TauT protects against cisplatin-induced acute kidney injury (AKI) established in a TauT transgenic mice model

Abstract

Cisplatin is a commonly used chemotherapeutic agent that has a major limitation because of its nephrotoxicity. Taurine is an important osmolyte that has been found to protect against cisplatin-induced apoptosis in renal cells in vitro. To determine whether over-expression of hTauT protects against cisplatin-induced acute kidney injury (AKI) in vivo, animals (wt and transgenic) were injected with cisplatin and the levels of BUN and serum creatinine were measured. Saline-injected mice were used as a control. The results showed that the levels of BUN and creatinine were significantly increased in the cisplatin-injected wild-type mice (110 ± 12 mg/dl and 0.98 ± 0.05 mg/dl) as compared to the saline-injected wild type mice (20 ± 2.5 mg/dl and 0.52 ± 0.06 mg/dl). However, over-expression of hTauT effectively prevented the progression of cisplatin-induced AKI in hTauT transgenic mice, as measured by the levels of BUN and serum creatininelevels (23 ± 3.5 mg/dl and 0.6 ± 0.05 mg/dl). © 2009 Springer Science+Business Media, LLC.