Abstract
Summary 1. Rat-liver mitochondria catalyzed an exchange of oxygen atoms between the carboxyl group of long-chain fatty acids and H2O(RCOOH−H218O exchange activity). This exchange was not inhibited by 2,4-dinitrophenol. The amount of RCO0H−H218O exchange activity for various individual long-chain fatty acids corresponded well with their effectiveness as inhibitors of orthophosphate-adenosine 5′-triphosphate exchange activity (32Pi-ATP exchange activity.) 2. Myristic acid, as a representative of the class of long-chain fatty acids, inhibited the exchange of oxygen atoms between orthophosphate and H2O (Pi−H218O exchange activity) catalyzed by rat-liver mitochondria. 3. Aging mitochondria resulted in inhibition of RCOOH−H218O exchange activity which was comparable with the extent of inhibition of [32P]Pi-ATP and Pi−H218O exchange activities. 4. It was proposed that RCOOH−H218O exchange activity may be mediated by a mechanism analogous to that for Pi−H218O exchange activity. It was further suggested that oxygen atoms from H2O may gain access to the carboxyl group of long-chain fatty acids or orthophosphate by lactonization of hydroxycarboxylic acid-like moieties which may form a part of the mechanism by which the energy of electron transport is conserved.
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