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Published on: June 7, 2014
Early sequential ultrastructural renal alterations induced by 2-bromoethylamine hydrobromide in the Swiss ICR mouse
D C Wolf1, J J Turek, W W Carlton
1Department of Veterinary Pathobiology, School of Veterinary Medicine, Purdue University, West Lafayette, IN.
Abstract:
Thirty-two male Swiss ICR mice were injected intraperitoneally with 300 mg 2-bromoethylamine hydrobromide/kg body weight, anesthetized, and perfused with glutaraldehyde-paraformaldehyde solution at 5, 15, 30, 60, 90, 120, 150, and 180 minutes after treatment. Eight control mice were injected intraperitoneally with sterile diluent, and one was perfused at each of the same time periods as the treated mice. Proximal tubule epithelial alterations progressed over time from increased secondary lysosome and myeloid body formation to cellular and mitochondrial swelling and eventually cell necrosis. The glomerular, peritubular, and vasa recta capillaries had endothelial cell swelling and desquamation and platelet aggregation. Bromoethylamine nephrotoxicosis in the male Swiss ICR mouse is an ischemic necrosis of the proximal tubules and papilla initiated by endothelial cell damage and makes an excellent model of chemically induced damage to endothelial cells and tubular necrosis.
Insights
2-bromoethylamine hydrobromide causes kidney damage in mice, leading to tubular necrosis and endothelial cell injury. This study establishes a model for chemically induced kidney damage.
Area of Science:
- Nephrology
- Toxicology
- Cell Biology
Background:
- Chemically induced kidney damage is a significant health concern.
- Understanding the mechanisms of nephrotoxicity is crucial for developing protective strategies.
Purpose of the Study:
- To investigate the temporal progression of kidney damage induced by 2-bromoethylamine hydrobromide in male Swiss ICR mice.
- To characterize the cellular and ultrastructural changes in renal tubules and capillaries following exposure.
- To establish a reliable animal model for studying chemically induced endothelial cell damage and tubular necrosis.
Main Methods:
- Male Swiss ICR mice were administered 2-bromoethylamine hydrobromide (300 mg/kg).
- Mice were euthanized and perfused at various time points (5-180 minutes) post-injection.
- Kidney tissues were examined for cellular alterations using electron microscopy.
Main Results:
- Progressive proximal tubule epithelial damage observed, including lysosome formation, swelling, and necrosis.
- Endothelial cell swelling, desquamation, and platelet aggregation occurred in glomerular, peritubular, and vasa recta capillaries.
- The damage pattern suggests ischemic necrosis initiated by endothelial cell injury.
Conclusions:
- 2-bromoethylamine hydrobromide induces ischemic necrosis of proximal tubules and papilla in mice.
- The observed endothelial cell damage and subsequent tubular necrosis provide a robust model for studying chemical nephrotoxicity.
- This model is valuable for research into chemically induced endothelial dysfunction and renal tubular injury.
