Abstract
Oxidative stress has been suggested to play a crucial role in the pathogenesis of diabetic complications including nephropathy. However, the exact mechanism of diabetic nephropathy is still not clearly understood. Since oxidative stress is known to be a major component in the induction of apoptosis, we investigated the occurrence of apoptosis in diabetic rat kidney. The status of oxidative stress was determined as thiobarbituric acid reactive substances (TBARS). The TBARS in the control and diabetic rat kidney were 2.00 ± 0.963 and 3.83 ± 0.715 μmol/mg protein, respectively (P< 0.05). Apoptosis was determined by evaluating the DNA fragmentation using an enzyme-linked immunoassay andin situend labeling. DNA fragmentation increased approximately fourfold in diabetic rat kidney compared to the normal kidney (P< 0.05). Apoptagin situlabeling displayed negligible apoptosis in nondiabetic kidney while significant areas of apoptosis were observed in diabetic kidney. Our results suggest that increased oxidative stress in diabetic kidney could induce apoptosis, which may contribute to the development of diabetic nephropathy.
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