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Related Experiment Videos

Normalizing renal reducing ability prevents adriamycin-induced proteinuria.

Takaaki Oteki1, Sohji Nagase, Hidekatsu Yokoyama

  • 1Pathophysiology of Renal Diseases, Medical Sciences for Control of Pathological Processes, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Ibaraki, Japan.

Biochemical and Biophysical Research Communications
|September 21, 2005
PubMed
Summary

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Adriamycin (ADR) nephropathy involves reactive oxygen species. This study shows that a decline in renal reducing ability (RRA) precedes proteinuria, and scavengers like DMSO and DMTU can improve RRA, linking RRA decline to ADR-induced kidney damage.

Area of Science:

  • Nephrology
  • Biochemistry
  • Toxicology

Background:

  • Reactive oxygen species (ROS) are implicated in adriamycin (ADR) nephropathy.
  • Adriamycin-induced kidney damage is a significant clinical concern.

Purpose of the Study:

  • To investigate the role of renal reducing ability (RRA) decline in ADR nephropathy.
  • To determine if scavengers alter RRA and subsequently affect proteinuria in ADR nephropathy.

Main Methods:

  • In vivo electron paramagnetic resonance (EPR) was used to measure RRA.
  • Administration of adriamycin (ADR) to induce nephropathy.
  • Treatment with scavengers dimethyl sulfoxide (DMSO) and dimethylthiourea (DMTU).

Main Results:

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  • A decline in RRA was observed on day 7 post-ADR administration.
  • Proteinuria appeared following the decrease in RRA.
  • DMSO and DMTU administration ameliorated the decline in RRA.

    • Conclusions:

    • The decline in RRA is closely linked to the development of proteinuria in ADR nephropathy.
    • Scavengers like DMSO and DMTU can mitigate the decline in RRA, suggesting a protective role.