Very few vertebrates survive without oxygen (anoxia) for more than a few minutes. The crucian carp (Carassius carassius) survive months of anoxia at low temperatures and we hypothesised that they maintain mitochondrial membrane potential and function.

Isolated crucian carp cardiomyocytes indeed maintained mitochondrial membrane potential after blocking complex-IV of the electron transport system with cyanide, while those of anoxia-intolerant trout depolarized. When complexes I-III were inhibited, crucian carp mitochondria depolarized, indicating that these complexes need to function during anoxia. Mitochondrial membrane potential depended on reversal of ATP synthase in chemical anoxia, as blocking with cyanide combined with oligomycin to inhibit ATP-synthase lead to depolarization. ATP-synthase activity was reduced in the heart after one week of anoxia in crucian carp, together with a downregulation of ATP-synthase subunit gene expression. However, the morphology of cardiac mitochondria were not affected by one-week anoxia, even with a large increase in mitofusin-2 expression. Cardiac citrate synthase activity was not affected by anoxia, while cytochrome-C oxidase activity was increased.

We show how mitochondria respond to anoxia. A mechanistic understanding of how mitochondrial function can be maintained in anoxia may provide new perspectives to reduce mitochondrial damage in anoxia-sensitive organisms.

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