1. Mitochondrial complexes I and II respond differently in two anoxia-tolerant species:
adaptive mitochondrial plasticity may be related to the ability to undergo metabolic
depression.
Gillian M.C. Renshaw1, Anthony J.R. Hickey2, Jules B.L. Devaux2
1School of Allied Sciences, Griffith University, QLD, Australia
2School of Biological Sciences, University of Auckland, Auckland, New-Zealand
Fig 1. The ETS coupling efficiency
from cerebellar mitochondria is
significantly higher for ES post-
anoxia compare to GCS
The Epaulette Shark (ES) is capable
of metabolic depression in response
to hypoxia or anoxia
The Grey Carpet Shark (GCS) is not
capable of metabolic depression in
response to hypoxia or anoxia
Fig 2. CI capacity of ES is
significantly higher (15%) than
GCS post-anoxia
Fig 3 & 4. Succinate stimulated CII respiration after 20min of anoxia compared to CII
respiration in controls was:
a) significantly higher in mitochondria from GCS (a 40% increase at 2.5mM)
b) significantly lower in mitochondria from ES (60% decrease at 0.5mM)
While anoxia tolerance is rare, the protective mechanisms are not uniform. The ES but not the GCS was able to maintain coupling
efficiency and CI capacity even after 20 mins of anoxia followed by reperfusion. The ES but not the GCS responded to succinate
accumulation by significantly decreasing CII respiration. Taken together these data suggest that the adaptive plasticity of ES
mitochondria would support entry into metabolic depression as a protective response to anoxia/reperfusion.
Homogenates of the cerebellum from two shark species were used to investigate
mitochondrial plasticity in response to anoxia followed by re-oxygenation
Fig 1. Fig 2. Fig 3. Fig 4.