Hickey 2013 Abstract MiP2013

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Hickey AJ, Iftikar FI, MacDonald J, Baker D (2013) Mitochondria in a changing climate? The role of mitochondrial in hyperthermic heart failure in different fish species. Mitochondr Physiol Network 18.08.
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Anthony Hickey
MiP2013, Book of Abstracts Open Access

Hickey AJ, Iftikar FI, MacDonald J, Baker D (2013)

Event: MiPNet18.08_MiP2013

Predictions of climate change mediated rises in ocean temperatures suggest that ectothermic hearts may place tight constraints on species. For many aquatic species, the upper temperature limit (Tmax) and the heart failure (HF) temperature (THF) is only a few degrees away from their current environmental temperatures [1,2]. For tropical fishes this window between Tmax and THF appears to be narrower than for temperate fishes, where only slight temperature increases induce heart failure (HF) [3]. Why heat stress induces HF remains unresolved, and for fishes elevated temperatures may result from energy and/or oxygen supply disruptions to and from cardiac mitochondria [2]. Damaged/stressed mitochondria may release ROS, trigger apoptosis, and/or simply may fail to produce enough ATP to sustain a heartbeat. Recent work within a common New Zealand wrasse (Notolabrus celidotus) found that ATP synthesis capacity collapses prior to THF alongside loss of cytochrome c [4]. However, is this effect limited to one species from one thermal habitat? We therefore compared heart mitochondria from three wrasse species that occupy cold temperate (N. cinctus), temperate (N. celidotus) and tropical (Thalassoma lunare) habitats. In all three species a drop in phosphorylation efficiency (inferred from RCR) occurred below the THF indicating that heart mitochondrial ATP supply is compromised at elevated temperatures. While acclimation of N. celidotus at their winter low of 15 °C and summer high of 21 °C revealed that the RCR values of heart mitochondria from warm acclimated animals adjusts, this appears to come at a cost of an increased dependence on anaerobic metabolism and an increased sensitivity of flux with Complex I and II substrates. These data indicate that mitochondrial integrity may well play a role in thermal stress tolerance and limit species distributions in our warming world.


O2k-Network Lab: NZ Auckland Hickey AJ


Labels: MiParea: Respiration, Comparative MiP;environmental MiP  Pathology: Cardiovascular  Stress:Oxidative stress;RONS, Temperature  Organism: Other mammals, Fishes  Tissue;cell: Heart  Preparation: Permeabilized tissue  Enzyme: Marker enzyme  Regulation: Flux control, Temperature, Threshold;excess capacity  Coupling state: LEAK, ROUTINE, OXPHOS, ET  Pathway: N, S, CIV, NS  HRR: Oxygraph-2k, TIP2k, O2k-Fluorometer 

MiP2013 

Affiliations and author contributions

School of Biological Sciences, University of Auckland, New Zealand. - Email: a.hickey@auckland.ac.nz


Supported by a Royal Society Marsden Grant to AJ H.


References

  1. Portner HO, Knust R (2007) Climate change affects marine fishes through the oxygen limitation of thermal tolerance. Science 315: 95-97.
  2. Portner HO, Mark FC, Bock C (2004) Oxygen limited thermal tolerance in fish? Answers obtained by nuclear magnetic resonance techniques. Resp Physiol Neurobiol 141: 243-260.
  3. Somero GN (2010) The physiology of climate change: How potentials for acclimatization and genetic adaptation will determine ‘winners’ and ‘losers’. J Exp Biol 213: 912-920.
  4. Iftikar FI, Hickey AJ (2013) Do mitochondria limit hot fish hearts? Understanding the role of mitochondrial function with heat stress in Notolabrus celidotus. Plos ONE 8: e64120.