Objectives: Hydrogen sulphide (H2S) has a protective effect against renal ischemia reperfusion injury (I/R), but it is toxic and have the limitation for its controlled in-vivo release to the system. However, its metabolite thiosulfate can release low amounts of H2S, is non toxic and clinically approved drug for end renal failure, cyanide toxicity and calcific nephrolithiasis, and may possess anti-ischemic reperfusion effect. The objective of this study was to determine the anti ischemia reperfusion (I/R) effect of sodium thiosulfate (STS).Methods: I/R was induced in LLC PK1 renal tubular epithelial cells by reversibly treatment of cells with glucose oxidase (3 mM/s) and catalase (998/s) in a glucose deprived media. STS was administered to the cells as pre-treated, preconditioned or post conditioned drug.Results: Pre-treatment of LLC PK1 cells with STS protects the cells from I/R injury but not, when the cells were preconditioned or post conditioned with STS, examined through cell viability tests like sulforhodamine B, crystal violet and LDH activity. Propargylglycine the endogenous H2S biosynthetic inhibitor treatment to the cells did not negate the renal protection mediated by STS pre-treatment indicate the possible release of H2S.Conclusion: This study indicates that STS plays a protective role in I/R induced renal injury when they were administered as pre-treated drug by modulating H2S metabolism.Â
