Decreased total ventricular protein synthesis and protein synthesis
into mitochondria during two or three hours of anoxic perfusion of
the turtle heart.
Bailey, J. R., and W. R. Driedzic.
Department of Biology, Mount Allison University, Sackville, New
Brunswick, Canada, E0A 3C0, Tel. (506)-364-2501, Fax. (506)-364
-2505
APStracts 3:0222R, 1996.
The turtle heart provides a model system to study the effects of
anoxia on protein synthesis without the potentially confounding
factor of contractile failure and decreased ATP levels. Protein
synthesis, as measured by 3H-labelled phenylalanine incorporation,
was studied under conditions of normoxia and anoxia in isolated
perfused turtle (Trachemys (=Pseudemys) scripta elegans) hearts at 15
C. Heart rate, cardiac output and ventricle pressure development were
unaffected by two or three hours of anoxia. Despite the anoxia energy
levels in the heart were presumably still high as contractility was
maintained. RNA content of ventricle decreased after anoxic
perfusion. Rates of total protein synthesis rates in ventricle were
3-fold lower under conditions of anoxia than under conditions of
normoxia. These findings suggest that the total level of RNA is one
determinant of protein synthesis. Incorporation of label into protein
extracted from mitochondria was also assessed. The ratio of
mitochondrial to whole ventricle protein synthesis was significantly
lower after anoxia revealing preferential control mechanisms under
anoxia between the synthesis of total cellular protein and protein
destined for mitochondria. Isolated mitochondria were still coupled
after two or three hours of anoxia. In effect, the mitochondria enter
into a state of hypometabolism in terms of rates of ATP synthesis and
protein synthesis but functional integrity is maintained. The
decrease in protein synthesis in general and mitochondrial protein
synthesis in particular may represent an adaptation to allow the
partitioning of the available energy resources towards mechanical
function during anoxia.
Received 7 February 1996; accepted in final form 23 May 1996.
APS Manuscript Number R79-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 June 96