Premium
Beating anoxia: mitochondrial plasticity in the turtle heart
Author(s) -
Galli Gina Lucia Jane,
Richards Jeffrey
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.887.3
Subject(s) - mitochondrion , anoxic waters , respiration , turtle (robot) , oxygen , reactive oxygen species , biology , cellular respiration , biochemistry , microbiology and biotechnology , chemistry , biophysics , anatomy , ecology , organic chemistry
Freshwater turtles can survive without oxygen for several months. The cellular mechanisms that allow the turtle heart to survive without oxygen have remained almost totally unexplored. In particular, it is not known how the turtle heart avoids anoxic damage to the mitochondria. The objective of this study was to make a comprehensive analysis of mitochondrial function in chronically and acutely anoxic mitochondria from the heart of Trachemys scripta . Turtles were acclimated to 5°C under either normoxic or anoxic (2 weeks) conditions. Mitochondrial respiration, electron transport chain (ETC) activities, ADP affinity, enzyme activities, proton leak and membrane potential were measured in permeabilized cardiac fibres and isolated mitochondria. 2 weeks of anoxia led to a decrease in aerobic capacity and an increase in proton conductance (proton leak) of the mitochondrial membrane. The mechanism behind this plasticity was a downregulation of Complex V in the ETC. This strategy serves two purposes; to conserve ATP when energy is limited and to reduce the production of reactive oxygen species. Turtle heart mitochondria endured 20 min of simulated anoxia followed by reperfusion without any impact on subsequent ADP stimulated oxygen consumption, State IV respiration or respiratory control ratio. Thus, turtle mitochondria are robust and intrinsically tolerant to anoxia/reoxygenation.