Effect of carbonyl cyanide m-chlorophenylhydrazone on respiration and respiration-dependent phosphorylation in Escherichia coli

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Abstract
The interference mechanism of carbonyl cyanide m-chloro-phenylhydrazone with the respiratory process and with phosphorylation coupled to respiration has been investigated in resting cells of E. coli. Preincubation of the cells with carbonyl cyanide m-chlorophenylhydra-zone in the absence of substrate caused strong inhibition of succinate oxidation. The inactivation of the respiratory system proved to be time-dependent and temperature-dependent and could be arrested by adding the substrate. Inhibition of incorporation of 32P into acid-soluble organic phosphate esters exceeded the inhibition of oxygen uptake. In contrast with succinate, the rate of oxidation of glucose was increased by carbonyl cyanide m-chlorophenylhydrazone. The sensitivity of other substrates to the inhibitor was less than that of succinate. Various observations are described in support of the view that respiratory inhibition induced by carbonyl cyanide m-chlorophenylhy-drazone is a result of its interference with ATP synthesis. The capacity of a given substrate to increase intracellular ATP concentration appeared to be directly related to its resistance to inhibition. In cell-free extracts carbonyl cyanide m-chlorophenylhydrazone still suppressed 32P incorporation but had no effect on respiration. Carbonyl cyanide m-chlorophenylhydrazone-induced stimulation of glucose oxidation and the acceleration of succinate oxidation by ADP or AMP in cells rendered permeable to nucleotides are tentatively interpreted as an indication that a certain part of respiration in E. coli is under phosphate-acceptor-mediated control.

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