Multiple sclerosis and oxidative stress—a clinical perspective

Kostić, Milica; Rajković, Jovana; Floranovic, M. S. Potic; Dimov, Irena; Pavlović, Dušica

doi:10.1134/s1819712412040083

Cited by 7 publications

(6 citation statements)

References 77 publications

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“…Many authors suggest that due to the harmful role of ROS in the pathology of neurodegenerative diseases, antioxidants reduce tissue damage caused by reactive species [32][33][34][35][36]. Some blood cells may play a similar role.…”

Section: Discussionmentioning

confidence: 99%

Do catalase and glutathione peroxidase protect blood platelets from lipid peroxidation in multiple sclerosis?

Fijałkowski¹,

Jędrzejczak-Pospiech²,

Błaszczyk³

2018

ppn

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Purpose: Catalase (cat) and glutathione peroxidase (GSH-Px) activities and thiobarbituric acid reactive substances (TBARS) concentration in blood platelets were determined in patients with multiple sclerosis (MS). Methods: The study was carried out in a group of 36 patients, men and women, aged 21-50 years old. They were divided into groups dependently on the degree of motor disability and duration of the disease. The control group included 15 healthy individuals of similar age to the study group. The activity of catalase was estimated according to the method by Beers and Sizer. Glutathione peroxidase activity was determined by the method of Sedlak and Lindsay, modified by Little and O'Brien. The concentration of thiobarbituric acid reactive substances in blood platelets was carried out using the method by Placer et al. Results: We observed a lower level of TBARS concentration in platelets of MS patients than in control group with an enhanced activities of both antioxidative enzymes on the basis of disability degree and duration of the disease. Conclusions: Catalase and glutathione peroxidase protect blood platelets from lipid peroxidation process in multiple sclerosis patients and may play a role in the course of the disease. It may also suggest involvement of lipid peroxidation in the activity of multiple sclerosis.

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Section: Discussionmentioning

confidence: 99%

Do catalase and glutathione peroxidase protect blood platelets from lipid peroxidation in multiple sclerosis?

Fijałkowski¹,

Jędrzejczak-Pospiech²,

Błaszczyk³

2018

ppn

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“…It has been demonstrated in studies with animal models of MS, the experimental autoimmune encephalomyelitis (EAE), where the primary event is the infiltration of lymphocytes and autoreactive CD4+ T cells that destroy myelin sheaths [23]. However, in some cases stress or death of oligodendrocytes could be an initial event in the MS presentation [24, 25]. The death of oligodendrocytes and the formation of new lesions may be triggered by a viral infection, followed by microglial activation and the recruitment of CD4, CD8 T cells, and macrophages (MQs) within the lesions [26].…”

Section: Immune Function In Multiple Sclerosismentioning

confidence: 99%

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

Ortíz

Pacheco-Moisés

Bitzer-Quintero

et al. 2013

Clinical and Developmental Immunology

159

125

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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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“…Increased neuronal apoptosis in the brain causes neuronal loss and reduces the number of synapses ( Glantz et al, 2006 ; Zhou et al, 2019 ). Neuronal excitotoxicity produced by high glutamate concentrations in patients with MS could be another mechanism to downregulate BDNF by inhibiting CREB binding to DNA ( Zou and Crews, 2006 ; Kostic et al, 2013 ). Oxidative stress is important in the pathogenesis of neuro-inflammatory diseases such as MS ( LeVine, 1992 ; Sayre et al, 2008 ).…”

Section: The Concurrent Effects Of Covid-19 and Ms On Mental And Psyc...mentioning

confidence: 99%

“…Inflammation in both diseases is associated with plaque formation ( Minagar et al, 2002 ; Minagar and Alexander, 2003 ; Nordvig et al, 2021 ). The formation of plaques/lesions leads to neurological symptoms that result from neuronal loss and oxidative stress ( Gilgun-Sherki et al, 2004 ; Kostic et al, 2013 ). Many patients with MS disease become less active and this inactivity leads to an accumulation of adipose tissue.…”

Section: Introductionmentioning

confidence: 99%

Multimodal Benefits of Exercise in Patients With Multiple Sclerosis and COVID-19

et al. 2022

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Multiple sclerosis (MS) is a demyelinating disease characterized by plaque formation and neuroinflammation. The plaques can present in various locations, causing a variety of clinical symptoms in patients with MS. Coronavirus disease-2019 (COVID-19) is also associated with systemic inflammation and a cytokine storm which can cause plaque formation in several areas of the brain. These concurring events could exacerbate the disease burden of MS. We review the neuro-invasive properties of SARS-CoV-2 and the possible pathways for the entry of the virus into the central nervous system (CNS). Complications due to this viral infection are similar to those occurring in patients with MS. Conditions related to MS which make patients more susceptible to viral infection include inflammatory status, blood-brain barrier (BBB) permeability, function of CNS cells, and plaque formation. There are also psychoneurological and mood disorders associated with both MS and COVID-19 infections. Finally, we discuss the effects of exercise on peripheral and central inflammation, BBB integrity, glia and neural cells, and remyelination. We conclude that moderate exercise training prior or after infection with SARS-CoV-2 can produce health benefits in patients with MS patients, including reduced mortality and improved physical and mental health of patients with MS.

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Multiple sclerosis and oxidative stress—a clinical perspective

Cited by 7 publications

References 77 publications

Do catalase and glutathione peroxidase protect blood platelets from lipid peroxidation in multiple sclerosis?

Do catalase and glutathione peroxidase protect blood platelets from lipid peroxidation in multiple sclerosis?

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

Multimodal Benefits of Exercise in Patients With Multiple Sclerosis and COVID-19

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