Limitation of apoptotic changes in renal tubular cell injury induced by hyperoxaluria

Urological Research
Kemal SaricaRamazan Uçak

Abstract

Renal tubular epithelium is the major target for oxalate induced injury, and sustained hyperoxaluria together with CaOx crystal formation/deposition may induce renal tubular cell damage and/or dysfunction. This may express itself in cell apoptosis. To evaluate the possible protective effects of certain agents (vitamin E, potassium citrate, allopurinol, verapamil and MgOH) on the presence and the severity of apoptotic changes caused by hyperoxaluria on renal tubular epithelium, an experimental study in rabbits was performed. Seventy rabbits were divided into seven different groups (each group n = 10): in group I severe hyperoxaluria was induced by continuous ethylene glycol (0.75%) administration started on day 0 and completed on day 14. Histologic alterations including crystal formation together with apoptotic changes (by using the TUNEL method) were evaluated on days 21 and 42, respectively. In the remaining experimental groups (groups II-VI), animals received some agents in addition to the induction of hyperoxaluria in an attempt to limit apoptotic changes. Group VII) animals constituted the controls. Kidneys were examined histopathologically under light microscopy for the presence and degree of crystal deposition in the tubu...Continue Reading

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Citations

Mar 20, 2009·Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association·Benjamin A VervaetMarc E De Broe
Sep 1, 2009·Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association·Benjamin A VervaetAnja Verhulst
Aug 4, 2010·Urological Research·Benjamin A VervaetPatrick C D'Haese
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Related Concepts

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

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