ◽  
Post Stroke ◽  
Mental Diseases ◽  
Post Stroke Depression ◽  
The Brain

The topic of post-stroke depression etiology is reviewed in two main approaches. Some suggest that post-stroke depression is caused by the brain damage itself. On the contrary, others assume that this is a psychologic response to injuries or loss. Many discoveries can be examined as evidence for both the physiological and psychosocial mechanism of post-stroke depression. The two methods are not self-excluding, but instead describe post-stroke depression as a complex and multifactorial disease with interactions between the physiological and environmental factor. One hypothesis about depression occurrence is the inflammatory, oxidative and nitrosative stress (IO&NS) depression theory. Oxidative stress mechanisms are implied in the pathogenesis of mental diseases. The brain is considered particularly vulnerable to oxidative damage, due to its relatively high oxygen utilization and thus generation of free radical subordinate products, its modest antioxidant protections and its lipid-rich resistance.

scholarly journals Modulation of microglial function by the antidepressant drug venlafaxine 28 November 2014

2014 ◽  
Vol 7 (4) ◽  
pp. 201-207 ◽  
Author(s):  
Michal Dubovický ◽  
Eszter Császár ◽  
Kristína Melicherčíková ◽  
Marcela Kuniaková ◽  
Lucia Račková
Keyword(s):  
Protective Effect ◽  
Nitrosative Stress ◽  
Antidepressant Drug ◽  
Blood Levels ◽  
Marginal Effect ◽  
Oxidative And Nitrosative Stress ◽  
Rapid Reduction ◽  
Microglia Cell ◽  
Inflammatory Parameters ◽  
The Brain

ABSTRACT An increasing amount of data suggests that depression is an inflammatory disease. Depressed patients have higher peripheral blood levels of inflammatory markers which have been shown to access the brain and interact with the pathophysiological domain known to be involved in depression. Furthermore, microglia activation may play an important role in the inflammatory pathophysiology of depression. In BV-2 microglia cell line, the present study investigated the potential anti-inflammatory effects of venlafaxine, along with its potential influence on injury of lipopolysaccharide (LPS)-stimulated cells. Although venlafaxine showed only marginal influence on the majority of the pro-inflammatory parameters assessed (in particular NO release, phagocytosis and proliferation), it significantly suppressed superoxide production by the stimulated cells. In addition, venlafaxine exerted also a protective effect on mitochondrial membrane potential and lysosomes of the stimulated microglia. In conclusion, our results suggest that although VEN might have only a marginal effect on major pro-inflammatory parameters of microglia, its inhibitory effect on superoxide generation can contribute to the prevention of harmful effects of oxidative and nitrosative stress involved in the pathogenesis of depression. Moreover, the protective effect of VEN on viability of microglia can prevent a rapid reduction of these cells, thus avoiding limitations of several physiological processes in the brain and possibly also the progression of depression

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