Stress and Cigarette Smoke Effects on Lung Mitochondrial Phosphorylation

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Abstract
The stress of forced mouth breathing and the superimposition of cigarette smoking on this stress cause losses in oxidative phosphorylation efficiency in guinea pig lung mitochondria in vivo. The loss of efficiency is greater in the mouth-breathing, air-inhaling animals than in cigarette smokers under the same conditions. The “tightness” of phosphorylation coupling at mitochondrial sites 2 and 3 was rneasured in these experiments, using artificial electron generators or acceptors. The mouth-breathing, nonsmoking animals lost efficiency at two phosphorylation locisites 2 and 3. Mouth-breathing smokers lost efficiency only at phosphorylation transfer site 3. These stress and cigarette smoke effects at sites 2 and 3, respectively, suggest that the losses of oxidative phosphorylation efficiency are due to different mechanisms acting at specific loci within the mitochondrion.