Date of this Version
Crop Protection 78 (2015) 35-39
Rodents have been noteworthy pests in agricultural areas for decades. Because rodents impact diverse ecosystems, anticoagulant rodenticides have been heavily used throughout the world to control rodent populations. This continued use has led to the development of resistance to anticoagulant rodenticides in some populations of targeted rodents. Although many studies have investigated the genetic and molecular basis of anticoagulant resistance, few have focused on potential changes in metabolic function of resistant animals. In this study, vole (Microtus californicus, Peale) liver microsome preparations were made from unexposed animals living in areas that had never used anticoagulant rodenticides for either crop protection or for the control of commensal rodents and exposed voles living in artichoke fields that have used anticoagulant rodenticides since the mid-1990s. Using these microsome preparations, the metabolism of diphacinone and chlorophacinone was tested. Microsomes from both male and female voles from exposed areas metabolized significantly more anticoagulant than unexposed animals. Also, both exposed and unexposed animals metabolized more diphacinone than chlorophacinone. These findings suggest that alterations in metabolic function may play a role in anticoagulant resistance.