Oxidation of citrate by mitochondria from guinea pig heart, liver and kidney

Abstract

There is no unanimity concerning the ability of mitochondrial systems from heart, liver and kidney to oxidize citrate. This disparity stems partly from lack of uniformity in the choice of species and partly from the mode of tissue preparation. The present results have been obtained with mitochondria prepared from guinea pig heart, liver and kidney. The QNOO2 for citrate at 2 mm ATP level is highest in kidney, 590, followed by liver, 417 and heart, 255. Kidney and liver oxidations are accompanied by phosphorylations while oxidation of citrate in the cardiac preparations are unaccompanied by any phosphorylation. Further differences are manifested by lowering ATP level in the medium to 0.33 mm. There is a decrease in the QNOO2 in liver and kidney with no change in phosphorylation ability, while the QNOO2 in the heart is increased by 25%. Greatest changes are those observed by addition of DPN and TPN which inordinately increase QNOO2 in the heart muscle, particularly at lower levels of ATP. Addition of CoA has virtually no effect on the QNOO2 or P/O ratios in any of the tissue preparations.