Oxidative modification of patient's plasma proteins and its role in pathogenesis of multiple sclerosis

Miller, Elżbieta; Walczak, Anna; Saluk‐Bijak, Joanna; Ponczek, Michał B.; Majsterek, Ireneusz

doi:10.1016/j.clinbiochem.2011.09.021

Cited by 79 publications

(61 citation statements)

References 26 publications

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“…Studies reporting increased CSF NOx (nitrite + nitrate) levels and decreased serum NO 2 -/NO 3 -levels [5] support our findings. However, contrary to our data; plasma and CSF nitrite and nitrate levels were observed to be elevated in MS in the studies conducted by C Larlori et al [10] and Miller et al [18]. Strengths of our study compared with previous studies are the selection of only RRMS patients as subtypes of MS and a higher number of patients.…”

Section: Discussioncontrasting

confidence: 53%

Original article Evaluation of oxidative and nitrosative stress in relapsing remitting multiple sclerosis: effect of corticosteroid therapy

Seven

Aslan²,

İncir³

et al. 2013

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Section: Discussioncontrasting

confidence: 53%

Original article Evaluation of oxidative and nitrosative stress in relapsing remitting multiple sclerosis: effect of corticosteroid therapy

Seven

Aslan²,

İncir³

et al. 2013

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“…Studies in plasma and serum in RRMS patients in remission using the reaction with dinitrophenylhydrazine products have consistently demonstrated increased protein carbonylation in MS compared to control groups [80][81][82]. One study of protein carbonylation in CSF [83] confirmed higher levels in a mixed MS population compared to controls (p=0.034).…”

Section: End-products Of Oxidation Protein Carbonylationmentioning

confidence: 88%

“…In serum and plasma, authors reported significantly higher mean 3-NT in MS compared to controls [62,81,84,85], including following acute relapse [84]. A single study also reported significantly higher 3-NT in an SPMS group compared to RRMS [81]. Conversely, Seven et al [27] reported reduced 3-NT immediately following relapse and following corticosteroid treatment (p<0.001).…”

Section: Protein Nitrosylationmentioning

confidence: 88%

Oxidative Stress-Related Biomarkers in Multiple Sclerosis: A Review

et al. 2016

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General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/pure/about/ebr-terms AbstractObjective: To provide an up to date review of oxidative stress biomarkers in multiple sclerosis and thus identify candidate molecules with greatest promise as biomarkers of diagnosis, disease activity or prognosis.Method: A semi-systematic literature search using PubMed and other databases.Results: Nitric oxide metabolites, superoxide dismutase, catalase, glutathione reductase, inducible nitric oxide synthase, protein carbonyl, 3-nitrotyrosine, isoprostanes, malondialdehyde and products of DNA oxidation have been identified across multiple studies as having promise as diagnostic, therapeutic or prognostic markers in MS.Conclusion: Heterogeneity of study design, particularly patient selection, limits comparability across studies. Further cohort studies are needed, and we would recommend promising markers be incorporated into future clinical trials to prospectively validate their potential.

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“…The increased 3-nitrotyrosine (3-NT) concentration, a stable footprint of peroxynitrite injury, has been also documented (21) in plasma of MS patients, showing the correlation with the disease development and intensity, as well as reflecting the patients' therapy response (14). 3-NT has direct detrimental effects on nerve tissue followed by nerve dysfunction (22).…”

Section: Nitric Oxide In the Experimental Autoimmune Encephalitis Andmentioning

confidence: 99%

Nitric oxide – mediated signalization and nitrosative stress in neuropathology / Azot oksid – posredovana signalizacija i nitrozativni stres u neuropatologiji

Stojanović¹,

Ljubisavljević²,

Stevanović³

et al. 2012

Journal of Medical Biochemistry

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Summary: Nitric oxide (NO) is an important signalling molecule in a variety of physiological processes. NO, a gas, is produced from L-arginine by different isoforms of the nitric oxide synthase and serves as mediator in important physiological functions, such as promoting vasodilation of blood vessels and mediating communication between nervous system cells. Contradictory to its physiologic actions, free radical activity of NO can cause cellular damage by the induction of nitrosative stress with significant implications on nervous system diseases. Although the mechanism of NOmediated neurodegeneration still remains unclear, numerous studies suggest its crucial role in modification of protein functions by nitrosylation and nitro-tyrosination. NO contributes to glutamate excitotoxicity, participates in organelle fragmentation, inhibits mitochondrial respiratory complexes and mobilizes zinc from the internal stores. Recently, NO has been emerged as a mediator of epigenetic gene expression and chromatin changes. Besides, NO is a key mediator in the regulation of inflammatory and immune response of the central nervous system. It is involved in down regulation of several aspects of CNS inflammation, but also has a dual role in that it is required for inflammation in some situations. Keywords: nitric oxide, nitrosative stress, protein S-nitrosylation, neuroinflammation, neurodegenerationKratak sadr`aj: Azot monoksid je va`an signalni molekul u brojnim fiziolo{kim procesima. Ovaj gas se stvara iz L-arginina dejstvom tri izoforme azot monoksid sintaze i medijator je va`nih fiziolo{kih funkcija, kao {to su posredovanje u regulaciji tonusa krvnih sudova i komunikaciji }elija nervnog sistema. Nasuprot ovim ulogama, kao slobodni radikal, NO mo`e izazvati }elijsko o{te}enje indukcijom nitrozativnog stresa, {to ima zna~ajne implikacije u bolestima nervnog sistema. Mada je mehanizam neurodegeneracije posredovane azot monoksidom jo{ uvek nerazja{njen, brojne studije ukazu ju na njegovu klju~nu ulogu u modifikaciji funkcije proteina kroz procese S-nitrozilacije i nitrovanja tirozina. On doprinosi glutamatnoj ekscitotoksi~nosti, u~estvuje u fragmentaciji organela, inhibi{e mitohondrijalne respiratorne komplekse i mobili{e cink iz unutra{njih depoa. Nedavno je ukazano da mo`e biti medijator epigenetske genske ekspresije i promena hromatina. Pored toga, NO je klju~ni posrednik u regulaciji inflamatornog i imunog odgovora CNS. On u~estvuje u nishodnoj regulaciji nekoliko aspekata inflamacije CNS, ali tako|e ispoljava dualisti~ke efekte u uslovima inflamacije.

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Oxidative modification of patient's plasma proteins and its role in pathogenesis of multiple sclerosis

Cited by 79 publications

References 26 publications

Original article Evaluation of oxidative and nitrosative stress in relapsing remitting multiple sclerosis: effect of corticosteroid therapy

Original article Evaluation of oxidative and nitrosative stress in relapsing remitting multiple sclerosis: effect of corticosteroid therapy

Oxidative Stress-Related Biomarkers in Multiple Sclerosis: A Review

Nitric oxide – mediated signalization and nitrosative stress in neuropathology / Azot oksid – posredovana signalizacija i nitrozativni stres u neuropatologiji

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