Oxidative Stress at Onset and in Early Stages of Type 1 Diabetes in Children and Adolescents

Carmen Domínguez; Elena Ruiz; Miguel Gussinye; Antonia Carrascosa

doi:10.2337/diacare.21.10.1736

Original Articles

Oxidative Stress at Onset and in Early Stages of Type 1 Diabetes in Children and Adolescents

Carmen Domínguez, PHD ,
Elena Ruiz, BSC ,
Miguel Gussinye, MD and
Antonia Carrascosa, MD, PHD

Biochemistry and Molecular Biology Research Centre, Pediatric Service, Vail d'Hebron Hospitals, Autonomous University of Barcelona Barcelona, Spain
Endocrinology and Adolescent Medicine Units, Pediatric Service, Vail d'Hebron Hospitals, Autonomous University of Barcelona Barcelona, Spain

Address correspondence and reprint requests to C. Domínguez, PhD, Centre d'Investigacions en Bioquimica y Biologia Molecular, Hospital Materno-Infantil Vail d'Hebron (Pl-14), Pg. Vail d'Hebron, 119-129, 08035, Barcelona, Spain. E-mail: cdomin{at}ar.vhebron.es

Diabetes Care 1998 Oct; 21(10): 1736-1742. https://doi.org/10.2337/diacare.21.10.1736

Abstract

OBJECTIVE 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.

RESEARCH DESIGN AND METHODS 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.

RESULTS 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 α-tocopherol/total lipids ratio and β-carotene levels during diabetes development (P < 0.001) were low.

CONCLUSIONS 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.