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Effects of aminoguanidine on lipid and protein oxidation in diabetic rat kidneys
Dilek Gogasyavuz1, Belgin Küçükkaya, H Onder Ersoz
1Department of Internal Medicine Section of Endocrinology and Metabolism, School of Medicine, Marmara University, Istanbul Turkey. dyavuz@turk.net
Abstract:
Nonenzymatic glycation of tissue and plasma proteins may stimulate the production of oxidant and carbonyl stress in diabetes. The aim of this study was to evaluate the effects of aminoguanidine (AG) on lipid peroxidation, protein oxidation and nitric oxide (NO) release in diabetic rat kidneys. After induction of diabetes with streptozotocin, female Wistar rats were divided into 2 groups. Group DAG (n=9) rats were given AG hydrogen carbonate (1 g/L) in drinking water and group D (n=8) was diabetic control rats given only tap water. Group H (n=8) was followed as healthy controls. At the end of an 8 week period, NO release, lipid and protein oxidation were determined in kidney tissues. NO release was significantly lower in diabetic rats compared with healthy controls (p<0.05). Lipid peroxidation was significantly high in group D (3.9 +/- 0.3 nmol MDA/g tissue) compared with the group DAG (2.6 0.1 nmol MDA/g tissue, p<0.01) and group H (2.4 +/- 0.2 nmol MDA/g tissue). Protein oxidation was significantly higher in diabetics than healthy controls (563.8 +/- 23.9, 655.8 +/- 7.2, 431.5 +/- 8.8 mmol carbonyl / g tissue for group DAG, D and H, respectively, p< 0.05). A positive correlation between albuminuria and thiobarbituric acid reactive substance (TBARS) levels (r= 0.54,p<0.005) and carbonyl content (r=0.70, p<0.0005) in kidney homogenate were observed. Although AG treatment had no effect on NO release, it significantly decreased lipid peroxidation in diabetic rat cortices. Consequently increased lipid peroxidation -as well as- protein oxidation could be involved in the pathogenesis of diabetic albuminuria.
Insights
Aminoguanidine (AG) reduced lipid peroxidation in diabetic rat kidneys but did not affect nitric oxide (NO) release. Increased lipid and protein oxidation are linked to diabetic albuminuria.
Area of Science:
- Biochemistry
- Nephrology
- Endocrinology
Background:
- Nonenzymatic glycation in diabetes elevates oxidant and carbonyl stress.
- Diabetic nephropathy is characterized by increased oxidative stress and impaired nitric oxide (NO) pathways.
- Protein and lipid oxidation contribute to the pathogenesis of diabetic complications.
Purpose of the Study:
- To investigate the effects of aminoguanidine (AG) on lipid peroxidation, protein oxidation, and NO release in diabetic rat kidneys.
- To evaluate the potential role of AG in mitigating oxidative stress in diabetes.
- To explore the relationship between oxidative stress markers and albuminuria in diabetic nephropathy.
Main Methods:
- Diabetes was induced in female Wistar rats using streptozotocin.
- Rats were treated with aminoguanidine (AG) hydrogen carbonate or received only tap water (diabetic control).
- Kidney tissues were analyzed for NO release, lipid peroxidation (malondialdehyde), and protein oxidation (carbonyl content) after 8 weeks.
Main Results:
- Diabetic rats exhibited significantly lower NO release and higher lipid and protein oxidation compared to healthy controls.
- AG treatment significantly reduced lipid peroxidation in diabetic rat kidneys.
- AG treatment did not significantly alter NO release in diabetic rats.
- Positive correlations were observed between albuminuria and markers of lipid peroxidation (TBARS) and protein oxidation (carbonyl content).
Conclusions:
- Increased lipid and protein oxidation are implicated in the development of diabetic albuminuria.
- Aminoguanidine (AG) demonstrates potential in reducing lipid peroxidation in diabetic kidneys.
- Further research is warranted to explore AG's therapeutic efficacy in managing diabetic nephropathy.
