1971 Volume 70 Issue 5 Pages 755-764
Mitochondrial metabolism was investigated in hypertrophied liver (in parts which still had portal circulation) and atrophied liver (in parts where portal circulation was lost) during early stages after ligation of the left branch of the portal vein.
In hypertrophied liver, enhanced respiratory control, state 3 respiration, an in-creased P:O ratio and ATP synthesis were observed as early as 12 hr after ligation of the left branch of the portal vein. These changes were not accompanied by in-crease in the amounts of respiratory carriers or activities of mitochondrial enzymes such as glutamate dehydrogenase [EC 1. 4. 1. 3], malate dehydrogenase [EC 1. 1. 1. 37] and glutamate-oxaloacetate transaminase [EC 2. 6. 1. 1]. The rate of phosphorylation with glutamate as substrate reached a maximum of about twice the control rate within 24 hr. The maximal rates of ATP hydrolysis by 2, 4-dinitrophenol (DNP) and of synthesis of ATP during oxidative phosphorylation were much higher than in sham-operated animals.
In atrophied liver, reduction of respiratory control, state 3 respiration, the P:O ratio and the rate of phosphorylation occurred over a period of 12 hr, but ATPase activity induced by DNP was not inhibited. The fatty acid content of mitochondria had increased about 3-fold after 12 hr and reached that of control liver within 48 hr, and then the intracellular ATP concentration returned to normal. The results sug-gest that the depression of mitochondrial function may be due to increase in the fatty acid content of mitochondria due to reduced fatty acid oxidation resulting from a lowering of the supply of ATP. The findings are discussed in the light of current knowledge on the mode of action of fatty acid in ischemic liver.
