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Updated: Apr 4, 2026
Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
Plasma antioxidant enzymes and lipoperoxidation status in children with Down syndrome
Jingyi He1, Tingyu Li1, Jie Chen1
1Children Nutrition Research Center, Ministry of Education Key Laboratory of Child Development and Disorders, Key Laboratory of Pediatrics in Chongqing, CSTC2009 CA5002, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing 400014, PR China.
Objectives:
Oxidative stress (OS) may play a critical role in cell aging and neurologic disorders that are often seen in Down syndrome (DS) patients. The aim of this study was to determine the antioxidant enzyme level and lipoperoxidation status in blood from DS children.
Design And Methods:
In a cross-sectional study, we recruited a total of 36 DS children and 40 healthy controls (HCs). All subjects were free of infection according to the C reactive protein (CRP) value and routine peripheral blood profile. The activities of total superoxide dismutases (SODs), extracellular glutathione peroxidase (GPx3),malondialdehyde (MDA) and nitric oxide synthase (NOS) concentrations in peripheral blood were measured by spectrophotometric methods. The relationship of SOD and GPx3 was analyzed in the two groups.
Results:
The two groups were similar with respect to age, gender and peripheral blood profiles. The total SOD activity was significantly increased, while the GPx3 activity was significantly reduced in the DS group compared to the HCs (p=0.000, p=0.033 respectively). The MDA level was higher in DS children (p=0.013). There was no significant difference in NOS between DS and HCs (p=0.708). A significant negative correlation between GPx3 and SOD activity was identified in DS (r=-0.14, p=0.018) but not in the HC group.
Conclusions:
Abnormal redox metabolism takes place in DS individuals. Reducing GPx3 may be a compensatory mechanism of protection against intracellular OS. Moreover, monitoring of decreases in GPx3 activity may be a useful biomarker for evaluating OS in DS patients.
