Full Length Research Paper
Abstract
Children’s diabetes is represented by the Type 1 diabetes mellitus (T1DM). In T1DM, 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 evaluate markers of oxidant/antioxidant status in diabetic children of Western Algeria. This study included 40 children with T1DM with mean age of 7.5 ± 1.7 years and 40 healthy age and sex matched controls. They were subjected to assessment of indicative parameters of lipoperoxidation, protein oxidation, changes in the status of antioxidant defense systems, plasma oxygen radical absorbance capacity (ORAC), glycated hemoglobin (HbA1c), total cholesterol and triglycerides. Malondialdehyde (MDA) and carbonyl proteins levels in plasma were significantly higher (4.03 ± 0.39 versus 2.53 ± 0.4 µmol/L, 5.03 ± 0.57 versus 3 ± 0.38 nmol/mg protein, respectively; P < 0.001) and a significant reduction in plasma total antioxidant capacity and vitamin C was observed in diabetic children than the controls (1.55 ± 0.28 versus 2.5 ± 0.23 AU, 37.58 ± 5.76 versus 48.8 ± 4.47 µmol/L, respectively; P < 0.001). Erythrocyte superoxide dismutase (SOD) and catalase (CAT) activities were significantly higher (520 ± 40.42 versus 392.7 ± 42.66 U/g hemoglobin, 71.08 ± 5.18 versus 56.6 ± 2.84 U/g hemoglobin, respectively; P < 0.001), whereas erythrocyte glutathione reductase (GSH) reduced significantly (34.98 ± 2.34 versus 42.68 ± 3.03 U/g hemoglobin, respectively; P < 0.001) in diabetic children than the control subject. The present finding suggested that young diabetic patients were susceptible to oxidative stress. Appropriate support for enhancing antioxidant supply in these patients may help prevent complications due to oxidative injury.
Key words: Children, oxidative stress, Type 1 diabetes mellitus.
Copyright © 2024 Author(s) retain the copyright of this article.
This article is published under the terms of the Creative Commons Attribution License 4.0