Different Rifampicin Inactivation Mechanisms in Nocardia and Related Taxa

J-STAGE 被引用文献3件 参考文献11件
  • TANAKA Yasushi
    Research Center for Pathogenic Fungi and Microbial Toxicoses, Chiba University
  • YAZAWA Katsukiyo
    Research Center for Pathogenic Fungi and Microbial Toxicoses, Chiba University
  • DABBS Eric R
    Research Center for Pathogenic Fungi and Microbial Toxicoses, Chiba University
  • NISHIKAWA Kazutaka
    Research Center for Pathogenic Fungi and Microbial Toxicoses, Chiba University
  • KOMAKI Hisayuki
    Research Center for Pathogenic Fungi and Microbial Toxicoses, Chiba University
  • MIKAMI Yuzuru
    Research Center for Pathogenic Fungi and Microbial Toxicoses, Chiba University
  • MIYAJI Makoto
    Research Center for Pathogenic Fungi and Microbial Toxicoses, Chiba University
  • MORISAKI Naoko
    Institute of Molecular and Cellular Bioscience, The University of Tokyo
  • IWASAKI Shigeo
    Institute of Molecular and Cellular Bioscience, The University of Tokyo

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Mycolic acid-containing bacteria inactivate rifampicin in a variety of ways such as glucosylation, ribosylation, phosphorylation and decolorization. These inactivations were found to be a species-specific phenomena in Nocardia and related taxa. Gordona, Tsukamurella and fast-growing Mycobacterium modified rifampicin by ribosylation of the 23-OH group of the antibiotic. Such ribosylation was not observed in Rhodococcus and Corynebacterium, but phosphorylation of the 21-OH group of rifampicin was observed in one strain of Rhodococcus. Nocardia modified the antibiotic by glucosylation (23-OH group) and phosphorylation, but ribosylation was not observed.

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