Domínguez C, Ruiz E, Gussinye M, Carrascosa A
Biochemistry and Molecular Biology Research Centre, Vall d'Hebron Hospitals, Autonomous University of Barcelona, Spain.
Diabetes Care. 1998 Oct;21(10):1736-42. doi: 10.2337/diacare.21.10.1736.
In diabetes, the persistence of hyperglycemia has been reported to cause increased production of oxygen free radicals through glucose autooxidation and nonenzymatic glycation. The aim of this study was to determine whether oxidative cellular damage occurs at the clinical onset of diabetes and in later stages of the disease in young patients.
Indicative parameters of lipoperoxidation, protein oxidation, and changes in the status of antioxidant defense systems were evaluated in single blood samples from 54 diabetic children, adolescents, and young adults and 60 healthy age- and sex-matched control subjects.
Malondialdehyde and protein carbonyl group levels in plasma were progressively higher in diabetic children and adolescents than in control subjects (P < 0.0001). The highest erythrocyte superoxide dismutase (SOD) activity was found in diabetic children at onset of clinical diabetes. In diabetic adolescents, SOD was also significantly higher (P < 0.0001) than in control subjects. Erythrocyte glutathione peroxidase was significantly lower in diabetic children and adolescents compared with control subjects (P < 0.002). A significant decline in blood glutathione content at the recent onset of diabetes was found (P < 0.0001). Furthermore, our results demonstrated progressive glutathione depletion during diabetes evolution. The plasma alpha-tocopherol/total lipids ratio and beta-carotene levels during diabetes development (P < 0.001) were low.
This cross-sectional study in young diabetic patients showed that systemic oxidative stress is present upon early onset of type 1 diabetes and is increased by early adulthood. Decreased antioxidant defenses may increase the susceptibility of diabetic patients to oxidative injury. Appropriate support for enhancing antioxidant supply in these young diabetic patients may help prevent clinical complications during the course of the disease.
据报道,在糖尿病中,高血糖的持续存在会通过葡萄糖自氧化和非酶糖基化导致氧自由基生成增加。本研究的目的是确定在年轻患者糖尿病临床发病时及疾病后期是否会发生细胞氧化损伤。
对54名糖尿病儿童、青少年和年轻成年人以及60名年龄和性别匹配的健康对照者的单次血样进行评估,检测脂质过氧化、蛋白质氧化的指示参数以及抗氧化防御系统状态的变化。
糖尿病儿童和青少年血浆中的丙二醛和蛋白质羰基水平逐渐高于对照者(P<0.0001)。临床糖尿病发病时的糖尿病儿童红细胞超氧化物歧化酶(SOD)活性最高。糖尿病青少年的SOD水平也显著高于对照者(P<0.0001)。与对照者相比,糖尿病儿童和青少年的红细胞谷胱甘肽过氧化物酶显著降低(P<0.002)。发现糖尿病近期发病时血中谷胱甘肽含量显著下降(P<0.0001)。此外,我们的结果表明糖尿病进展过程中谷胱甘肽逐渐耗竭。糖尿病发展过程中血浆α-生育酚/总脂质比值和β-胡萝卜素水平较低(P<0.001)。
这项针对年轻糖尿病患者的横断面研究表明,1型糖尿病早期发病时存在全身氧化应激,到成年早期会加剧。抗氧化防御能力下降可能会增加糖尿病患者对氧化损伤的易感性。适当支持这些年轻糖尿病患者增强抗氧化物质供应可能有助于预防疾病过程中的临床并发症。