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Gliotoxin induces Mg2+ efflux from intact brain mitochondria

Mauro Salvi1, Aleksandra Bozac, Antonio Toninello

  • 1Dipartimento di Chimica Biologica, Universita' di Padova and Istituto di Neuroscienze del C.N.R., Unita' per lo Studio delle Biomembrane, Via G. Colombo 3, 35121 Padua, Italy.

Neurochemistry International
|July 6, 2004
PubMed

Insights

Gliotoxin induces mitochondrial permeability transition (MPT) by opening a pore, causing swelling and ion efflux. It also activates a separate magnesium (Mg2+) efflux system in brain mitochondria.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Neuroscience

Background:

  • Gliotoxin (GT) is a fungal metabolite impacting cellular membranes.
  • It belongs to the epipolythiodioxopiperazine class and reacts with thiols.

Purpose of the Study:

  • To investigate the effects of gliotoxin on energized brain mitochondria.
  • To elucidate the mechanisms of gliotoxin-induced mitochondrial changes and ion efflux.

Main Methods:

  • Energized brain mitochondria were treated with gliotoxin.
  • Effects on matrix swelling, membrane potential (DeltaPsi), and cation efflux (Ca2+, Mg2+) were measured.
  • The influence of cyclosporin A (CsA), ADP, Mg2+, and spermine was assessed.

Main Results:

  • Gliotoxin induced low-amplitude matrix swelling, DeltaPsi collapse, and Ca2+ and Mg2+ efflux, indicative of mitochondrial permeability transition (MPT).
  • Cyclosporin A and ADP partially inhibited MPT-related effects but not Mg2+ efflux.
  • Exogenous Mg2+ or spermine protected against MPT but only slightly affected Mg2+ efflux.

Conclusions:

  • Gliotoxin induces MPT in brain mitochondria via pore opening.
  • Gliotoxin also activates a distinct Mg2+ efflux system independent of MPT.

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