Evidence for different forms of monoamine oxidase in perfused rabbit lung.

mitochondrial space was not completely reduced. This indicates some mitochondrial oxidative activity when alveolar Po, was in the 0.5-1.0 mrn Hg range. These studies have demonstrated substrate oxidation and respiratory control with isolated lung mitochondria. Measurements of surface fluorescence and tissue redox couples show intracellular reduction of pyridine nucleotides in response to oxidative inhibitors. These studies indicate in situ activity of lung mitochondria and demonstrate the involvement of these organelles in mainte nance of lung intracellular redox state. An additional feature of lung mitochondria is the relatively rapid rate of a-glycerophosphate oxidation and the CaU requirement for activation of lung mitochondrial aGP dehydrogenase. Inbcellular Ca* may influence the aGP/DHAP ratio and thereby determine the relative availability of these triose phosphates for incorporation into lung phospholipids. Activity of lung mitochondria was studied with a preparation of isolated mitochondria. This was correlated with responses of the isolated perfused lung as determined from surface fluorescence measurements and tissue redox couples. Lung mitochondria demonstrated substrate oxidation, respiratory control, and Ca++ activation of a-glycerophosphate dehydrogenase. In response to oxidative inhibitors, the isolated lung showed increased surface fluorescence and increased tissue ratios of redox couples indicating reduction of pyridine nucleotides. The results demonstrate functional activity of lung mitochondria in situ.