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2019 Fiscal Year Final Research Report

Relationship between anthracycline anticancer drug and reactive oxygen species; reconstruction of information for its elucidation

Research Project

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Project/Area Number 16K08420
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Medical pharmacy
Research InstitutionKinjo Gakuin University

Principal Investigator

Mizutani Hideki  金城学院大学, 薬学部, 教授 (80397504)

Project Period (FY) 2016-04-01 – 2020-03-31
Keywordsアントラサイクリン / 抗がん剤 / 活性酸素
Outline of Final Research Achievements

We reconstructed the relational information between anthracycline anticancer drug (AC) and reactive oxygen species (ROS). Experiments were evaluated for DNA damage and cell death in doxorubicin (DOX), epirubicin (EPI), daunorubicin (DNR), idarubicin (IDR), aclarubicin (ACL). AC damaged DNA in the presence of Cu (II), and its intensity was (DOX, EPI) > (THP, IDR) > ACR >> DNR, and no damage was observed in DNR. On the other hand, as a result of detailed examination of cell death of THP, ACR and IDR, it was suggested that ROS was involved in cell death of THP and ACR, but ROS was not involved in IDR. In addition, Cu (I) was involved in ACR cell death, and the importance of Cu was clarified.

Free Research Field

がん治療薬学、酸化ストレス学、医療薬学、医療薬剤学

Academic Significance and Societal Importance of the Research Achievements

アントラサイクリン系抗がん剤の作用機序として活性酸素種の関与が知られているが、その詳細については明らかでない。我々はこれまでドキソルビシンのCu(II) 存在下での新しい酸化的DNA損傷機構を明らかにしたが、今回、ピラルビシン、アクラルビシン、イダルビシンでも同様にCu(II)存在下でDNA損傷することを明らかにし、アクラルビシンによる細胞死でCu(I)の関与を明らかにした。これらの成果はアントラサイクリンの新しい作用機序の解明につながり、創薬の場、臨床の場へフィードバックすることにより、新規抗がん剤の開発、がんの薬物治療の進展につながり、社会への還元が期待される。

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Published: 2021-02-19  

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