Pesticide resistance in wild mammals : Mechanisms of anticoagulant resistance in wild rodents

Access this Article

Author(s)

Abstract

Warfarin is commonly used worldwide as a rodenticide. It inhibits coagulation of blood by inhibiting vitamin K 2,3-epoxide reductase (VKOR) activity. An inadequate supply of vitamin K blocks the production of prothrombin and causes hemorrhage. It has been reported that repeated or long-term treatments with this drug cause resistance in wild rodents. However, the mechanism of warfarin resistance in rodents is still not known precisely. Recent studies reported and identified the function of the molecule, vitamin K epoxide reductase complex subunit 1 (VKORC1), which is the main unit of VKOR. An amino acid substitution in VKORC1 is one of the supposed mechanisms of warfarin resistance. An accelerated detoxification system involving cytochrome P450 (CYP) could also cause the rodenticide resistance. Administration of SKF-525A, a potent inhibitor for P450, increased the mortality due to reduction of warfarin metabolism in warfarin-resistant rats. Meanwhile, the appearance of warfarin-resistant rodents has led to the development of the more effective and toxic rodenticide superwarfarin, which is widely used in Europe and the USA. However, animals resistant to this second-generation rodenticide have already been reported in Europe. In this review, we focus on the mechanism and the pleiotropic effects of pesticide resistance in wild rodents.

Journal

  • The Journal of Toxicological Sciences

    The Journal of Toxicological Sciences 33(3), 283-291, 2008-08-23

    The Japanese Society of Toxicology

References:  56

Cited by:  1

Codes

  • NII Article ID (NAID)
    110006862204
  • NII NACSIS-CAT ID (NCID)
    AN00002808
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    03881350
  • NDL Article ID
    9609101
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z19-1022
  • Data Source
    CJP  CJPref  NDL  NII-ELS  J-STAGE 
Page Top