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Adverse effects of antimicrobials via predictable or idiosyncratic inhibition of host mitochondrial components

Alison E Barnhill1, Matt T Brewer, Steve A Carlson

  • 1Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, Iowa, USA.

Antimicrobial Agents and Chemotherapy
|May 23, 2012
PubMed

Insights

Antibiotics can cause nonantibacterial side effects by damaging mitochondria, which share bacterial ancestors. This review examines how drugs like aminoglycosides and fluoroquinolones impact mitochondrial function, offering insights for safer drug development.

Area of Science:

  • Mitochondrial biology
  • Pharmacology
  • Toxicology

Background:

  • Mitochondria, with their bacterial ancestry, are potential targets for antibiotic-host interactions.
  • Antibiotic-induced mitochondrial damage can manifest as nonantibacterial side effects.
  • Understanding these interactions is crucial for predicting and mitigating drug toxicity.

Purpose of the Study:

  • To review the role of mitochondria in antibiotic-induced nonantibacterial side effects.
  • To explore the mechanisms by which specific antibiotics (aminoglycosides, chloramphenicol, fluoroquinolones, linezolid/oxazolidinones) affect mitochondrial function.
  • To highlight the implications for future antibiotic drug design.

Main Methods:

  • Literature review of studies investigating antibiotic effects on mitochondria.
  • Analysis of reported side effects of common antibiotics in relation to mitochondrial targets.
  • Comparative examination of drug mechanisms and their mitochondrial consequences.

Main Results:

  • Aminoglycosides and oxazolidinones can inhibit mitochondrial ribosomes, similar to their antibacterial action.
  • Chloramphenicol and fluoroquinolones, while targeting mitochondrial components, appear to cause idiosyncratic mitochondrial damage.
  • Mitochondrial side effects are a potential consequence of antibiotics targeting shared prokaryotic and mitochondrial pathways.

Conclusions:

  • Antibiotic-host interactions at the mitochondrial level contribute to nonantibacterial side effects.
  • Drug design should consider the potential for mitochondrial toxicity, especially for antibiotics with targets conserved in mitochondria.
  • Further research into mitochondrion-specific drug effects can lead to safer therapeutic agents.

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