Warm Acclimation Increases Mitochondrial Efficiency in Fish: A Compensatory Mechanism to Reduce the Demand for Oxygen.

AbstractIn ectotherms, it is well described that thermal acclimation induces compensatory adjustments maintaining mitochondrial functions across large shifts in temperature. However, until now, studies mostly focused on fluxes of oxygen without knowing whether mitochondrial efficiency to produce ATP (ATP/O ratio) is also dependent on temperature acclimation. We thus measured thermal reaction norms of oxidative phosphorylation activity and efficiency in isolated mitochondria from skeletal muscle of sea bass (Dicentrarchus labrax) juveniles acclimated at optimal (22°C), low (18°C), and high (26°C) temperatures. The mitochondrial fluxes (oxygen consumption and ATP synthesis) increased with increasing assay temperatures and were on the whole higher in fishes acclimated at 18°C than in the other two groups. However, these mitochondrial rates were not significantly different between experimental groups when they were compared at the acclimation temperature. In contrast, we show that acclimation to high, and not low, temperature improved mitochondrial efficiency (on average >15%). This higher efficiency in high-temperature-acclimated fishes is also apparent when compared at respective acclimation temperatures. This mitochondrial phenotype would favor an economical management of oxygen in response to harsh energetic constraints associated with warming water.

Mechanical ventilation preserves diaphragm mitochondrial function in a rat sepsis model.

BACKGROUND: To describe the effect of mechanical ventilation on diaphragm mitochondrial oxygen consumption, ATP production, reactive oxygen species (ROS) generation, and cytochrome c oxidase activity and content, and their relationship to diaphragm strength in an experimental model of sepsis. METHODS: A cecal ligation and puncture (CLP) protocol was performed in 12 rats while 12 controls underwent sham operation. Half of the rats in each group were paralyzed and mechanically ventilated. We performed blood gas analysis and lactic acid assays 6 h after surgery. Afterwards, we measured diaphragm strength and mitochondrial oxygen consumption, ATP and ROS generation, and cytochrome c oxidase activity. We also measured malondialdehyde (MDA) content as an index of lipid peroxidation, and mRNA expression of the proinflammatory interleukin-1ß (IL-1ß) in diaphragms. RESULTS: CLP rats showed severe hypotension, metabolic acidosis, and upregulation of diaphragm IL-1ß mRNA expression. Compared to sham controls, spontaneously breathing CLP rats showed lower diaphragm force and increased susceptibility to fatigue, along with depressed mitochondrial oxygen consumption and ATP production and cytochrome c oxidase activity. These rats also showed increased mitochondrial ROS generation and MDA content. Mechanical ventilation markedly restored mitochondrial oxygen consumption and ATP production in CLP rats; lowered mitochondrial ROS production by the complex 3; and preserved cytochrome c oxidase activity. CONCLUSION: In an experimental model of sepsis, early initiation of mechanical ventilation restores diaphragm mitochondrial function.

Consequences of electroshock-induced narcosis in fish muscle: from mitochondria to swim performance.

Adult zebrafish Danio rerio were exposed to an electric shock of 3 V and 1A for 5 s delivered by field backpack electrofishing gear, to induce a taxis followed by a narcosis. The effect of such electric shock was investigated on both the individual performances (swimming capacities and costs of transport) and at cellular and mitochondrial levels (oxygen consumption and oxidative balance). The observed survival rate was very high (96·8%) independent of swimming speed (up to 10 body length s-1 ). The results showed no effect of the treatment on the metabolism and cost of transport of the fish. Nor did the electroshock trigger any changes on muscular oxidative balance and bioenergetics even if red muscle fibres were more oxidative than white muscle. Phosphorylating respiration rates rose between (mean 1 s.e.) 11·16 ± 1·36 pmol O2 s-1  mg-1 and 15·63 ± 1·60 pmol O2 s-1  mg-1 for red muscle fibres whereas phosphorylating respiration rates only reached 8·73 ± 1·27 pmol O2 s-1  mg-1 in white muscle. Such an absence of detectable physiological consequences after electro-induced narcosis both at organismal and cellular scales indicate that this capture method has no apparent negative post-shock performance under the conditions of this study.