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The mitochondrion: a perpetrator of acquired hearing loss

Erik C Böttger1, Jochen Schacht

  • 1Institut für Medizinische Mikrobiologie, Universität Zürich, Zürich, Switzerland.

Hearing Research
|January 31, 2013
PubMed

Insights

Mitochondria dysfunction and reactive oxygen species (ROS) contribute to acquired hearing loss. Understanding these mechanisms may lead to non-ototoxic antibacterials.

Area of Science:

  • Oto-science
  • Cellular Biology
  • Biochemistry

Background:

  • Acquired hearing loss stems from aging, drugs, and noise.
  • Reactive oxygen species (ROS) are implicated in hair cell death, but ROS formation mechanisms are unclear.
  • Mitochondria are primary sites of cellular ROS production.

Purpose of the Study:

  • To review evidence linking mitochondrial pathology and respiratory chain dysfunction to acquired hearing loss.
  • To explore diverse pathways of ROS generation and their causal role in acquired hearing loss.
  • To discuss advances in developing non-ototoxic antibacterials based on aminoglycoside-mitochondria interactions.

Main Methods:

  • Literature review focusing on mitochondrial dysfunction in acquired hearing loss.
  • Analysis of evidence for ROS generation pathways.
  • Examination of aminoglycoside-mitochondria interactions for therapeutic development.

Main Results:

  • Mitochondrial pathology and respiratory chain dysfunction are evident in acquired hearing loss.
  • Multiple pathways can generate ROS, and oxidative stress is not always causal.
  • Aminoglycoside-mitochondria interactions offer a basis for novel antibacterial strategies.

Conclusions:

  • Mitochondrial dysfunction is a key factor in acquired hearing loss.
  • Further research into ROS pathways is needed to clarify causality.
  • Targeting aminoglycoside-mitochondria interactions holds promise for developing safer antibiotics.
Keywords:
ROSSODmitochondrial DNAmtDNArRNAreactive oxygen speciesribosomal RNAsuperoxide dismutase

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