Renal cortical mitochondria are the source of oxygen free radicals enhanced by gentamicin

C L Yang1, X H Du, Y X Han

  • 1Department of Nephrology, China-Japan Friendship Hospital, Beijing.

Renal Failure
|January 1, 1995
PubMed

Insights

Gentamicin increases oxygen free radicals in rat kidney mitochondria. Antioxidants like DMSO, CAT, and DFO partially reduced these radicals, suggesting mitochondria are a key source in gentamicin nephrotoxicity.

Area of Science:

  • Nephrology
  • Biochemistry
  • Toxicology

Background:

  • Gentamicin is an antibiotic known to cause kidney damage (nephrotoxicity).
  • The exact mechanisms, particularly the role of oxygen free radicals in the kidneys, are not fully understood.

Purpose of the Study:

  • To investigate if renal cortical mitochondria are a source of oxygen free radicals enhanced by gentamicin.
  • To determine the specific types of oxygen free radicals involved and their modulation by antioxidants.

Main Methods:

  • Isolated rat renal cortical mitochondria.
  • Incubated mitochondria with and without gentamicin, and various antioxidants (DMSO, DFO, CAT, SOD, MT1).
  • Quantified superoxide anions and hydroxyl radicals.

Main Results:

  • Gentamicin significantly increased both superoxide anion and hydroxyl radical production in mitochondria.
  • Dimethylsulfoxide (DMSO), deferoxamine (DFO), and catalase (CAT) inhibited hydroxyl radicals.
  • Superoxide dismutase (SOD) inhibited superoxide anions, while MT1 showed no significant effect on either radical type.

Conclusions:

  • Renal cortical mitochondria are a primary source of oxygen free radicals exacerbated by gentamicin.
  • Hydroxyl radicals and superoxide anions play a significant role in gentamicin-induced nephrotoxicity.
  • Specific antioxidants show differential effects on radical types, offering potential therapeutic insights.

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