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Toxicity of emestrin, a new macrocyclic dithiodioxopiperazine mycotoxin, to mitochondrial function

K Kawai1, K Ishizaki, T Nakamaru

  • 1Faculty of Home Economics, Chukyo Women's University, Ohbu 474, Aichi, Japan.

Mycotoxin Research
|April 23, 2013
PubMed

Insights

Emestrin, a mycotoxin, disrupts cellular energy production by inhibiting ATP synthesis and causing mitochondrial swelling in rats and mice. This mycotoxin impacts oxidative phosphorylation, revealing its toxic molecular mechanism.

Area of Science:

  • Biochemistry
  • Toxicology
  • Mitochondrial Biology

Background:

  • Emericella species produce emestrin, a novel macrocyclic epidithiodioxopiperazine mycotoxin.
  • The in vivo toxicity of emestrin in rats and mice necessitates understanding its molecular mechanisms.

Purpose of the Study:

  • To investigate the effects of emestrin on mitochondrial reactions.
  • To elucidate the molecular basis of emestrin's in vivo toxicity.

Main Methods:

  • Isolated rat liver mitochondria were used to study emestrin's effects.
  • Mitochondrial respiration, ATP synthesis, and structural changes (swelling) were assessed.
  • The influence of calcium ions on emestrin-induced mitochondrial swelling was examined.

Main Results:

  • Emestrin inhibited ATP synthesis and uncoupled oxidative phosphorylation.
  • A depression of respiration (state 3) was observed with emestrin.
  • Emestrin induced significant mitochondrial swelling, enhanced by calcium ions.
  • Emestrin B, a related compound, uncoupled oxidative phosphorylation but did not depress state 3 respiration.

Conclusions:

  • Emestrin disrupts mitochondrial function by inhibiting ATP synthesis and causing structural damage.
  • The observed mitochondrial effects provide insight into emestrin's in vivo toxicity.
  • Emestrin's mechanism involves interference with oxidative phosphorylation and mitochondrial integrity.

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