Increased levels of autoantibodies against catalase and superoxide dismutase associated with oxidative stress in patients with rheumatoid arthritis and systemic lupus erythematosus

Mansour, Riadh Ben; Lassoued, Saloua; Gargouri, Bilel; Gaïd, A El; Attia, Hamadi; Fakhfakh, Feiza

doi:10.1080/03009740701772465

Cited by 88 publications

(80 citation statements)

References 49 publications

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“…Similarly, the rate of eryptosis was positively correlated with the ROS abundance as shown in this study. The increased percentage of eryptosis in fresh blood from SLE patients was equivalent to an increased ROS abundance, which may be attributed to the excessive production of ROS and antibodies against anti-oxidant enzymes [37][38][39]. Notably, in the present study, neither of the plasma total antioxidant capacity of patients and ROS in erythrocytes incubated in plasma from patients exhibited a significant change as compared to the control groups.…”

Section: Discussioncontrasting

confidence: 48%

Eryptosis as an Underlying Mechanism in Systemic Lupus Erythematosus-Related Anemia

Jiang

Bian²,

Ma³

et al. 2016

Cell Physiol Biochem

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Background: The progression of systemic lupus erythematosus (SLE) leads to anemia in patients, adversely affecting prognosis. The diverse causes of anemia may include excessive eryptosis or premature suicidal erythrocyte death characterized by cell shrinkage and phosphatidylserine (PS) exposure on the cell surface. The present study explored if SLE enhances eryptosis and the underlying mechanisms. Materials and Methods: Eryptosis was assessed using flow cytometry in healthy volunteers (n = 20) and anemic patients hospitalized for SLE (n = 22), for parameters including PS exposure, cell volume, cytosolic calcium ion (Ca²⁺) levels and reactive oxygen species (ROS) and ceramide abundance. These indicators were measured in erythrocytes of experimental subjects and erythrocytes treated with plasma from healthy volunteers or SLE patients. Results: The hemoglobin and hematocrit levels were significantly lower in anemic SLE patients than in healthy volunteers (***p<0.001, p<0.001, respectively). The percentage of PS-exposing erythrocytes was significantly higher in SLE patients than in healthy volunteers (p<0.001), accompanied by an increase in cytosolic Ca²⁺ levels, oxidative stress. The measurements of PS and Ca²⁺ levels were significantly higher in the erythrocytes of healthy volunteers following incubation in plasma of SLE patients than in plasma of healthy volunteers for 24h (***p<0.001, *p<0.05 respectively). Conclusion: Eryptosis is enhanced in SLE and may contribute to anemia. The probable underlying mechanisms may be an excessive formation of ROS in erythrocytes. Also, some plasma components may trigger eryptosis by increasing the cytosolic Ca²⁺ concentration.

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Section: Discussioncontrasting

confidence: 48%

Eryptosis as an Underlying Mechanism in Systemic Lupus Erythematosus-Related Anemia

Jiang

Bian²,

Ma³

et al. 2016

Cell Physiol Biochem

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“…Oxidative stress and the inactivation of nitric oxide (NO) by vascular superoxide anion (O 2 ·− ) play a critical role in the pathogenesis of endothelial dysfunction, an early event in most cardiovascular diseases, including hypertension. 8,9 Reactive oxygen species (ROS) have been considered as risk and enhancer factors for autoimmune diseases, 10 and oxidation is one of the major factors responsible for atheroma development in this context. Indeed, SLE is a disease characterized by an increased oxidative damage.…”

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confidence: 99%

Chronic Hydroxychloroquine Improves Endothelial Dysfunction and Protects Kidney in a Mouse Model of Systemic Lupus Erythematosus

et al. 2014

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S ystemic lupus erythematosus (SLE) is a multisystemic chronic autoimmune inflammatory disorder that is associated with a high risk for the development of renal and cardiovascular disease, 1,2 which are major causes of mortality in these patients. 3 It predominantly affects young women of child-bearing age, the same population that is at lowest relative risk of atherosclerotic heart disease. In fact, women with lupus (age, 35-44 years) are >50 times as likely as healthy women without lupus to have a myocardial infarction. 4 Indeed, SLE is characterized by a high incidence of hypertension, 5-7 a wellestablished risk factor for the development and acceleration of atherosclerosis and ischemic heart disease. Oxidative stress and the inactivation of nitric oxide (NO) by vascular superoxide anion (O 2 ·− ) play a critical role in the pathogenesis of endothelial dysfunction, an early event in most cardiovascular diseases, including hypertension. 8,9 Reactive oxygen species (ROS) have been considered as risk and enhancer factors for autoimmune diseases, 10 and oxidation is one of the major factors responsible for atheroma development in this context. Indeed, SLE is a disease characterized by an increased oxidative damage.11-14 Free radical-mediated reactions are implicated in endothelial dysfunction in SLE, 15 and renal oxidative stress plays an important mechanistic role in the development of autoimmune-mediated hypertension. 16Abstract-Hydroxychloroquine has been shown to be efficacious in the treatment of autoimmune diseases, including systemic lupus erythematosus. Hydroxychloroquine-treated lupus patients showed a lower incidence of thromboembolic disease. Endothelial dysfunction, the earliest indicator of the development of cardiovascular disease, is present in lupus.Whether hydroxychloroquine improves endothelial function in lupus is not clear. The aim of this study was to analyze the effects of hydroxychloroquine on hypertension, endothelial dysfunction, and renal injury in a female mouse model of lupus. NZBWF1 (lupus) and NZW/LacJ (control) mice were treated with hydroxychloroquine 10 mg/kg per day by oral gavage, or with tempol and apocynin in the drinking water, for 5 weeks. Hydroxychloroquine treatment did not alter lupus disease activity (assessed by plasma double-stranded DNA autoantibodies) but prevented hypertension, cardiac and renal hypertrophy, proteinuria, and renal injury in lupus mice. Aortae from lupus mice showed reduced endotheliumdependent vasodilator responses to acetylcholine and enhanced contraction to phenylephrine, which were normalized by hydroxychloroquine or antioxidant treatments. No differences among all experimental groups were found in both the relaxant responses to acetylcholine and the contractile responses to phenylephrine in rings incubated with the nitric oxide synthase inhibitor N G -nitro-l-arginine methyl ester. Vascular reactive oxygen species content and mRNA levels of nicotinamide adenine dinucleotide phosphate oxidase subunits NOX-1 and p47 phox were increased in lupus...

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“…The primary factor causing oxidative stress observed in SLE is excessive free radical production rather than impaired antioxidant activity [4].…”

Section: Notesmentioning

confidence: 99%

“…There have been major advancements in the pathological mechanisms of SLE. Reactive oxygen species (ROS) have been considered as risk and enhancer factors for autoimmune diseases [4], and free radical-mediated reactions are implicated in SLE. Oxidative stress has a potential to elicit an autoimmune response and to contribute to the disease pathogenesis thus being useful when determining its prognosis [5].…”

Section: Introductionmentioning

confidence: 99%

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Measurement of Malondialdehyde, Glutathione, and Glutathione Peroxidase in SLE Patients

Gheita

Kenawy

2014

Methods in Molecular Biology

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Oxidative stress contributes to chronic inflammation of tissues and plays a central role in immunomodulation, which may lead to autoimmune diseases such as systemic lupus erythematosus (SLE) and antiphospholipid syndrome. Markers of oxidative damage include malondialdehyde (MDA), antioxidant scavengers as glutathione (GSH), and glutathione peroxidase (GSH Px), which all correlate well with SLE disease activity. Amelioration of some clinical manifestations of SLE may be expected by targeting lipid peroxidation with dietary or pharmacological antioxidants. Here, we describe the detection of the key players of oxidant/antioxidant imbalance in SLE.

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Increased levels of autoantibodies against catalase and superoxide dismutase associated with oxidative stress in patients with rheumatoid arthritis and systemic lupus erythematosus

Abstract: Collectively, these results suggested that the primary factor causing the oxidative stress observed in RA and SLE is excessive free radical production rather than impaired CAT or SOD activity due to autoantibody inhibition.

Cited by 88 publications

References 49 publications

Eryptosis as an Underlying Mechanism in Systemic Lupus Erythematosus-Related Anemia

Eryptosis as an Underlying Mechanism in Systemic Lupus Erythematosus-Related Anemia

Chronic Hydroxychloroquine Improves Endothelial Dysfunction and Protects Kidney in a Mouse Model of Systemic Lupus Erythematosus

Measurement of Malondialdehyde, Glutathione, and Glutathione Peroxidase in SLE Patients

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