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首页> 外文期刊>Journal of diabetes >Oxidants, antioxidants and mitochondrial function in non-proliferative diabetic retinopathy
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Oxidants, antioxidants and mitochondrial function in non-proliferative diabetic retinopathy

机译：氧化剂、抗氧化剂和线粒体功能在non-proliferative糖尿病性视网膜病变

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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 F0/F1-ATPase. Results: Levels of LPO and NO were significantly increased in T2DM patients with severe NPDR (3.19±0.05μmol/mL and 45.62±1.27pmol/mL, respectively; P0.007 and P0.0001 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±0.48mEq/mL (P0.0001). In contrast with TAC, erythrocyte catalase and GPx activity was increased in patients with severe NPDR (139.4±4.4 and 117.13±14.84U/mg, respectively; P0.0001 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 (P0.0001 for all). Furthermore, there was a significant increase in the hydrolytic activity of the F0/F1-ATPase in T2DM patients with mild NPDR (265.07±29.55nmol/PO4; P0.0001 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.
机译：背景:糖尿病视网膜病变(DR)是一个可预防的导致的视觉残疾。本研究的研究水平和氧化应激标记和行为线粒体功能non-proliferative博士(NPDR)和建立之间的关系的严重性NPDR和氧化的标记压力和线粒体功能。横向分析,2型糖尿病(2型糖尿病)患者轻微、中等和严重non-proliferative博士(NPDR)进行评估氧化应激的标记(即产品脂质过氧化和一氧化氮(NO)分解产物)和(即总抗氧化活性抗氧化能力(TAC)、过氧化氢酶和谷胱甘肽过氧化物酶(GPx)的活动红细胞)。决定的流动性血小板和亚线粒体粒子F0 / F1-ATPase水解活动。水平的法律流程外包和没有显著增加在2型糖尿病患者严重NPDR(3.19±0.05μ摩尔/毫升和45.62±1.27 pmol /毫升,分别;分别为水平在健康志愿者),表明氧化应激的存在。和最小峰值明显降低的水平了吗在严重视网膜病变为7.98±0.48毫克当量/毫升术中,0.0001)。过氧化氢酶GPx活性增加严重患者NPDR(139.4±4.4分别为117.13±14.84 u /毫克;健康志愿者为),表明一个氧化剂和抗氧化剂之间的不平衡。膜亚线粒体粒子的流动性在2型糖尿病患者显著降低轻度,中度或严重NPDR相比在健康志愿者(术;0.0001)。此外,有一个显著增加F0 / F1-ATPase的水解活性2型糖尿病患者轻度NPDR(265.07±29.55 nmol /警察丁;志愿者),建议增加分解代谢。结论:患者NPDR表现出氧化放松管制与膜流动性降低亚线粒体粒子和增加的系统性分解代谢(线粒体功能障碍)潜在的广义系统的损害T2DM。

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