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Citrinin-induced mitochondrial permeability transition

E J Da Lozzo1, M B Oliveira, E G Carnieri

  • 1Departamento de Bioquímica, Universidade Federal do Paraná, Curitiba, PR, Brasil.

Journal of Biochemical and Molecular Toxicology
|July 17, 1998
PubMed
Summary

The mycotoxin citrinin causes calcium (Ca2+) efflux and membrane permeabilization in rat liver mitochondria. This suggests citrinin induces mitochondrial permeability transition without oxidative damage.

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Area of Science:

  • Biochemistry
  • Toxicology
  • Cell Biology

Background:

  • Mycotoxins are toxic secondary metabolites produced by fungi.
  • Citrinin is a mycotoxin with known nephrotoxic effects.
  • Mitochondrial dysfunction is implicated in various toxicological processes.

Purpose of the Study:

  • To investigate the effects of citrinin on calcium (Ca2+) efflux in isolated rat liver mitochondria.
  • To determine if citrinin induces mitochondrial membrane permeabilization.
  • To elucidate the mechanism of citrinin-induced mitochondrial permeability transition.

Main Methods:

  • Isolated rat liver mitochondria were used.
  • Calcium efflux was measured using ruthenium red.
  • Mitochondrial swelling was assessed spectrophotometrically.

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  • Protective effects of antioxidants (catalase, BHT, DTT) and pore inhibitors (ATP-Mg2+, cyclosporin A) were evaluated.

    • Main Results:

    • Citrinin significantly increased Ca2+ efflux from mitochondria.
    • Citrinin induced Ca2+-dependent mitochondrial swelling, indicating membrane permeabilization.
    • Antioxidants did not prevent citrinin-induced swelling.
    • ATP-Mg2+ and cyclosporin A partially protected against swelling, suggesting pore formation.

    Conclusions:

    • Citrinin induces mitochondrial permeability transition.
    • The mechanism involves pore formation and does not appear to rely on oxidative damage.
    • Citrinin's effects on mitochondrial calcium handling may contribute to its toxicity.