Mitochondria in the Cold

Gnaiger, Erich; Kuznetsov, Andrej V.; Schneeberger, Stefan; Seiler, R.; Brandacher, Gerald; Steurer, Wolfgang; Margreiter, Raimund

doi:10.1007/978-3-662-04162-8_45

Cited by 166 publications

(133 citation statements)

References 24 publications

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“…The cold-adapted N. fucicola also needed higher FCCP concentrations for similar assay temperatures to N. celidotus (Fig. 7B, inset), indicating a tightly coupled ETS in N. fucicola, or differences in FCCP mobility and inner membrane composition (Gnaiger et al, 2000). This was also reflected in the UCR observed for N. fucicola, which remained unaffected as assay temperatures increased (Fig.…”

Section: The Impact Of Heat Stress On Mitochondrial Bioenergeticsmentioning

confidence: 80%

Could thermal sensitivity of mitochondria determine species distribution in a changing climate?

Iftikar

MacDonald

Baker

et al. 2014

Journal of Experimental Biology

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For many aquatic species, the upper thermal limit (T max ) and the heart failure temperature (T HF ) are only a few degrees away from the species' current environmental temperatures. While the mechanisms mediating temperature-induced heart failure (HF) remain unresolved, energy flow and/or oxygen supply disruptions to cardiac mitochondria may be impacted by heat stress. Recent work using a New Zealand wrasse (Notolabrus celidotus) found that ATP synthesis capacity of cardiac mitochondria collapses prior to T HF . However, whether this effect is limited to one species from one thermal habitat remains unknown. The present study confirmed that cardiac mitochondrial dysfunction contributes to heat stress-induced HF in two additional wrasses that occupy cold temperate (Notolabrus fucicola) and tropical (Thalassoma lunare) habitats. With exposure to heat stress, T. lunare had the least scope to maintain heart function with increasing temperature. Heat-exposed fish of all species showed elevated plasma succinate, and the heart mitochondria from the cold temperate N. fucicola showed decreased phosphorylation efficiencies (depressed respiratory control ratio, RCR), cytochrome c oxidase (CCO) flux and electron transport system (ETS) flux. In situ assays conducted across a range of temperatures using naive tissues showed depressed complex II (CII) and CCO capacity, limited ETS reserve capacities and lowered efficiencies of pyruvate uptake in T. lunare and N. celidotus. Notably, alterations of mitochondrial function were detectable at saturating oxygen levels, indicating that cardiac mitochondrial insufficiency can occur prior to HF without oxygen limitation. Our data support the view that species distribution may be related to the thermal limits of mitochondrial stability and function, which will be important as oceans continue to warm.

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Section: The Impact Of Heat Stress On Mitochondrial Bioenergeticsmentioning

confidence: 80%

Could thermal sensitivity of mitochondria determine species distribution in a changing climate?

Iftikar

MacDonald

Baker

et al. 2014

Journal of Experimental Biology

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“…After gentle shaking (30min, 0°C) the tissue was removed from the permeabilising solution and washed three times in a modified mitochondrial respiratory medium [MiRO5, in mmoll −1 unless otherwise indicated: 0.5 EGTA, 3 MgCl 2 ·6H 2 O, 60 K-lactobionate, 20 taurine, 10 KH 2 PO 4 , 20 Hepes, 160 sucrose and 1gl −1 bovine serum albumin (Gnaiger et al, 2000)]. Fibres were removed from MiRO5, blotted dry and weighed into bundles (~5-10mg) for respirometric determinations.…”

Section: Mitochondrial Respirationmentioning

confidence: 99%

Low O2 acclimation shifts the hypoxia avoidance behaviour of snapper (Pagrus auratus) with only subtle changes in aerobic and anaerobic function

Cook

Iftikar

Baker

et al. 2012

Journal of Experimental Biology

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SUMMARYIt was hypothesised that chronic hypoxia acclimation (preconditioning) would alter the behavioural low-O 2 avoidance strategy of fish as a result of both aerobic and anaerobic physiological adaptations. Avoidance and physiological responses of juvenile snapper (Pagrus auratus) were therefore investigated following a 6week period of moderate hypoxia exposure (10.2-12.1kPa P O2 , 21±1°C) and compared with those of normoxic controls (P O2 =20-21kPa, 21±1°C). The critical oxygen pressure (P crit ) limit of both groups was unchanged at ~7kPa, as were standard, routine and maximum metabolic rates. However, hypoxia-acclimated fish showed increased tolerances to hypoxia in behavioural choice chambers by avoiding lower P O2 levels (3.3±0.7 vs 5.3±1.1kPa) without displaying greater perturbations of lactate or glucose. This behavioural change was associated with unexpected physiological adjustments. For example, a decrease in blood O 2 carrying capacity was observed after hypoxia acclimation. Also unexpected was an increase in whole-blood P 50 following acclimation to low O 2 , perhaps facilitating Hb-O 2 off-loading to tissues. In addition, cardiac mitochondria measured in situ using permeabilised fibres showed improved O 2 uptake efficiencies. The proportion of the anaerobic enzyme lactate dehydrogenase, at least relative to the aerobic marker enzyme citrate synthase, also increased in heart and skeletal red muscle, indicating enhanced anaerobic potential, or in situ lactate metabolism, in these tissues. Overall, these data suggest that a prioritization of O 2 delivery and O 2 utilisation over O 2 uptake during long-term hypoxia may convey a significant survival benefit to snapper in terms of behavioural low-O 2 tolerance.

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“…The rate of oxygen consumption at the basal level and upon treatment with oligomycin, p-trifluoromethoxy carbonyl cyanide phenylhydrazone (FCCP), or rotenone was recorded sequentially. Respiration by ESCs was determined using an Oxygraph-2K-based workshop (OROBOROS, Innsbruck, Austria) by re-suspending cells in MiR05 respiration buffer (20 mM HEPES, 10 mM KH 2 PO 4 , 110 mM sucrose, 20 mM taurine, 60 mM K-lactobionate, 0.5 mM EGTA, 3 mM MgCl 2 , 0.1% fatty acid-free BSA) (30) at the cell density of 1 ϫ 10 6 /ml. Prior to permeabilization, the basal level of oxygen consumption was monitored and the cells were then permeabilized with digitonin and different mitochondrial respiration substrates were added sequentially to determine the level of oxygen consumption (31).…”

Section: ⌬/ϫmentioning

confidence: 99%

Cited2, a Transcriptional Modulator Protein, Regulates Metabolism in Murine Embryonic Stem Cells

Hakimi

Liu

et al. 2014

Journal of Biological Chemistry

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Background:The function of HIF-1, a master regulator of metabolism, is in part modulated by Cited2. The role of Cited2 in murine embryonic stem cell (mESC) glucose metabolism remains unknown. Results: Deletion of Cited2 in mESCs results in impaired mitochondria morphology, reduced glucose oxidation, increased glycolysis, and defective mESC differentiation. Conclusion: Cited2 coordinates glucose metabolism to regulate mESC differentiation. Significance: Cited2 is a potential target for metabolic reprogramming in mESCs.

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Mitochondria in the Cold

Cited by 166 publications

References 24 publications

Could thermal sensitivity of mitochondria determine species distribution in a changing climate?

Could thermal sensitivity of mitochondria determine species distribution in a changing climate?

Low O2 acclimation shifts the hypoxia avoidance behaviour of snapper (Pagrus auratus) with only subtle changes in aerobic and anaerobic function

Cited2, a Transcriptional Modulator Protein, Regulates Metabolism in Murine Embryonic Stem Cells

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