Of the oxidative stress-related damage, the prediction of disease prognosis and
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. Keywords: Oxidative stress, Biomarkers, Antioxidant therapy, Systemic lupus erythematosusIntroduction Systemic lupus erythematosus is an autoimmune inflammatory disease characterized by the presence of flare of autoantibodies, especially against nuclear components. Although it is believed that the etiology of SLE is multifactorial, including immune dysfunction, genetic, hormonal and environmental, the molecular mechanisms underlying this systemic autoimmune response remain largely unknown. A key issue in the pathogenesis of lupus is how intracellular antigens become exposed and targeted by the immune system [1,2]. In this regard, excessive production of ROS and altered redox state which may cause abnormal activation of apoptosis [3,4], are considered as imperative factors involved in production, expansion of antibody flares and various clinical features in SLE [2]. Several studies have shown the role of ROS in the deregulation of apoptosis and cause Mangafodipir (trisodium) site increased apoptosis and delayed in clearance of apoptotic bodies. The delay in clearance of* Correspondence: [email protected] 1 Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA Full list of author information is available at the end of the articleapoptotic cells may prolong interaction between ROS and nuclear debris and generate neo-epitopes that subsequently stimulate broad spectrum of autoantibody formation leading to inflammation and organ damage in SLE [5]. The noxious effects of ROS may cause the following consequence: i) shift of intracellular redox (i.e. decrease GSH/GSSH ratio) condition, ii) oxidative modification of lipid, protein and DNA, iii) gene activation of oxidative stress and gene mutation related to antioxidant enzymes. Considerable genetic studies in SLE patients and animal models implicate the role of oxidative stress in the pathogenesis of SLE. Numerous gene polymorphisms encoding superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and NADPH oxidase encoding gene NCF2 have been identified in association with SLE risk, however some of these associations appear to be ethicity dependent [6]. The Nrf2-Keap1 pathway is important in protection against oxidative stress and inflammation. A strong association between Nrf2-653 G/A polymorphism and the development of nephritis has been reported in PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25768400 Mexican SLE patients [7]. CAT polymorphism (-330CC genotype) is significantly associated with thrombocytopenia,?2014 Shah et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution Lic.
