MITOCHONDRIAL VULNERABILITY AND LIPID METABOLISM - BRAIN AND PANCREATIC MITOCHONDRIA

Oxidative phosphorylation of pancreatic mitochondria was found to be very labile to ischemia in vivo or aging in vitro, as is the case for brain mitochondria. Marked differences were, however, noted in the mechanism responsible for the lability in the two types of mitochondria. In pancreatic mitochondria the decrease in oxidative phosphorylation was accompanied by a fall in the lipid acyl ester bonds and a concomitant increase in lysolecithin, probably due to the action of endogenous phospholipase A (EC 3.1.1.4). On the other hand, in a similar condition the content and composition of phospholipids in brain mitochondria did not change significantly. In brain mitochondria active incorporation of [2-14C]acetate into free fatty acids in the absence of any added cofactors was observed, but this activity was not detected in pancreatic, liver and kidney mitochondria. The possible biochemical mechanism underlying the inhibitory reaction in brain mitochondrial metabolism by ischemia or aging is discussed with particular reference to the increased pool size of endogenously synthesized free fatty acids. © 1969 BY THE JOURNAL OF BIOCHEMISTRY.