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Updated: Feb 14, 2026

Simultaneous Measurement of Mitochondrial Calcium and Mitochondrial Membrane Potential in Live Cells by Fluorescent Microscopy
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Simultaneous Measurement of Mitochondrial Calcium and Mitochondrial Membrane Potential in Live Cells by Fluorescent Microscopy

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The mycotoxin phomoxanthone A disturbs the form and function of the inner mitochondrial membrane

Philip Böhler1, Fabian Stuhldreier1, Ruchika Anand2

  • 1Institute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, 40225, Düsseldorf, Germany.

Cell Death & Disease
|February 21, 2018
PubMed

Insights

Phomoxanthone A (PXA), a fungal toxin, disrupts mitochondrial calcium (Ca2+) regulation and inner membrane structure, leading to apoptosis. This novel mitochondrial toxin inhibits respiration and causes fragmentation independent of standard fission/fusion pathways.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Mycology

Background:

  • Mitochondria are vital organelles regulating cellular energy, calcium homeostasis, and apoptosis.
  • Mitochondrial toxins, often microbial, disrupt these essential functions.
  • Phomoxanthone A (PXA) is a mycotoxin from Phomopsis longicolla.

Purpose of the Study:

  • To identify and characterize phomoxanthone A (PXA) as a novel mitochondrial toxin.
  • To elucidate the specific mechanisms by which PXA affects mitochondrial function and structure.
  • To explore PXA's potential as a research tool for studying mitochondrial dynamics.

Main Methods:

  • Treatment of cells with phomoxanthone A (PXA).
  • Measurement of mitochondrial calcium (Ca2+) release and endoplasmic reticulum (ER) Ca2+ levels.
  • Assessment of mitochondrial membrane potential using CCCP as a control.
  • Analysis of cellular respiration and electron transport chain activity.
  • Microscopy to observe mitochondrial network structure and fragmentation.
  • Investigation of the roles of DRP1 and OPA1 in PXA-induced fragmentation.
  • Analysis of inner mitochondrial membrane integrity and cristae structure.
  • Detection of pro-apoptotic protein release.

Main Results:

  • PXA induces significant Ca2+ release from mitochondria, but not the ER.
  • PXA depolarizes mitochondria and inhibits cellular respiration and electron transport chain activity.
  • PXA causes rapid fragmentation of the mitochondrial network, independent of DRP1 and OPA1.
  • PXA disrupts the inner mitochondrial membrane and cristae, leading to apoptosis via pro-apoptotic protein release.

Conclusions:

  • Phomoxanthone A (PXA) is identified as a novel mitochondrial toxin.
  • PXA exhibits a unique mechanism of action, affecting mitochondrial Ca2+ homoeostasis and inner membrane integrity.
  • PXA's distinct effects on mitochondrial structure and function suggest its utility in studying mitochondrial ion transport and membrane dynamics.

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