Abstract
IN an investigation of the biochemical mechanism of chloramphenicol (CM) resistance in Pseudomonas fluorescence, Kuschner1 reported that oxidation of succinate by intact cells of a CM-resistant strain was not affected by CM, although this reaction by the wild strain was moderately inhibited. On the other hand, the same reaction in cell-free systems of both strains was found to be equally sensitive to CM inhibition. From this result, he proposed that CM resistance in the resistant strain was due to decreased permeability against CM. Ramsey2 investigated the action of CM on the formation of inducible enzymes by ultra-socially disrupted cell preparation of Staphylococcus aureus, and observed that the preparation from the CM-resistant strain still retained the resistance of intact cells so that changes in permeability was not the main source of resistance in this organism.
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References
Kuschner, D. J., Arch. Biochim. Biophys., 58, 347 (1955).
Ramsey, H. H., Nature, 182, 602 (1958).
Yokota, T., and Akiba, T., Medicine and Biol. (Tokyo), 58, 172 (1961).
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OKAMOTO, S., MIZUNO, D. Inhibition by Chloramphenicol of Protein Synthesis in the Cell-free System of a Chloramphenicol-resistant Strain of Escherichia coli. Nature 195, 1022–1023 (1962). https://doi.org/10.1038/1951022a0
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DOI: https://doi.org/10.1038/1951022a0
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