For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
10
views
61
references
 Top references
cited by
2
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      330
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The Evaluation of Oxidative Stress Parameters in Serum Patients with Relapsing-Remitting Multiple Sclerosis Treated with II-Line Immunomodulatory Therapy

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objectives

          The assessment of oxidative stress (OS) in serum relapsing-remitting multiple sclerosis patients treated with II-line immunomodulatory therapy (fingolimod, natalizumab) compared to newly diagnosed patients (de novo group) treated with interferon (IFN) beta and controls. The relationship between OS parameters and gender, age, disease duration, Expanded Disability Status Scale, annualized relapse rate, MRI lesions in patients treated with II-line.

          Materials and Methods

          One hundred and twenty-one patients with RRMS were enrolled in the study. Patients were divided into groups: de novo group, IFN, fingolimod (FG), natalizumab (NT), and controls. Lipid hydroperoxides (LHP), malondialdehyde (MDA), lipofuscin (LPS), and total oxidative status (TOS) were determined.

          Results

          LHP, MDA, and TOS were lower in NT and FG groups compared to the de novo group. Levels of OS were different between NT and FG patients and the IFN group. Women treated with FG and NT had lower MDA, LPH, and TOS than women who were not treated while in men only LPH was lowered. Positive correlations were found between MDA, LHP, TOS, and ARR in the NT group.

          Conclusion

          The II-line immunomodulatory treatment decreased OS particularly among women. No difference in OS levels was observed between II-line therapy and IFN beta.

          Related collections

          Most cited references61

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Oxidative damage in multiple sclerosis lesions

          Lukas Haider, Marie T. Fischer, Josa M. Frischer … (2011)
          Multiple sclerosis is a chronic inflammatory disease of the central nervous system, associated with demyelination and neurodegeneration. The mechanisms of tissue injury are currently poorly understood, but recent data suggest that mitochondrial injury may play an important role in this process. Since mitochondrial injury can be triggered by reactive oxygen and nitric oxide species, we analysed by immunocytochemistry the presence and cellular location of oxidized lipids and oxidized DNA in lesions and in normal-appearing white matter of 30 patients with multiple sclerosis and 24 control patients without neurological disease or brain lesions. As reported before in biochemical studies, oxidized lipids and DNA were highly enriched in active multiple sclerosis plaques, predominantly in areas that are defined as initial or ‘prephagocytic’ lesions. Oxidized DNA was mainly seen in oligodendrocyte nuclei, which in part showed signs of apoptosis. In addition, a small number of reactive astrocytes revealed nuclear expression of 8-hydroxy-d-guanosine. Similarly, lipid peroxidation-derived structures (malondialdehyde and oxidized phospholipid epitopes) were seen in the cytoplasm of oligodendrocytes and some astrocytes. In addition, oxidized phospholipids were massively accumulated in a fraction of axonal spheroids with disturbed fast axonal transport as well as in neurons within grey matter lesions. Neurons stained for oxidized phospholipids frequently revealed signs of degeneration with fragmentation of their dendritic processes. The extent of lipid and DNA oxidation correlated significantly with inflammation, determined by the number of CD3 positive T cells and human leucocyte antigen-D expressing macrophages and microglia in the lesions. Our data suggest profound oxidative injury of oligodendrocytes and neurons to be associated with active demyelination and axonal or neuronal injury in multiple sclerosis.
          Article 0 comments Cited 233 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Radical changes in multiple sclerosis pathogenesis.

            Jack van Horssen, Maarten Witte, Gerty Schreibelt … (2011)
            Reactive oxygen species (ROS) contain one or more unpaired electrons and are formed as intermediates in a variety of normal biochemical reactions. However, when generated in excess amounts or not appropriately controlled, ROS initiate extensive cellular damage and tissue injury. ROS have been implicated in the progression of cancer, cardiovascular disease and neurodegenerative and neuroinflammatory disorders, such as multiple sclerosis (MS). In the last decade there has been a major interest in the involvement of ROS in MS pathogenesis and evidence is emerging that free radicals play a key role in various processes underlying MS pathology. To counteract ROS-mediated damage, the central nervous system is equipped with an intrinsic defense mechanism consisting of endogenous antioxidant enzymes. Here, we provide a comprehensive overview on the (sub)cellular origin of ROS during neuroinflammation as well as the detrimental effects of ROS in processing underlying MS lesion development and persistence. In addition, we will discuss clinical and experimental studies highlighting the therapeutic potential of antioxidant protection in the pathogenesis of MS. 2010 Elsevier B.V. All rights reserved.
            Article 0 comments Cited 99 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              MRI outcomes in a placebo-controlled trial of natalizumab in relapsing MS.

              D Soon, Michael Panzara, E Havrdová … (2007)
              In a 2-year, placebo-controlled trial (the Natalizumab Safety and Efficacy in Relapsing Remitting Multiple Sclerosis [AFFIRM] study), involving 942 patients with relapsing multiple sclerosis (MS), natalizumab significantly reduced the relapse rate by 68% and progression of sustained disability by 42% vs placebo. We report the effect of natalizumab on MRI measures from the AFFIRM study. The number and volume of gadolinium (Gd)-enhancing, new or enlarging T2-hyperintense, and new T1-hypointense lesions and brain parenchymal fraction were measured from annual scans obtained at baseline, 1 year, and 2 years. Compared with placebo, natalizumab produced a 92% decrease in Gd-enhancing lesions (means 2.4 vs 0.2; p < 0.001), an 83% decrease in new or enlarging T2-hyperintense lesions (means 11.0 vs 1.9; p < 0.001), and a 76% decrease in new T1-hypointense lesions (means 4.6 vs 1.1; p < 0.001) over 2 years. Median T2-hyperintense lesion volume increased by 8.8% in the placebo group and decreased by 9.4% in the natalizumab group (p < 0.001); median T1-hypointense lesion volume decreased by 1.5% in the placebo group and decreased by 23.5% in the natalizumab group (p < 0.001). Brain atrophy was greater in year 1 and less in year 2 in natalizumab-treated patients. Natalizumab has a sustained effect in preventing the formation of new lesions in patients with relapsing multiple sclerosis.
              Article 0 comments Cited 87 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Bożena Adamczyk:
                ORCID: http://orcid.org/0000-0003-1641-5350
                Journal
                Journal ID (nlm-ta): Oxid Med Cell Longev
                Journal ID (iso-abbrev): Oxid Med Cell Longev
                Journal ID (publisher-id): OMCL
                Title: Oxidative Medicine and Cellular Longevity
                Publisher: Hindawi
                ISSN (Print): 1942-0900
                ISSN (Electronic): 1942-0994
                Publication date (Print): 2017
                Publication date (Electronic): 12 September 2017
                Volume: 2017
                Electronic Location Identifier: 9625806
                Affiliations
                1Department of Neurology in Zabrze, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, ul. 3 Maja 13-15, 41-800 Zabrze, Poland
                2Department of Neurology, 10th Military Research Hospital and Polyclinic, Independent Public Healthcare Centre, ul. Powstańców Warszawy 5, 85-681 Bydgoszcz, Poland
                3Department of Biochemistry in Zabrze, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, ul. 3 Jordana 19, 41-808 Zabrze, Poland
                Author notes

                Academic Editor: Francisco J. Romero

                Author information
                http://orcid.org/0000-0003-1641-5350
                Article
                DOI: 10.1155/2017/9625806
                PMC ID: 5613460
                SO-VID: 732eba4d-a0f9-45ee-9827-a8f94794cd3d
                Copyright © Copyright © 2017 Bożena Adamczyk et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 7 June 2017
                Date revision received : 30 July 2017
                Date accepted : 20 August 2017
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

                Comments

                Comment on this article

                scite_

                Similar content330

                See all similar

                Cited by2

                See all cited by

                Most referenced authors795

                See all reference authors