Oxidative protein damage and antioxidant status in systemic lupus erythematosus

Zhang, Q.; Ye, D. Q.; Chen, G. P.; Zheng, Yongri

doi:10.1111/j.1365-2230.2009.03437.x

Cited by 38 publications

(41 citation statements)

References 23 publications

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“…In our study, SH group levels were found to be signifi cantly decreased in SLE patients compared to normal controls (260.2 ± 182.7 versus 339.4 ± 104.3 µmol/L), similar to the report of Zhang et al 25 This supports the role of oxidative stress in the pathogenesis of SLE.…”

supporting

confidence: 92%

Malondialdeído e grupo sulfidrila como biomarcadores do estresse oxidativo em pacientes com lúpus eritematoso sistêmico

Pérez

Netto

et al. 2012

Rev. Bras. Reumatol.

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supporting

confidence: 92%

Malondialdeído e grupo sulfidrila como biomarcadores do estresse oxidativo em pacientes com lúpus eritematoso sistêmico

Pérez

Netto

et al. 2012

Rev. Bras. Reumatol.

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“…Our data further agree with the results found by Zhang et al in plasma of SLE patients. 48 In the present study, the overall oxidative status was mostly evaluated in WBCs, instead of plasma. Thus, our results confirm previous studies and show that oxidative stress is further promoted in circulating WBCs, including monocytes and neutrophils of APS patients.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial dysfunction in antiphospholipid syndrome: implications in the pathogenesis of the disease and effects of coenzyme Q10 treatment

Pérez-Sánchez

Ruiz-Limón

Aguirre

et al. 2012

Blood

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The exact mechanisms underlying the role of oxidative stress in the pathogenesis and the prothrombotic or proinflammatory status of antiphospholipid syndrome (APS) remain unknown. Here, we investigate the role of oxidative stress and mitochondrial dysfunction in the proatherothrombotic status of APS patients induced by IgG-antiphospholipid antibodies and the beneficial effects of supplementing cells with coenzyme Q 10 (CoQ 10 ). A significant increase in relevant prothrombotic and inflammatory parameters in 43 APS patients was found compared with 38 healthy donors. Increased peroxide production, nuclear abundance of Nrf2, antioxidant enzymatic activity, decreased intracellular glutathione, and altered mitochondrial membrane potential were found in monocytes and neutrophils from APS patients. Accelerated atherosclerosis in APS patients was found associated with their inflammatory or oxidative status. CoQ 10 preincubation of healthy monocytes before IgG-antiphospholipid antibody treatment decreased oxidative stress, the percentage of cells with altered mitochondrial membrane potential, and the induced expression of tissue factor, VEGF, and Flt1. In addition, CoQ 10 significantly improved the ultrastructural preservation of mitochondria and prevented IgG-APS-induced fission mediated by Drp-1 and Fis-1 proteins. In conclusion, the oxidative perturbation in APS patient leukocytes, which is directly related to an inflammatory and proatherothrombotic status, relies on alterations in mitochondrial dynamics and metabolism that may be prevented, reverted, or both by treatment with CoQ 10 .

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“…Severity of the disease might be enhanced by the imbalance between oxidative stress and helper T-cell (Th1)-derived cytokines in SLE [15]. The SLEDAI correlates with serum markers of oxidant stress in SLE [18] and correlated negatively with levels of GSH and GSH Px [16] which may aid in the evaluation of treatment effectiveness [7]. It is suggested that in active SLE, oxidative status is increased without a corresponding elevation of the antioxidants, which verifies the value of using potent antioxidant therapy in preventing oxidative damage in SLE [19].…”

Section: Calculationmentioning

confidence: 97%

“…Px, and antioxidant molecules such as GSH are significantly reduced in erythrocytes [15,16] and lymphocytes [17], and the levels of lipid peroxidation, measured as MDA, are significantly higher in SLE patients [5,15].…”

Section: Calculationmentioning

confidence: 99%

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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Oxidative protein damage and antioxidant status in systemic lupus erythematosus

Abstract: The findings suggest that protein oxidation may play a role in the pathogenesis of chronic organ damage in SLE.

Cited by 38 publications

References 23 publications

Malondialdeído e grupo sulfidrila como biomarcadores do estresse oxidativo em pacientes com lúpus eritematoso sistêmico

Malondialdeído e grupo sulfidrila como biomarcadores do estresse oxidativo em pacientes com lúpus eritematoso sistêmico

Mitochondrial dysfunction in antiphospholipid syndrome: implications in the pathogenesis of the disease and effects of coenzyme Q10 treatment

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

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