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Biotin amelioration of nephrotoxicity in streptozotocin-induced diabetic mice
Badr A Aldahmash1, Doaa M El-Nagar2, Khalid E Ibrahim1
1Zoology Department, College of Science, King Saud University, Riyadh, Saudi Arabia.
Abstract:
The current study was carried out to investigate the protective role of biotin in kidney injury and oxidative stress in diabetic mice type 1. Male Swiss albino mice were randomly divided into 3 groups. Control group received saline. Diabetes type 1 was induced in second and third groups by intraperitoneal injection of streptozotocin as a single dose (150 mg/kg). Second group remained as the untreated diabetic group and the third group received 15 mg/kg daily oral dose of biotin for 12 successive days. Biochemical results showed significant elevation in blood glucose and urea levels in both diabetic groups. Also, there is an increase in glomerular areas and decrease in glomerular cellularity in both diabetic groups. Histopathological results showed severe alterations in the untreated diabetic group represented by distorted glomeruli, inflammatory cells, and giant macrophages. In addition, there was an intense immune-reaction response toward acrolein indicator of oxidative damage. Upon biotin administration of diabetic mice, the above mentioned histopathological changes were reduced and also acroline reaction of oxidative damage was diminished. Our findings prove that biotin has a protective role against streptozotocin-induced oxidative damage in kidneys of laboratory mice.
Insights
Biotin, a B vitamin, demonstrated a protective effect against kidney injury and oxidative stress in a mouse model of type 1 diabetes. This vitamin reduced kidney damage markers and improved overall kidney health in diabetic mice.
Area of Science:
- Nephrology
- Endocrinology
- Nutritional Science
Background:
- Type 1 diabetes is associated with significant kidney complications, including injury and oxidative stress.
- Diabetic nephropathy is a major cause of kidney failure worldwide.
- Oxidative stress plays a critical role in the pathogenesis of diabetic kidney disease.
Purpose of the Study:
- To investigate the protective effects of biotin against kidney injury in a type 1 diabetes mouse model.
- To evaluate the impact of biotin on oxidative stress markers in the kidneys of diabetic mice.
- To determine if biotin can mitigate streptozotocin-induced nephropathy.
Main Methods:
- Male Swiss albino mice were induced with type 1 diabetes using streptozotocin.
- Diabetic mice were treated with daily oral doses of biotin (15 mg/kg) for 12 days.
- Kidney injury was assessed through biochemical analysis (blood glucose, urea), glomerular morphology, and histopathological examination, including acrolein staining for oxidative damage.
Main Results:
- Diabetic mice exhibited elevated blood glucose and urea levels, increased glomerular area, and decreased cellularity.
- Histopathology revealed severe kidney damage in untreated diabetic mice, characterized by distorted glomeruli, inflammation, and macrophages.
- Biotin treatment significantly reduced histopathological alterations and diminished the oxidative damage marker (acrolein) in diabetic mice.
Conclusions:
- Biotin exhibits a protective role against kidney injury in type 1 diabetes.
- Biotin effectively mitigates oxidative stress in the kidneys of diabetic mice.
- These findings suggest biotin as a potential therapeutic agent for diabetic nephropathy.
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