Abstract
Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease whose etiology remains largely unknown. The uncontrolled oxidative stress in SLE contributes to functional oxidative modifications of cellular protein, lipid and DNA and consequences of oxidative modification play a crucial role in immunomodulation and trigger autoimmunity. Measurements of oxidative modified protein, lipid and DNA in biological samples from SLE patients may assist in the elucidation of the pathophysiological mechanisms of the oxidative stress-related damage, the prediction of disease prognosis and the selection of adequate treatment in the early stage of disease. Application of these biomarkers in disease may indicate the early effectiveness of the therapy. This review is intended to provide an overview of various reactive oxygen species (ROS) formed during the state of disease and their biomarkers linking with disease. The first part of the review presents biochemistry and pathophysiology of ROS and antioxidant system in disease. The second part of the review discusses the recent development of oxidative stress biomarkers that relates pathogenesis in SLE patients and animal model. Finally, this review also describes the reported clinical trials of antioxidant in the disease that have evaluated the efficacy of antioxidant in the management of disease with ongoing conventional therapy.
Highlights
Systemic lupus erythematosus is an autoimmune inflammatory disease characterized by the presence of flare of autoantibodies, especially against nuclear components
This review examines the available evidence for the involvement of cellular oxidants in the pathogenesis of Systemic lupus erythematosus (SLE) and the current biomarkers of oxidative stress focusing on their association with disease complication, which may be useful for developing ideal biomarkers in disease
Oxidative stress biomarkers may have a role in the future to assist clinical decisions regarding the use of antioxidant therapies and their efficacy
Summary
Systemic lupus erythematosus is an autoimmune inflammatory disease characterized by the presence of flare of autoantibodies, especially against nuclear components. All biomolecules (lipid, protein and DNA) can be damaged by excessive production of ROS (including ONOO−) and may be deleterious and concomitant Product of these cascades of oxidative modification can be detected in biological fluid and their abundance correlates with disease activity and organ damage in SLE patients, which suggest that oxidative modification act as biomarkers. Interaction of reactive oxygen species with lipids, proteins and DNA ROS, in particular the hydroxyl radical, react with lipid membrances and generate reactive aldehydes including MDA and HNE, in three phase reactions (Figure 2), which can ‘spread’ oxidative damage through the circulation in SLE [58]. The end products/metabolites of ROS/RNS are stable, can accumulate to detectable concentrations, reflect specific oxidation pathways, and correlate with disease severity Some are known to have direct effects
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