Abstract
Extracellular superoxide dismutase (ecSOD) is the major extracellular scavenger of reactive oxygen species and associated with the diabetic complication in patients with type 2 diabetes mellitus (T2DM). We aimed to investigate the serum ecSOD activity in Chinese patients with different stages of diabetic retinopathy (DR) and evaluate the association between the serum ecSOD activity and the severity of DR. A total of 343 T2DM patients were categorized into three groups: nondiabetic retinopathy (NDR) group, nonproliferative diabetic retinopathy (NPDR) group, and proliferative diabetic retinopathy (PDR) group. Serum ecSOD activities were measured by the autoxidation of the pyrogallol method. In this study, 271, 46, and 26 patients were enrolled in the NDR, NPDR, and PDR groups, respectively. We found a significantly decreased trend of serum ecSOD activity among NDR subjects (118.0 ± 11.5 U/mL) compared to NPDR subjects (108.5 ± 11.9 U/mL) (P < 0.001) and NPDR subjects compared to PDR subjects (102.7 ± 12.4 U/mL) (P = 0.041). Serum ecSOD activity was an independent risk factor for DR (OR = 0.920, P < 0.001) and was associated with the progression of DR. Serum ecSOD activity might be a biomarker for DR screening and evaluation of the clinical severity of DR in Chinese T2DM patients.
Highlights
Diabetic retinopathy (DR) is the most common and severe microvascular complication in patients with type 2 diabetes mellitus (T2DM), which is the main cause of blindness or serious visual impairment [1]
Various mechanisms contributing to the pathogenesis of DR such as inflammation, polyol pathway, accumulation of advanced glycation end products (AGEs), flux of hexosamine pathway, and protein kinase C (PKC) activation are associated with the overproduction of reactive oxygen species (ROS) by the mitochondria [5]
All selected patients were categorized into three groups: nondiabetic retinopathy (NDR) group, nonproliferative diabetic retinopathy (NPDR) group, and proliferative diabetic retinopathy (PDR) group
Summary
Diabetic retinopathy (DR) is the most common and severe microvascular complication in patients with type 2 diabetes mellitus (T2DM), which is the main cause of blindness or serious visual impairment [1]. Chronic uncontrolled hyperglycemia is thought to be the crucial influencing factor for the dysfunction of retinal microvascular pericyte and endothelial cell in T2DM patients [2]. The accumulation of ROS can lead to oxidative stress, which is one of the key factors of the pathogenesis of DR [3]. Various mechanisms contributing to the pathogenesis of DR such as inflammation, polyol pathway, accumulation of advanced glycation end products (AGEs), flux of hexosamine pathway, and protein kinase C (PKC) activation are associated with the overproduction of ROS by the mitochondria [5]. Maugeri et al [6] have demonstrated that the pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) could inhibit the hyperglycemia/hypoxia-induced retinal dysfunction in patients with DR. The markers of oxidative stress were worthy of further study in patients with DR
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