Osmoregulation and salinity-induced oxidative stress: is oxidative adaptation determined by gill function?

Osmoregulating decapods such as the Mediterranean green crab Carcinus aestuarii possess two groups of spatially segregated gills: anterior gills serve mainly respiratory purposes, while posterior gills contain osmoregulatory structures. The co-existence of similar tissues serving different functions allows the study of differential adaptation, in terms of free radical metabolism, upon salinity change. Crabs were immersed for 2 weeks in seawater (SW, 37 ppt), diluted SW (dSW, 10 ppt) and concentrated SW (cSW, 45 ppt). Exposure to dSW was the most challenging condition, elevating respiration rates of whole animals and free radical formation in hemolymph (assessed fluorometrically using C-H2DFFDA). Further analyses considered anterior and posterior gills separately, and the results showed that posterior gills are the main tissues fueling osmoregulatory-related processes because their respiration rates in dSW were 3.2-fold higher than those of anterior gills, and this was accompanied by an increase in mitochondrial density (citrate synthase activity) and increased levels of reactive oxygen species (ROS) formation (1.4-fold greater, measured through electron paramagnetic resonance). Paradoxically, these posterior gills showed undisturbed caspase 3/7 activity, used here as a marker for apoptosis. This may only be due to the high antioxidant protection that posterior gills benefit from [superoxide dismutase (SOD) in posterior gills was over 6 times higher than in anterior gills]. In conclusion, osmoregulating posterior gills are better adapted to dSW exposure than respiratory anterior gills because they are capable of controlling the deleterious effects of the ROS production resulting from this salinity-induced stress.journal articleresearch support, non-u.s. gov't2016 Jan2015 11 13importe

Fasting enhances mitochondrial efficiency in duckling skeletal muscle by acting on the substrate oxidation system

International audienceDuring food deprivation, animals must develop physiological responses to maximize energy conservation and survival. At the subcellular level, energy conservation is mainly achieved by a reduction in mitochondrial activity and an upregulation of oxidative phosphorylation efficiency. The aim of this study was to decipher mechanisms underlying the increased mitochondrial coupling efficiency reported in fasted birds. Mitochondrial oxidative phosphorylation activity, efficiency and membrane potential were measured in mitochondria isolated from the gastrocnemius muscle of ducklings. The content and activities of respiratory chain complexes were also determined. Results from ducklings fasted for 6 days were compared with ducklings fed ad libitum. Here, we report that 6 days of fasting improved coupling efficiency in muscle mitochondria of ducklings by depressing proton-motive force through the downregulation of substrate oxidation reactions. Fasting did not change the basal proton conductance of mitochondria but largely decreased the oxidative phosphorylation activity, which was associated with decreased activities of succinate–cytochrome c reductase (complexes II–III) and citrate synthase, and altered contents in cytochromes b and c+c1. In contrast, fasting did not change cytochrome aa3 content or the activity of complexes I, II and IV. Altogether, these data show that the lower capacity of the respiratory machinery to pump protons in ducklings fasted for 6 days generates a lower membrane potential, which triggers a decreased proton leak activity and thus a higher coupling efficiency. We propose that the main site of action would be located at the level of co-enzyme Q pool/complex III of the electron transport chain

Body mass dependence of oxidative phosphorylation efficiency in liver mitochondria from mammals

International audienceIn eukaryotes, the performances of an organism are dependent on body mass and chemically supported by the mitochondrial production of ATP. Although the relationship between body mass and mitochondrial oxygen consumption is well described, the allometry of the transduction efficiency from oxygen to ATP production (ATP/O) is still poorly understood. Using a comparative approach, we investigated the oxygen consumption and ATP production of liver mitochondria from twelve species of mammals ranging from 5 g to 600 kg. We found that both oxygen consumption and ATP production are mass dependent but not the ATP/O at the maximal phosphorylating state. The results also showed that for sub-maximal phosphorylating states the ATP/O value positively correlated with body mass, irrespective of the metabolic intensity. This result contrasts with previous data obtained in mammalian muscles, suggesting a tissue-dependence of the body mass effect on mitochondrial efficiency

Threshold effect in the H2O2 production of skeletal muscle mitochondria during fasting and refeeding

International audienceUnder nutritional deprivation, the energetic benefits of reducing mitochondrial metabolism are often associated with enhanced harmful pro-oxidant effects and a subsequent long-term negative impact on cellular integrity. However, the flexibility of mitochondrial functioning under stress has rarely been explored during the transition from basal non-phosphorylating to maximal phosphorylating oxygen consumption. Here, we experimentally tested whether ducklings (Cairina moscnata), fasted for 6 days and subsequently refed for 3 days, exhibited modifications to their mitochondrial fluxes, i.e. oxygen consumption, ATP synthesis, reactive oxygen species generation (ROS) and associated ratios, such as the electron leak (% ROS/O) and the oxidative cost of ATP production (% ROS/ATP). This was carried out at different steady-state rates of oxidative phosphorylation in both pectoralis (glycolytic) and gastrocnemius (oxidative) muscles. Fasting induced a decrease in the rates of oxidative phosphorylation and maximal ROS release. These changes were completely reversed by 3 days of refeeding. Yet, the fundamental finding of the present study was the existence of a clear threshold in ROS release and associated ratios, which remained low until a low level of mitochondrial activity was reached (30-40% of maximal oxidative phosphorylation activity)

Improved mitochondrial coupling as a response to high mass-specific metabolic rate in extremely small mammals

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Does high mitochondrial efficiency carry an oxidative cost? The case of the African pygmy mouse (Mus mattheyi)

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