Persistent increase in mitochondrial superoxide mediates cisplatin-induced chronic kidney disease.

ABSTRACT: Severe and recurrent cisplatin-induced acute kidney injury (AKI) as part of standard cancer therapy is a known risk factor for development of chronic kidney disease (CKD). The specific role of superoxide (O₂^•-)-mediated disruption of mitochondrial oxidative metabolism in CKD after cisplatin treatment is unexplored. Cisplatin is typically administered in weekly or tri-weekly cycles as part of standard cancer therapy. To investigate the role of O₂^•- in predisposing patients to future renal injury and in CKD, mice were treated with cisplatin and a mitochondrial-specific, superoxide dismutase (SOD) mimetic, GC4419. Renal function, biomarkers of oxidative stress, mitochondrial oxidative metabolism, and kidney injury markers, as well as renal histology

SUBMITTER: Mapuskar KA 

PROVIDER: S-EPMC6174865 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature