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Related Experiment Videos

Cell surface oxygen consumption by mitochondrial gene knockout cells.

Patries M Herst1, An S Tan, Debbie-Jane G Scarlett

  • 1Department of Radiation Therapy, Wellington School of Medicine and Health Sciences, University of Otago, PO Box 7343, Wellington, New Zealand.

Biochimica Et Biophysica Acta
|June 5, 2004
PubMed
Summary

Mitochondrial gene knockout cells utilize trans-plasma membrane electron transport (tPMET) for energy. This study reveals oxygen as the terminal electron acceptor for tPMET, supporting cell growth without mitochondria.

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Mitochondrial Function

Background:

  • Mitochondrial gene knockout (rho(0)) cells rely on glycolysis for energy.
  • These cells exhibit enhanced reduction of tetrazolium dyes via plasma membrane electron transport.
  • The role of oxygen in this non-mitochondrial pathway was previously unclear.

Purpose of the Study:

  • To investigate oxygen's role as a terminal electron acceptor in trans-plasma membrane electron transport (tPMET) in HL60rho(0) cells.
  • To elucidate the association between cell surface oxygen consumption and oxygen-dependent cell growth in rho(0) cells.
  • To identify the specific pathways and components involved in non-mitochondrial oxygen consumption.

Main Methods:

  • Utilized HL60rho(0) cells, which lack mitochondrial DNA.

Related Experiment Videos

  • Measured non-mitochondrial oxygen consumption and WST-1 dye reduction.
  • Employed various inhibitors targeting glycolysis, electron transport, and specific enzymes (e.g., diphenyleneiodonium, dicoumarol).
  • Assessed the effect of extracellular NADH, NADPH, and NAD(+) on oxygen consumption.

    • Main Results:

    • Oxygen was identified as the terminal electron acceptor for tPMET in HL60rho(0) cells.
    • Cell surface oxygen consumption was linked to oxygen-dependent cell growth in the absence of mitochondrial function.
    • Extracellular NADH and NADPH, but not NAD(+), inhibited non-mitochondrial oxygen consumption, indicating a cell surface localization.
    • Inhibitors of glycolysis, ubiquinone redox cycle, flavin center, and NQO1 significantly reduced oxygen consumption.
    • Inhibition profiles for oxygen consumption and WST-1 reduction were similar, suggesting a shared tPMET pathway.

    Conclusions:

    • Oxygen serves as a crucial terminal electron acceptor for tPMET in rho(0) cells, supporting growth.
    • The tPMET pathway in these cells is localized at the cell surface and is dependent on glycolysis and specific enzymes.
    • This non-mitochondrial pathway provides an alternative energy source for cells lacking functional mitochondria.