Normalizing renal reducing ability prevents adriamycin-induced proteinuria.

Author(s): Oteki T, Nagase S, Yokoyama H, Ohya H, Akatsuka T, Tada M, Ueda A, Hirayama A, Koyama A

Affiliation(s): Pathophysiology of Renal Diseases, Medical Sciences for Control of Pathological Processes, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Ibaraki, Japan.

Publication date & source: 2005-11-11, Biochem Biophys Res Commun., 337(1):48-51.

Reactive oxygen species play an important role in adriamycin (ADR) nephropathy. We showed by in vivo electron paramagnetic resonance (EPR) that renal reducing ability (RRA) declined on the 7th day after ADR administration. Proteinuria appeared after the decline in RRA. The aim of this study was to prove by in vivo EPR whether the decline in RRA is altered by scavengers such as dimethyl sulfoxide (DMSO) and dimethylthiourea (DMTU) and that it is this change which is responsible for the proteinuria in ADR nephropathy. By showing that DMSO and DMTU ameliorate the RRA, we demonstrate that the decline in RRA is related to ADR-induced proteinuria.