Abstract
Reductions in glutathione (GSH) levels have been shown to be associated with aging and the pathogenesis of a variety of diseases, including systemic lupus erythematosus (SLE). Glutamate cysteine ligase (GCL) catalyzes the first and rate-limiting step of GSH synthesis. In order to appraise the correlation between oxidative stress and the severity and activity of SLE, GSH, oxidized GSH (GSSG) and thioredoxin (TRX) concentrations and the enzymatic activity levels of GCL in peripheral blood mononuclear cells (PBMCs) from patients with SLE and healthy controls were studied. In patients with SLE, the levels of GCL activity and GSH decreased, while TRX and GSSG levels increased when compared with those in the healthy controls. GSH concentrations and GCL activity levels negatively correlated with the SLE disease activity index and erythrocyte sedimentation rate. Furthermore, patients with SLE and nephritis had lower levels of GSH and GCL activity and higher levels of TRX and GSSG compared with those in SLE patients without nephritis. Therefore, the results of the present study indicate that insufficient levels of GSH and GCL activity in PBMCs may contribute to the pathogenesis of SLE.
Highlights
Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease
Several previous studies have indicated that the chronic immune activation present in the disease is caused by the depletion of intracellular glutathione (GSH) through oxygen‐derived free radical production, known as oxidative stress [4,5,6]
The results demonstrated that the levels of GSH in the peripheral blood mononuclear cells (PBMCs) negatively correlated with SLE disease activity index (SLEDAI)
Summary
Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease. The assortment of autoantibodies produced is broad and, as a consequence, the manifestations of the disease are diverse [1]. Inflammatory and/or immuno‐mediated disorders, have been associated with oxidative stress in terms of increased ROS formation, and with impaired antioxidant status mainly in terms of reduced GSH levels and lowered cellular redox potential [7]. Reductions in GSH levels are associated with aging and the pathogenesis of a variety of diseases, autoimmune or not, including SLE, rheumatoid arthritis (RA), autoimmune thyroiditis, muscular dystrophy, amyotrophic lateral sclerosis, acquired immunodeficiency syndrome (AIDS), Alzheimer's, alcoholic liver disease, cataract genesis, respiratory distress syndrome and Werner syndrome [8,9,10,11]. Altered GSH concentrations may play an important role in a number of autoimmune pathological conditions, prevalently elicited, determined and maintained by inflammatory/immune responses mediated by oxidative stress reactions [12]
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