Xpression is usually accompanied by inflammatory lesions, resulting in the conversion of NO to various reactive nitrogen species (RNS.), which PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25957400 include nitrosonium cation (NO+), nitroxyl anion (NO-) and peroxynitrite (ONOO.). Many independent studies show a significant correlation between global lupus disease activity and markers of systemic NO production [17].Sources of reactive oxygen species and their scavengersReviewReactive oxygen and nitrogen speciesROS is a collective term for the chemical species that are formed as a result of incomplete reduction of oxygen. It includes superoxide anion radical (O2?), peroxy radical (ROO-), hydrogen peroxide (H2O2), singlet oxygen (1O2), perhydroxyl radical (HO2.) and extremely reactive hydroxyl radical (.OH). ROS are short-lived molecules produced by normal cellular metabolism that are well recognized for playing a dual role; they are both deleterious and beneficial species. At low or moderateReactive oxygen species mostly originate from mitochondria, blood cells (lymphocytes, RBC) and vascular endothelial cells in patients with SLE and these ROS cause hyperpolarization of mitochondria, activated T lymphocytes, apoptosis and endothelial activation [23,48]. Several studies have shown increased production of ROS or diminished levels of intracellular reduced glutathione in various blood components in SLE patients [19,24]. In addition, ROS can be produced by other sources like NADPH oxidase (NOX enzyme) in activated phagocytes [49] and to a lesser extent in macrophage and polymononuclear cells [50,51], lysosome (myeloperoxidase undergoes a complex array of redox transformations and produces HOCl) and microsomes [52,53]. Hydroxyl radicals are generated from peroxynitrite, which is in turn rapidly formed through the reaction between NO?and O2�� under appropriate stoichiometric conditions. Hydrogen peroxide is formed through the dismutation of O2�� catalyzed by the enzyme superoxide dismutase, and is also produced via. action of several other oxidase enzymes (e.g. aminoacid oxidases). Tissue BAY 11-7085 web inflammation and chronic infection lead to the overproduction of O and O2��, which rapidly combine to yield peroxynitrite: O2 + O ONO2?. In addition, ROS may amplify the inflammation process of gene expression involved in the inflammatory response, particularly via. activation of the nuclear transcription factor NFk, which in turn upregulates pro-inflammatory cytokines and leukocyte adhesion molecules. Exogenous sources of ROS include; radiation, UV light, x-rays, gamma rays, chemicals that react to form peroxides, ozone and singlet oxygen, chemicals that promote superoxide formation,Shah et al. Journal of Biomedical Science 2014, 21:23 http://www.jbiomedsci.com/content/21/1/Page 3 ofTable 1 A summary of reported oxidant and antioxidant biomarkers in SLEStudy Shah et al. [14,19-22] Perl et al. [23,24] Turi et al. [25] Hassan et al. [26] Kurient Scofied [4,27] Taysi et al. [28] Serban et al. [29] Turgay et al. [30] Segal et. al. [31] Bae et al. [32] Jovanovic et al. [13] Abou-raya et al. [33] Vipartene et al. [28] Mohan Das [34] Tewthanan et. al. [16,35] Morgan et. al. [36,37] Zhang et al. [38,39] Ahsan et al. [40] Lunec et al. [41] Evan et al. [42] Maeshima et al. [43] Ho et al. [44] Gilkeson et al. [17] Wanchu et al. [45], significantly elevated levels; , significantly diminished levels.ROSLipid peroxidationSODCatalaseGlutathione peroxidaseGSHNitric oxideProtein oxidationDNA oxidationTissue/Cell studied RBC,.
