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Diabetes-induced apoptosis in rat kidney
1Department of Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston 77555-0647, USA.
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 in 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 mumol/mg protein, respectively (P < 0.05). Apoptosis was determined by evaluating the DNA fragmentation using an enzyme-linked immunoassay and in situ end labeling. DNA fragmentation increased approximately fourfold in diabetic rat kidney compared to the normal kidney (P < 0.05). Apoptag in situ labeling 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.
Insights
Increased oxidative stress in diabetic rat kidneys leads to significant apoptosis, a key factor in the development of diabetic nephropathy. This study highlights the role of oxidative stress in kidney cell death.
Area of Science:
- Nephrology
- Molecular Biology
- Biochemistry
Background:
- Diabetic nephropathy is a significant complication of diabetes.
- The precise mechanisms underlying diabetic nephropathy remain incompletely understood.
- Oxidative stress is implicated in the pathogenesis of diabetic complications.
Purpose of the Study:
- To investigate the occurrence of apoptosis in the kidneys of diabetic rats.
- To determine the relationship between oxidative stress and apoptosis in diabetic nephropathy.
Main Methods:
- Oxidative stress was quantified using thiobarbituric acid reactive substances (TBARS) assay.
- Apoptosis was assessed via DNA fragmentation using enzyme-linked immunoassay and in situ end labeling (Apoptag).
Main Results:
- TBARS levels were significantly elevated in diabetic rat kidneys compared to controls (3.83 vs. 2.00 mumol/mg protein, P < 0.05).
- DNA fragmentation increased approximately fourfold in diabetic kidneys.
- Apoptag labeling revealed significant apoptosis in diabetic kidneys, unlike in control kidneys.
Conclusions:
- Increased oxidative stress in diabetic kidneys is associated with elevated apoptosis.
- Apoptosis induced by oxidative stress may contribute to the development of diabetic nephropathy.