Literature DB >> 20201076

Markers of oxidative and nitrosative stress in systemic lupus erythematosus: correlation with disease activity.

Gangduo Wang1, Silvia S Pierangeli, Elizabeth Papalardo, G A S Ansari, M Firoze Khan.   

Abstract

OBJECTIVE: Free radical-mediated reactions have been implicated as contributors in a number of autoimmune diseases, including systemic lupus erythematosus (SLE). However, the potential for oxidative/nitrosative stress to elicit an autoimmune response or to contribute to disease pathogenesis, and thus be useful when determining a prognosis, remains largely unexplored in humans. This study was undertaken to investigate the status and contribution of oxidative/nitrosative stress in patients with SLE.
METHODS: Sera from 72 SLE patients with varying levels of disease activity according to the SLE Disease Activity Index (SLEDAI) and 36 age- and sex-matched healthy controls were evaluated for serum levels of oxidative/nitrosative stress markers, including antibodies to malondialdehyde (anti-MDA) protein adducts and to 4-hydroxynonenal (anti-HNE) protein adducts, MDA/HNE protein adducts, superoxide dismutase (SOD), nitrotyrosine (NT), and inducible nitric oxide synthase (iNOS).
RESULTS: Serum analysis showed significantly higher levels of both anti-MDA/anti-HNE protein adduct antibodies and MDA/HNE protein adducts in SLE patients compared with healthy controls. Interestingly, not only was there an increased number of subjects positive for anti-MDA or anti-HNE antibodies, but also the levels of both of these antibodies were statistically significantly higher among SLE patients whose SLEDAI scores were > or = 6 as compared with SLE patients with lower SLEDAI scores (SLEDAI score <6). In addition, a significant correlation was observed between the levels of anti-MDA or anti-HNE antibodies and the SLEDAI score (r = 0.734 and r = 0.647, respectively), suggesting a possible causal relationship between these antibodies and SLE. Furthermore, sera from SLE patients had lower levels of SOD and higher levels of iNOS and NT compared with healthy control sera.
CONCLUSION: These findings support an association between oxidative/nitrosative stress and SLE. The stronger response observed in serum samples from patients with higher SLEDAI scores suggests that markers of oxidative/nitrosative stress may be useful in evaluating the progression of SLE and in elucidating the mechanisms of disease pathogenesis.

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Year:  2010        PMID: 20201076      PMCID: PMC2935652          DOI: 10.1002/art.27442

Source DB:  PubMed          Journal:  Arthritis Rheum        ISSN: 0004-3591


  49 in total

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Journal:  Autoimmun Rev       Date:  2008-05-27       Impact factor: 9.754

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  80 in total

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3.  Proteomic identification of carbonylated proteins in the kidney of trichloroethene-exposed MRL+/+ mice.

Authors:  Xiuzhen Fan; Gangduo Wang; Robert D English; M Firoze Khan
Journal:  Toxicol Mech Methods       Date:  2013-10-07       Impact factor: 2.987

Review 4.  Metabolic abnormalities and oxidative stress in lupus.

Authors:  Yaima L Lightfoot; Luz P Blanco; Mariana J Kaplan
Journal:  Curr Opin Rheumatol       Date:  2017-09       Impact factor: 5.006

5.  Oxidative stress and dietary micronutrient deficiencies contribute to overexpression of epigenetically regulated genes by lupus T cells.

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6.  Increased lipid and protein oxidation and lowered anti-oxidant defenses in systemic lupus erythematosus are associated with severity of illness, autoimmunity, increased adhesion molecules, and Th1 and Th17 immune shift.

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7.  Oxidative hotspots on actin promote skeletal muscle weakness in rheumatoid arthritis.

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8.  iNOS null MRL+/+ mice show attenuation of trichloroethene-mediated autoimmunity: contribution of reactive nitrogen species and lipid-derived reactive aldehydes.

Authors:  Gangduo Wang; Maki Wakamiya; Jianling Wang; G A S Ansari; M Firoze Khan
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9.  Cytochrome P450 2E1-deficient MRL+/+ mice are less susceptible to trichloroethene-mediated autoimmunity: Involvement of oxidative stress-responsive signaling pathways.

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10.  Mitochondrial dysfunctions in myalgic encephalomyelitis/chronic fatigue syndrome explained by activated immuno-inflammatory, oxidative and nitrosative stress pathways.

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