Study of urinary 8-hydroxydeoxyguanosine as a biomarker of oxidative DNA damage in diabetic nephropathy patients

Increased oxidative stress induced by hyperglycemia may contribute to the pathogenesis of diabetic complications. Urinary 8-hydroxydeoxyguanosine (8-OHdG) has been reported to serve as a sensitive biomarker of oxidative DNA damage and also of oxidative stress. This article studied oxidative DNA dama...

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Veröffentlicht in:Journal of pharmaceutical and biomedical analysis 2004-09, Vol.36 (1), p.101-104
Hauptverfasser: Xu, G.W., Yao, Q.H., Weng, Q.F., Su, B.L., Zhang, X., Xiong, J.H.
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Sprache:eng
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Zusammenfassung:Increased oxidative stress induced by hyperglycemia may contribute to the pathogenesis of diabetic complications. Urinary 8-hydroxydeoxyguanosine (8-OHdG) has been reported to serve as a sensitive biomarker of oxidative DNA damage and also of oxidative stress. This article studied oxidative DNA damage in patients with diabetic nephropathy and in healthy control subjects by urinary 8-OHdG evaluations. Contents of 8-OHdG in urine were analyzed by capillary electrophoresis with end-column amperometric detection (CE-AD) after a single-step solid-phase extraction (SPE). Levels of urinary 8-OHdG in diabetic nephropathy patients with macroalbuminuria was significant higher than in control subjects (5.72±6.89 μmol/mol creatinine versus 2.33±2.83 μmol/mol creatinine, P = 0.018). A significant difference of 24 h urinary 8-OHdG excretions exists between the patients with macroalbuminuria and the patients with normoalbuminuria (19.2±16.8 μg/24 h versus 8.1±1.7 μg/24 h, P = 0.015). There was a positive correlation between urinary excretion of 8-OHdG and glycosylated hemoglobin (HbA 1c) ( r = 0.287, P = 0.022). A weak correlation exists between the levels of 8-OHdG and triglyceride ( r = 0.230, P = 0.074). However, the urinary 8-OHdG contents are not correlated with blood pressure and total cholesterol. The increased excretion of urinary 8-OHdG is seen as indicating an increased systemic level of oxidative DNA damage in diabetic nephropathy patients.
ISSN:0731-7085
1873-264X
DOI:10.1016/j.jpba.2004.04.016