Oxidative Stress in Multiple Sclerosis Disease (Review Article)

Background: Multiple sclerosis (MS) is an inflammatory disease of the central nervous system, in which the myelin sheaths got injured. The prevalence of MS is on grow, as well as, it affects the young ages. Females are most common to have MS compared to males. Oxidative stress is the situation of imbalance between oxidants (free radicals and reactive oxygen species (ROS)) and antioxidants in a living system, in which either the oxidants are elevated or antioxidants are reduced, or sometimes both. ROS and oxidative stress have been implicated in the progression of many degenerative diseases, which is important in cracking the unrevealed mysteries of MS. In this review article, some of the proposed mechanisms that link oxidative stress with MS disease would be described. Keywords: Oxidative stress, ROS, multiple sclerosis, antioxidants

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

Clinical and Developmental Immunology ◽

10.1155/2013/708659 ◽

2013 ◽

Vol 2013 ◽

pp. 1-14 ◽

Cited By ~ 86

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.

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Differential susceptibility of a few members of the nasuta–albomicans complex of Drosophila to paraquat-induced lethality and oxidative stress

Genome ◽

10.1139/g11-049 ◽

2011 ◽

Vol 54 (10) ◽

pp. 829-835 ◽

Cited By ~ 2

Author(s):

Mysore S. Ranjini ◽

Ravikumar Hosamani ◽

Muralidhara ◽

Nallur B. Ramachandra

Keyword(s):

Oxidative Stress ◽

Biochemical Analysis ◽

Reduced Glutathione ◽

Differential Susceptibility ◽

Activity Levels ◽

Oxygen Species ◽

Stress Markers ◽

The Status ◽

Markers Of Oxidative Stress ◽

And Oxidative Stress

The evolution of karyotypically stabilized short-lived (SL) and long-lived (LL) cytoraces in the laboratory have been established and validated through our previous lifespan studies. In the present investigation, we examined the possible reason(s) for the differential longevity among selected members of SL and LL cytoraces, employing the well known paraquat (PQ) resistance bioassay. Exposure of these races to varying concentrations of PQ revealed relatively higher resistance among LL cytoraces than SL cytoraces, as evident by the lower incidence of mortality. Biochemical analysis for endogenous markers of oxidative stress revealed that LL-2 cytorace exhibited lower reactive oxygen species (ROS) and lipid peroxidation (LPO) levels, higher activity levels of superoxide dismutase (SOD), and coupled with higher levels of reduced glutathione (GSH) compared with the levels found in SL-2 cytorace. These findings suggest that the higher susceptibility of SL cytoraces to PQ challenge may be, at least in part, related to the higher endogenous levels of oxidative stress markers. Although the precise mechanisms responsible for the longer longevity among LL cytoraces of the nasuta–albomicans complex of Drosophila merits further investigation, our data suggest that the relatively longer lifespan may be related to the status of endogenous markers that renders them more resistant towards oxidative-stress-mediated lethality, as evident in the PQ assay.

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Recent advances on immunosuppressive drugs and remyelination enhancers for the treatment of multiple sclerosis

Current Pharmaceutical Design ◽

10.2174/1381612827666210127121829 ◽

2021 ◽

Vol 27 ◽

Author(s):

Jennifer Cadenas-Fernández ◽

Pablo Ahumada-Pascual ◽

Luis Sanz Andreu ◽

Ana Velasco

Keyword(s):

Multiple Sclerosis ◽

Intracellular Signaling ◽

Demyelinating Disease ◽

Lipid Synthesis ◽

Immunosuppressive Drugs ◽

Nerve Fibers ◽

Myelin Sheaths ◽

Demyelinating Lesions ◽

The Central Nervous System ◽

Lipid Structures

: Mammalian nervous systems depend crucially on myelin sheaths covering the axons. In the central nervous system, myelin sheaths consist of lipid structures which are generated from the membrane of oligodendrocytes (OL). These sheaths allow fast nerve transmission, protect axons and provide them metabolic support. In response to specific traumas or pathologies, these lipid structures can be destabilized and generate demyelinating lesions. Multiple sclerosis (MS) is an example of a demyelinating disease in which the myelin sheaths surrounding the nerve fibers of the brain and spinal cord are damaged. MS is the leading cause of neurological disability in young adults in many countries, and its incidence has been increasing in recent decades. Related to its etiology, it is known that MS is an autoimmune and inflammatory CNS disease. However, there are no effective treatments for this disease and the immunomodulatory therapies that currently exist have proven limited success since they only delay the progress of the disease. Nowadays, one of the main goals in the MS research is to find treatments which allows the recovery of neurological disabilities due to demyelination. To this end, different approaches, such as modulating intracellular signaling or regulating the lipid metabolism of OLs, are being considered. Here, in addition to immunosuppressive or immunomodulatory drugs that reduce the immune response against myelin sheaths, we review a diverse group of drugs that promotes endogenous remyelination in MS patients and whose use may be interesting as potential therapeutic agents in MS disease. To this end, we compile specific treatments against MS that are currently in the market with remyelination strategies which have entered into human clinical trials for future reparative MS therapies. The method used in this study is a systematic literature review on PubMed, Web of Science and Science Direct databases up to May 31, 2020. To narrow down the search results in databases, more specific keywords, such as, “myelin sheath”, “remyelination”, “demyelination”, “oligodendrocyte” and “lipid synthesis” were used to focus the search. We favoured papers published after January, 2015, but did not exclude earlier seminal papers.

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Immunopathological Mechanisms and Oxidative Stress Damage in Multiple Sclerosis

Role of Oxidative Stress in Chronic Diseases ◽

10.1201/b16653-27 ◽

2014 ◽

pp. 549-588

Author(s):

Sayonara Oliveira ◽

Ana Kallaur ◽

Damacio Kaimen-Maciel ◽

Edna Vissoci Reiche

Keyword(s):

Oxidative Stress ◽

Multiple Sclerosis ◽

Stress Damage ◽

And Oxidative Stress

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Oxidative Stress Inside the Pathogenesis of Ascending Aorta Aneurysms: A Clearer Vision for Identifying Promising Biomarkers and Therapeutic Targets

10.20944/preprints202111.0346.v1 ◽

2021 ◽

Author(s):

Carmela Balistreri ◽

Calogera Pisano ◽

Giovanni Ruvolo

Keyword(s):

Oxidative Stress ◽

Risk Factors ◽

Genetic Variants ◽

Complex Disease ◽

Ascending Aorta ◽

Oxygen Species ◽

Aorta Aneurysm ◽

Independent Risk Factors ◽

The Impact ◽

And Oxidative Stress

Ascending aorta aneurysm (AsAA) is a complex disease, currently defined an inflammatory disease. In the sporadic form, AsAA has, indeed, a complex physiopathology with a strong inflammatory basis, significantly modulated by genetic variants in innate/inflammatory genes, acting as independent risk factors and as largely evidenced in our recent studies performed during the last 10 years. Based on these premises, here, we want to revise the impact of reactive oxygen species (ROS) and oxidative stress on AsAA pathophysiology and consequently on the onset and progression of sporadic AsAA. This might consent to add other important pieces in the intricate puzzle of the pathophysiology of this disease with the translational aim to identify biomarkers and targets to apply in the complex management of AsAA, by facilitating the AsAA diagnosis currently based only on imaging evaluations, and the treatment exclusively founded on surgery approaches.

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Oxidative stress in animals: a pathophysiologist's view

Russian veterinary journal ◽

10.32416/2500-4379-2020-4-10-18 ◽

2020 ◽

Vol 2020 (4) ◽

pp. 10-18

Author(s):

Dmitriy Gildikov

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Antioxidant System ◽

Review Article ◽

Publication Activity ◽

Pathophysiological Mechanism ◽

Oxygen Species ◽

The World ◽

Intracellular Oxidative Stress

In the review article, from the modern standpoint, oxidative stress is considered as a universal pathophysiological mechanism of the vast majority of diseases in animals. A brief review of the publication activity in the world on this topic; the significance of reactive oxygen species in the physiology and development of intracellular oxidative stress, the role of etiological factors that initiate their hyperproduction are presented, as well the methods of detecting oxidative stress are characterizited. General concepts of the antioxidant system of the animal body are examined, and the pathophysiological targets of oxidative stress in animals are generalized.

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Advanced Glycation End Products and Oxidative Stress in a Hyperglycaemic Environment

10.5772/intechopen.97234 ◽

2021 ◽

Author(s):

Akio Nakamura ◽

Ritsuko Kawahrada

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Advanced Glycation End Products ◽

Reactive Oxygen ◽

Protein Glycation ◽

Oxygen Species ◽

Advanced Glycation ◽

Glycation End Products ◽

End Products ◽

And Oxidative Stress

Protein glycation is the random, nonenzymatic reaction of sugar and protein induced by diabetes and ageing; this process is quite different from glycosylation mediated by the enzymatic reactions catalysed by glycosyltransferases. Schiff bases form advanced glycation end products (AGEs) via intermediates, such as Amadori compounds. Although these AGEs form various molecular species, only a few of their structures have been determined. AGEs bind to different AGE receptors on the cell membrane and transmit signals to the cell. Signal transduction via the receptor of AGEs produces reactive oxygen species in cells, and oxidative stress is responsible for the onset of diabetic complications. This chapter introduces the molecular mechanisms of disease onset due to oxidative stress, including reactive oxygen species, caused by AGEs generated by protein glycation in a hyperglycaemic environment.

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The Role of MicroRNAs in Diabetes-Related Oxidative Stress

International Journal of Molecular Sciences ◽

10.3390/ijms20215423 ◽

2019 ◽

Vol 20 (21) ◽

pp. 5423 ◽

Cited By ~ 3

Author(s):

Mirza Muhammad Fahd Qadir ◽

Dagmar Klein ◽

Silvia Álvarez-Cubela ◽

Juan Domínguez-Bendala ◽

Ricardo Luis Pastori

Keyword(s):

Oxidative Stress ◽

Target Gene ◽

Cellular Stress ◽

Cellular Damage ◽

Oxygen Species ◽

Non Coding Rnas ◽

And Oxidative Stress

Cellular stress, combined with dysfunctional, inadequate mitochondrial phosphorylation, produces an excessive amount of reactive oxygen species (ROS) and an increased level of ROS in cells, which leads to oxidation and subsequent cellular damage. Because of its cell damaging action, an association between anomalous ROS production and disease such as Type 1 (T1D) and Type 2 (T2D) diabetes, as well as their complications, has been well established. However, there is a lack of understanding about genome-driven responses to ROS-mediated cellular stress. Over the last decade, multiple studies have suggested a link between oxidative stress and microRNAs (miRNAs). The miRNAs are small non-coding RNAs that mostly suppress expression of the target gene by interaction with its 3’untranslated region (3′UTR). In this paper, we review the recent progress in the field, focusing on the association between miRNAs and oxidative stress during the progression of diabetes.

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