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the pre-requisite for the development of renal stone

A direct co-relation between renal mitochondrial dysfunction and ethylene glycol induced calcium oxalate formation was reported, where the exposure of the proximal tubule with calcium oxalate crystals resulted in rapid and progressive osmotic swelling and dissipation of transmembrane potential of mitochondria resulted in its damage . The peroxidation of protein had greater influence on the nucleation and aggregation property of calcium oxalate crystal growth and that predominantly occur in mitochondria Mitochondrial permeability transition pore (mPTP) opening is a terminal event leading to mitochondrial dysfunction and cell death under conditions of oxidative stress. In fact, the vulnerability of the renal tissue towards oxidative stress depends on the functional cross talks between mPTP and mitochondrial KATP channel In the present study, we evaluated the specific role of mitochondrial potassium ATP channel in the sodium thiosulfate mediated renal protection.

Acccording to previous study results, it is believed that renal protection mediated by sodium thiosulfate is mainly attributed to its chelation and antioxidant potential However, thiosulfates are metabolized in mitochondria, and thus we anticipated a mitochondria based mechanism for its renal protection. In this connection, we used a mitochondrial potassium channel blocker glibenclamide (binds to sulphonylurea receptor subtypes of KATP channel) and channel opener diazoxide (binds to ATP binding sites of sulphonylurea receptor subtypes of KATP channel) to evaluate the renal status as supported by biochemical parameters and histopatholog