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Gentamicin rapidly inhibits mitochondrial metabolism in high-frequency cochlear outer hair cells

Heather C Jensen-Smith1, Richard Hallworth, Michael G Nichols

  • 1Department of Biomedical Sciences, Creighton University, Omaha, Nebraska, United States of America. heathersmith@creighton.edu

Plos One
|June 21, 2012
PubMed

Insights

Gentamicin (GM) antibiotics damage hearing by harming cochlear outer hair cells (OHCs). Differences in OHC and inner hair cell (IHC) metabolism may explain why OHCs are more vulnerable to this hearing loss.

Area of Science:

  • Ototoxicity
  • Mitochondrial Metabolism
  • Auditory Neuroscience

Background:

  • Aminoglycosides (AG), like gentamicin, are widely used antibiotics.
  • AG ototoxicity can cause irreversible hearing loss (HL) in a significant portion of patients.
  • High-frequency outer hair cells (OHCs) are particularly vulnerable to HL, similar to AG ototoxicity.

Purpose of the Study:

  • To investigate if differences in inner hair cell (IHC) and OHC mitochondrial metabolism influence their sensitivity to AG-induced HL.
  • To compare IHC- and OHC-specific metabolic changes during gentamicin exposure.

Main Methods:

  • Measured mitochondrial reduced nicotinamide adenine dinucleotide (NADH) fluorescence in IHCs and OHCs.
  • Assessed succinate dehydrogenase activity.
  • Compared metabolic responses to gentamicin and elevated glucose in high-frequency basal turn OHCs.

Main Results:

  • Gentamicin caused rapid decreases in NADH fluorescence and succinate dehydrogenase activity.
  • High-frequency basal turn OHCs showed metabolic biases, responding quickly to environmental changes like gentamicin and glucose.
  • These metabolic biases may increase OHC susceptibility to reactive oxygen species (ROS) production during injury.

Conclusions:

  • Mitochondrial metabolism plays a crucial role in regulating aminoglycoside ototoxicity.
  • Fundamental metabolic differences between IHCs and OHCs likely dictate their differing fates in various HL pathologies.
  • Understanding these metabolic differences is key to developing strategies against hearing loss.

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