Subcellular distribution of the enzymes of the malate-aspartate shuttle in rat heart and effect of experimental cardiac hypertrophy.
The effect of experimental cardiac hypertrophy on the enzymes of the malate-aspartate shuttle aspartate aminotransferase (AAT) and malate dehydrogenase (MDH) was studied. Aortic constriction in adult rats resulted in 25% cardiac hypertrophy in 21/2-3 weeks. Total DNA (mg per heart) did not change. The proportions of mitochondrial and cytosolic isozymes of AAT and MDH did not change as a result of cardiac hypertrophy. About two-thirds of each enzyme occurred in the mitochondrial form and one-third in the cytosolic form. Total AAT in hypertrophic hearts, in enzyme units per mg DNA, increased by 24% compared to AAT content in the hearts of sham-operated animals. Total MDH did not change. Solubilized protein increased by 20%. Normal hearts contained 10 times more enzyme units of MDH than of AAT. Cardiac growth stimulation induced in newborn rats did not result in specific changes of either enzyme. It is suggested that true cardiac hypertrophy acts as a specific stimulus for the possibly rate-limiting enzyme AAT of the shuttle.
Mavrides
C
C
Korecky
B
B
D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism*; D001835:Body Weight; D006332:Cardiomegaly / Q000201:enzymology*; D004247:DNA / Q000032:analysis; D008291:Malate Dehydrogenase / Q000378:metabolism*; D009206:Myocardium / Q000648:ultrastructure*; D009929:Organ Size; D051381:Rats; D011919:Rats, Inbred Strains; D013347:Subcellular Fractions / Q000201:enzymology*; D014018:Tissue Distribution
D004247:DNA; D008291:Malate Dehydrogenase; D001219:Aspartate Aminotransferases