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Background  Diabetic retinopathy ( DR ) is a preventable cause of visual disability. The aims of the present study were to investigate levels and behavior oxidative stress markers and mitochondrial function in non‐proliferative  DR  ( NPDR ) and to establish the correlation between the severity of  NPDR  and markers of oxidative stress and mitochondrial function.    Methods  In a transverse analysis, type 2 diabetes mellitus ( T2DM ) patients with mild, moderate and severe non‐proliferative  DR  ( NPDR ) were evaluated for markers of oxidative stress (i.e. products of lipid peroxidation ( LPO ) and nitric oxide ( NO ) catabolites) and antioxidant activity (i.e. total antioxidant capacity ( TAC ), catalase, and glutathione peroxidase ( GPx ) activity of erythrocytes). Mitochondrial function was also determined as the fluidity of the submitochondrial particles of platelets and the hydrolytic activity of  F  0 / F  1 ‐ ATP ase.    Results  Levels of  LPO  and  NO  were significantly increased in  T2DM  patients with severe  NPDR  (3.19 ± 0.05 μmol/m L  and 45.62 ± 1.27 pmol/m L , respectively;  P   <  0.007 and  P   <  0.0001 vs levels in health volunteers, respectively), suggesting the presence of oxidative stress.  TAC  had significant decrease levels with minimum peak in severe retinopathy with 7.98 ± 0.48 m E q/m L  ( P  < 0.0001). In contrast with  TAC , erythrocyte catalase and  GPx  activity was increased in patients with severe  NPDR  (139.4 ± 4.4 and 117.13 ± 14.84  U /mg, respectively;  P  < 0.0001 vs healthy volunteers for both), suggesting an imbalance between oxidants and antioxidants. The fluidity of membrane submitochondrial particles decreased significantly in  T2DM  patients with mild, moderate, or severe  NPDR  compared with that in healthy volunteers ( P  < 0.0001 for all). Furthermore, there was a significant increase in the hydrolytic activity of the  F  0 / F  1 ‐ ATP ase in  T2DM  patients with mild  NPDR  (265.07 ± 29.55 nmol/ PO  4 ;  P  < 0.0001 vs healthy volunteers), suggesting increased catabolism.    Conclusions  Patients with  NPDR  exhibit oxidative deregulation with decreased membrane fluidity of submitochondrial particles and increased systemic catabolism (mitochondrial dysfunction) with the potential for generalized systemic damage in  T2DM .

Oxidants, antioxidants and mitochondrial function in non‐proliferative diabetic retinopathy (在非增殖性糖尿病视网膜病变中的氧化剂、抗氧化剂以及线粒体功能)