| Project/Area Number |
16K15034
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Veterinary medical science
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
池中 良徳 北海道大学, 獣医学研究院, 准教授 (40543509)
中山 翔太 北海道大学, 獣医学研究院, 助教 (90647629)
水川 葉月 北海道大学, 獣医学研究院, 助教 (60612661)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 殺鼠剤 / 抵抗性 / ラット / 殺鼠剤抵抗性 / 薬剤耐性 / ワルファリン / クマネズミ / 薬物代謝 / シトクロムP440 / 野生齧歯類 / クローズドコロニー |
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| Outline of Final Research Achievements |
Anti-blood coagulation rodenticides, such as warfarin, have been used all over the world. They inhibit vitamin K epoxide reductase (VKOR), which is necessary for producing several blood clotting factors. This inhibition by rodenticides results in lethal hemorrhage in rodents. However, heavy usage of these agents has led to the appearance of rodenticide-resistant rats. The mutation of the target enzyme of warfarin, VKOR, is considered as major cause for rodenticide resistance in wild rats. However, there have been few studies regarding the hepatic metabolism of warfarin. We investigated warfarin metabolism in resistant rats, and our results showed new mechanism for the rodenticide resistance in wild black rats in Japan.
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