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The mitochondrial T1095C mutation increases gentamicin-mediated apoptosis.

Hakan Muyderman1, Neil R Sims, Masashi Tanaka

  • 1Discipline of Medical Biochemistry and Centre for Neuroscience, School of Medicine, Flinders University, Adelaide, South Australia, Australia. hakan.muyderman@flinders.edu.au

Mitochondrion
|June 28, 2012
PubMed
Summary

A mitochondrial DNA mutation (T1095C) is linked to maternally inherited diseases. This mutation increases cellular vulnerability to aminoglycoside antibiotics, raising concerns for patient safety.

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Area of Science:

  • Genetics
  • Mitochondrial Biology
  • Neuroscience

Background:

  • A heteroplasmic mitochondrial DNA (mtDNA) mutation, T1095C, in the 12S ribosomal RNA (rRNA) gene was previously identified in an Italian family.
  • This family exhibited maternally inherited parkinsonism, antibiotic-mediated deafness, and peripheral neuropathy.

Purpose of the Study:

  • To investigate the pathogenic role of the T1095C mtDNA mutation.
  • To determine the mutation's effect on cellular function and susceptibility to antibiotic toxicity.

Main Methods:

  • Generation of a transmitochondrial cybrid cell line from the proband.
  • Assessment of mitochondrial glutathione levels and activity of respiratory chain complex II/III.
  • Exposure of cybrid cells to an aminoglycoside antibiotic and measurement of apoptosis.

Main Results:

  • The cybrid cell line showed selective depletion of mitochondrial glutathione.
  • A decrease in the activity of mitochondrial respiratory chain complex II/III was observed.
  • Cells with the mutation exhibited a ten-fold increase in apoptosis when exposed to aminoglycoside antibiotics compared to controls.

Conclusions:

  • The T1095C mutation plays a pathogenic role in the observed family phenotype.
  • The mutation confers increased risk for aminoglycoside-induced cellular toxicity.
  • This finding has implications for managing patients with this mtDNA mutation, particularly regarding antibiotic treatment.