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hypothesis for stone formation and growth

The protective mechanism induced by the opening of mito KATP is well-studied in cardiovascular diseases. Analogous to the heart system, renal protection by diazoxide may well be claimed due to i) Changes in the mitochondrial Ca2+ levels ii) Mitochondrial matrix swelling and changes in ATP synthesis iii) Changes in the ROS levels. Sodium thiosulfate is a known calcium chelating agent with antioxidant properties (30) and can render electrons to complex IV upon its metabolism. Furthermore, several lines of the reports suggest that mitochondrial KATP channel opening may inhibit mitochondrial permeability transition through inhibiting calcium overload and thereby preserve mitochondrial functions. A proven relationship between mitochondrial membrane potential, mitochondrial dependent apoptosis and calcium overload predicts the possibility of thiosulfate mediated calcium signaling mechanism through calcium/calmodulin-dependent protein kinase for its action, proposed for the future study.

The present study enhances the existing knowledge of STS mediated anti urolithiatic mechanism that emphasizes the calcium chelation and antioxidant property of STS alone. Based on our findings, we suggest that thiosulfate modulate the mitochondrial KATP channel to render renal protection against stone formation.

CONCLUSIONS