Abstract
Abstract Studies are described which show that when intact rat liver mitochondria are incubated with 74As-inorganic arsenate a new radioactive substance is produced which has been isolated and shown to possess properties that would be expected for a stable low molecular weight arsenate ester. The formation of this new compound by mitochondria is inhibited by KCN, 2,4-dinitrophenol, and oligomycin, suggesting that a functional electron transport chain and at least part of the coupling reactions of oxidative phosphorylation are required. The relationship of the new arsenylated compound to the mechanism of oxidative phosphorylation is unclear, and studies designed to clarify this aspect of the research are in progress.
Highlights
The formation of this new compound by mitochondria is inhibited by KCN, 2,4-dinitrophenol, and oligomycin, suggesting that a functional electron transport chain and at least part of the coupling reactions of oxidative phosphorylation are required
Numerous studies of the effects of inorganic arsenate on respiration [1, 2], ATP synthesis [2, 3], ATPase [2, 4], the ATP-32P r exchange reaction,l and the ATP-ADP exchange reaction [5] catalyzed by intact mitochondria suggest that inorganic arsenate compet.es with inorganic phosphate at a step of the coupling mechanism at which inorganic phosphate normally interacts with a component generated during oxidative phosphorylation
The inhibition of As-X formation produced by potassium cyanide, 2,4-dinitrophenol, and oligomycin shown in Experiment 1 indicates that electron transport and at least a portion of the coupling mechanism of oxidative phosphorylation are involved in its formation
Summary
Studies are described which show that when intact rat liver mitochondria are incubated with 74As-inorganic arsenate a new radioactive substance is produced which has been isolated and shown to possess properties that would be expected for a stable low molecular weight arsenate ester. A similar mechanism has been invoked to rationalize the observed stimulation of respiration, inhibition of ATP synthesis, stimulation of ATPase activity, and inhibition of the ATP-ADP exchange reaction catalyzed by intact mitochondria [2, 4, 5] In this communication we wish to report the formation by intact mitochondria during respiration of a stable arsenylated derivative of a mitochondrial constituent and to describe pertinent kinetic and chemical properties which provide evidence for a possible role of a low molecular weight mitochondrial component in the reactions associated with oxidative phosphorylation
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