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Rifampin: Mechanisms of Action and Resistance
Reviews of Infectious Diseases
Vol. 5, Supplement 3. The Use of Rifampin in the Treatment of Nontuberculous Infections (Jul. - Aug., 1983), pp. S407-S411
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/4453139
Page Count: 5
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Rifampin specifically inhibits bacterial RNA polymerase, the enzyme responsible for DNA transcription, by forming a stable drug-enzyme complex with a binding constant of 10⁻⁹ M at 37 C. The corresponding mammalian enzymes are not affected by rifampin. Bacterial resistance to rifampin is caused by mutations leading to a change in the structure of the β subunit of RNA polymerase. Such resistance is not an all-or-nothing phenomenon; rather, a large number of RNA polymerases with various degrees of sensitivity to rifampin have been found. No strict correlation exists between enzyme sensitivity and MIC values, since inhibition of RNA synthesis does not always show up to the same extent in the two different test systems used for the determination of these values.
Reviews of Infectious Diseases © 1983 Oxford University Press