# Mitochondrial responses to anoxia-reoxygenation exposure in crucian carp (Carassius carassius)

## TL;DR

Crucian carp mitochondria produce less harmful oxygen byproducts during oxygen deprivation and recovery, helping them survive in low-oxygen environments.

## Contribution

The study reveals tissue-specific mitochondrial adaptations in crucian carp that reduce oxidative stress during anoxia-reoxygenation.

## Key findings

- Crucian carp mitochondria emit up to 4-fold less hydrogen peroxide than common carp.
- Heart mitochondria show a 40% reduction in Complex II-mediated flux after anoxia-reoxygenation.
- Tissue-specific increases in protein and mtDNA oxidation suggest varied oxidative stress responses.

## Abstract

The crucian carp (Carassius carassius) is one of the most anoxia-tolerant vertebrates. While physiological underpinnings of its ability to withstand O2 deprivation are well studied, the ability to tolerate the return to normoxia is still enigmatic. Such reoxygenation is associated with detrimental oxidation damage in other organisms, where mitochondria play a central role in the damaging effects. This leads to the question whether mitochondrial adaptations play a central role in the anoxia and reoxygenation tolerance of crucian carp. We here address whether mitochondria from crucian carp circumvent the negative effects of anoxia–reoxygenation exposure, namely the generation of reactive oxygen species (ROS) and subsequent oxidative stress. Crucian carp brain and heart mitochondria generated up to 4-fold less hydrogen peroxide (H2O2; a major ROS) compared with the closely related, anoxia-intolerant, common carp (Cyprinus carpio). The lower H2O2 emission was partly explained by higher (∼15–30%) total oxidant scavenging capacity. Complex II-mediated flux was ∼40% reduced after anoxia–reoxygenation in crucian carp heart mitochondria. Mitochondrial H2O2 generation measured in vivo was unaffected by anoxia–reoxygenation exposure in heart, brain and gill, but reduced by ∼25% in liver. There were also tissue-specific increases in protein carbonylation (∼1.8-fold in brain and gills) and mitochondrial DNA (mtDNA) damage (∼1.5-fold in liver and heart), indicating that biphasic oxidative stress responses affect tissues differently. Our data show that crucian carp avoid excessive mitochondrial ROS generation upon exposure to anoxia–reoxygenation. The tissue-specific distribution of protein and mtDNA oxidation indicate that crucian carp balance body redox signalling to secure resilience during fluctuating O2 availability.

Summary: Crucian carp mitochondria show lower H2O2 emission compared with anoxia-intolerant common carp and anoxia–reoxygenated crucian carp show tissue-specific oxidative damage, but no H2O2 accumulation with reduced complex II flux.