Antioxidant and oxidative stress status in type 2 diabetes and diabetic foot ulcer

被引:0
|
作者
Bolajoko, Elizabeth Bosede [1 ]
Mossanda, Kensese Sontin [1 ]
Adeniyi, Francis [3 ]
Akinosun, Olubayo [3 ]
Fasanmade, Adesoji [4 ]
Moropane, Mpho [2 ]
机构
[1] Univ Limpopo, Dept Chem Pathol, Garankuwa, South Africa
[2] Univ Limpopo, Dept Anat Pathol, Garankuwa, South Africa
[3] Univ Ibadan, Dept Chem Pathol, Ibadan, Nigeria
[4] Univ Ibadan, Dept Med, Ibadan, Nigeria
来源
SAMJ SOUTH AFRICAN MEDICAL JOURNAL | 2008年 / 98卷 / 08期
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中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective. Oxidative stress (OS) has been implicated in the aetiology and progression of diabetic complications including diabetic foot ulcer. In this Study, the levels of lipid peroxides (LPO) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) as well as the enzymatic antioxidant activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in type 2 diabetes mellitus and diabetic foot ulcer subjects were assessed and compared with apparently healthy normal Subjects to understand the involvement of OS in the subjects. Method. The abovementioned OS markers were measured in 50 Subjects for each of the following groups: type 2 diabetes mellitus (DM), diabetic foot ulcer (DF) and non-diabetic control (NC). Results: Significant elevated values of LPO (39.86%) and 8-OHdG (45.53%) were found in DM subjects compared with the NC subjects. This increase in both parameters was greater for DF subjects: 80.23% and 53.91% respectively. SOD activities were significantly reduced in DM (14.82%) and DF (4.09%) subjects in contrast with elevated activities of GPx observed in DM (21.87%) and DF (20.94%) subjects. Glycated haemoglobin/fasting plasma glucose (HbA1c/FPG) correlated positively with LPO, 8-OHdG and GPx, whereas a negative correlation was observed for SOD. Conclusion. Increased oxidation subsequent to diabetic conditions induces an over-expression of GPx activity suggesting a compensatory mechanism by the body to prevent further tissue damage in the subjects.
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页码:614 / 617
页数:4
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