Turtles maintain mitochondrial integrity but reduce mitochondrial respiratory capacity in the heart after cold acclimation and anoxia
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Turtles maintain mitochondrial integrity but reduce mitochondrial respiratory capacity in the heart after cold acclimation and anoxia. / Bundgaard, Amanda; Qvortrup, Klaus; Rasmussen, Lene Juel; Fago, Angela.
In: Journal of Experimental Biology, Vol. 222, No. 11, jeb200410, 2019.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - Turtles maintain mitochondrial integrity but reduce mitochondrial respiratory capacity in the heart after cold acclimation and anoxia
AU - Bundgaard, Amanda
AU - Qvortrup, Klaus
AU - Rasmussen, Lene Juel
AU - Fago, Angela
PY - 2019
Y1 - 2019
N2 - Mitochondria are important to cellular homeostasis, but can become a dangerous liability when cells recover from hypoxia. Anoxia-tolerant freshwater turtles show reduced mitochondrial respiratory capacity and production of reactive oxygen species (ROS) after prolonged anoxia, but the mechanisms are unclear. Here, we investigated whether this mitochondrial suppression originates from downregulation of mitochondrial content or intrinsic activity by comparing heart mitochondria from (1) warm (25 degrees C) normoxic, (2) cold-acclimated (4 degrees C) normoxic and (3) cold-acclimated anoxic turtles. Transmission electron microscopy of heart ventricle revealed that these treatments did not affect mitochondrial volume density and morphology. Furthermore, neither enzyme activity, protein content nor supercomplex distribution of electron transport chain (ETC) enzymes changed significantly. Instead, our data imply that turtles inhibit mitochondrial respiration rate and ROS production by a cumulative effect of slight inhibition of ETC complexes. Together, these results show that maintaining mitochondrial integrity while inhibiting overall enzyme activities are important aspects of anoxia tolerance.
AB - Mitochondria are important to cellular homeostasis, but can become a dangerous liability when cells recover from hypoxia. Anoxia-tolerant freshwater turtles show reduced mitochondrial respiratory capacity and production of reactive oxygen species (ROS) after prolonged anoxia, but the mechanisms are unclear. Here, we investigated whether this mitochondrial suppression originates from downregulation of mitochondrial content or intrinsic activity by comparing heart mitochondria from (1) warm (25 degrees C) normoxic, (2) cold-acclimated (4 degrees C) normoxic and (3) cold-acclimated anoxic turtles. Transmission electron microscopy of heart ventricle revealed that these treatments did not affect mitochondrial volume density and morphology. Furthermore, neither enzyme activity, protein content nor supercomplex distribution of electron transport chain (ETC) enzymes changed significantly. Instead, our data imply that turtles inhibit mitochondrial respiration rate and ROS production by a cumulative effect of slight inhibition of ETC complexes. Together, these results show that maintaining mitochondrial integrity while inhibiting overall enzyme activities are important aspects of anoxia tolerance.
KW - Electron microscopy
KW - Respirometry
KW - Mitochondria
KW - Reactive oxygen species
KW - Supercomplex
KW - Oxygen
U2 - 10.1242/jeb.200410
DO - 10.1242/jeb.200410
M3 - Journal article
C2 - 31097599
VL - 222
JO - Journal of Experimental Biology
JF - Journal of Experimental Biology
SN - 0022-0949
IS - 11
M1 - jeb200410
ER -
ID: 223923532