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Part of the book series: Springer Series in Applied Biology ((SSAPPL.BIOLOGY))

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Abstract

It has been well documented that the common target of quinolone antibacterials is the bacteria-specific type II DNA topoisomerase, i.e. DNA gyrase (for reviews, see Cozzarelli 1980; Geliert 1981; Wang 1985; Drlica and Franco 1988). These drugs share a common mode of action with anti-cancer drugs by forming a ternary complex with the enzyme and the DNA substrate (Geliert et al. 1977; Sugino et al. 1977; Chen and Liu 1986; Glisson and Ross 1987). The biological consequence of the formation of such a “cleavable complex” is at least two-fold:

  1. i)

    the enzyme is inactivated, leading to the arrest of DNA synthesis in bacterial cells

  2. ii)

    the cleavable complex formation causes unrepairable DNA damage which is believed to trigger recA-dependent SOS repair response and alternatively leading to cell death, presumably by the expression of certain lethal proteins in the cell (Drlica 1984).

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© 1990 Springer-Verlag London Limited

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Shen, L.L. et al. (1990). Aspects of Quinolone-DNA Interactions. In: Crumplin, G.C. (eds) The 4-Quinolones: Anti Bacterial Agents in Vitro. Springer Series in Applied Biology. Springer, London. https://doi.org/10.1007/978-1-4471-3449-7_10

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  • DOI: https://doi.org/10.1007/978-1-4471-3449-7_10

  • Publisher Name: Springer, London

  • Print ISBN: 978-1-4471-3451-0

  • Online ISBN: 978-1-4471-3449-7

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