Display Settings:

Format

Send to:

Choose Destination
    Drug Resist Updat. 2001 Oct;4(5):322-9.

    Are cytochrome b gene mutations the only cause of atovaquone resistance in Pneumocystis?

    Source

    Department of Biological Sciences, University of Cincinnati, Cincinnati, OH 45221, USA. Edna.Kaneshiro@uc.edu

    Abstract

    There is evidence that exposure of the opportunistic pathogen Pneumocystis to atovaquone enhances the development of resistance to the drug. Atovaquone is a structural analog of ubiquinone, which binds to the mitochondrial cytochrome bc(1) complex and inhibits electron transport. Like the parasites Plasmodium and Toxoplasma, atovaquone resistance can result from mutations in the cytochrome b gene of Pneumocystis. However, atovaquone resistance cannot be explained by cytochrome b gene mutations in all cases. The discovery that atovaquone also inhibits biosynthesis of ubiquinone in P. carinii may unfold other mechanisms by which drug resistance develops.

    Copyright 2002, Elsevier Science Ltd. All rights reserved.

    PMID:
    11991686
    [PubMed - indexed for MEDLINE]

      Supplemental Content

      Icon for Elsevier Science

      Save items

      loading

      Recent activity

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      Write to the Help Desk