Metformin ameliorates arsenic trioxide hepatotoxicity via inhibiting mitochondrial complex I
Arsenic trioxide (ATO) is a well-accepted chemotherapy agent in managing promyelocytic leukemia. ATO often causes severe health hazards such as hepatotoxicity, dermatosis, neurotoxicity, nephrotoxicity and cardiotoxicity. The production of reactive oxygen species, (ROS) play a significant role in AT...
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creator | Ling, Sunbin Shan, Qiaonan Liu, Peng Feng, Tingting Zhang, Xuanyu Xiang, Penghui Chen, Kangchen Xie, Haiyang Song, Penghong Zhou, Lin Liu, Jimin Zheng, Shusen Xu, Xiao |
description | Arsenic trioxide (ATO) is a well-accepted chemotherapy agent in managing promyelocytic leukemia. ATO often causes severe health hazards such as hepatotoxicity, dermatosis, neurotoxicity, nephrotoxicity and cardiotoxicity. The production of reactive oxygen species, (ROS) play a significant role in ATO-induced hepatotoxicity. The oral hypoglycemic drug, metformin, is considered to be a potential novel agent for chemoprevention in the treatment of cancer. Moreover, metformin has also been shown to have hepatoprotective effects. In the present study, we demonstrated that metformin protected normal hepatocytes from ATO-induced apoptotic cell death
in vitro
and
in vivo
. Gene expression screening revealed that glucose metabolism might be related to the metformin-induced protective effect on ATO-treated AML12 cells. The metformin-promoted or induced glycolysis was not responsible for the protection of AML12 cells from ATO-induced apoptotic cell death. Instead, metformin increased the intracellular NADH/NAD+ ratio by inhibiting mitochondrial respiratory chain complex I, further decreasing the intracellular ROS induced by ATO. Treatment with low glucose or rotenone, a mitochondrial respiratory chain complex I inhibitor, also protected AML12 cells from ATO-induced apoptotic cell death. We show for the first time that metformin protects the hepatocyte from ATO by regulating the mitochondrial function. With its properties of chemoprevention, chemosensitization and the amelioration of liver damage, metformin has great prospects for clinical application other than type 2 diabetes mellitus (T2DM). |
doi_str_mv | 10.1038/cddis.2017.482 |
format | Article |
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in vitro
and
in vivo
. Gene expression screening revealed that glucose metabolism might be related to the metformin-induced protective effect on ATO-treated AML12 cells. The metformin-promoted or induced glycolysis was not responsible for the protection of AML12 cells from ATO-induced apoptotic cell death. Instead, metformin increased the intracellular NADH/NAD+ ratio by inhibiting mitochondrial respiratory chain complex I, further decreasing the intracellular ROS induced by ATO. Treatment with low glucose or rotenone, a mitochondrial respiratory chain complex I inhibitor, also protected AML12 cells from ATO-induced apoptotic cell death. We show for the first time that metformin protects the hepatocyte from ATO by regulating the mitochondrial function. With its properties of chemoprevention, chemosensitization and the amelioration of liver damage, metformin has great prospects for clinical application other than type 2 diabetes mellitus (T2DM).</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/cddis.2017.482</identifier><identifier>PMID: 29095437</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/31 ; 38 ; 38/39 ; 38/47 ; 631/80/82/23 ; 64 ; 64/60 ; 692/4022/1585 ; 692/700/565/1436 ; 692/700/565/2194 ; 96 ; Antibodies ; Antidiabetics ; Apoptosis ; Arsenic ; Arsenic trioxide ; Biochemistry ; Biomedical and Life Sciences ; Cancer ; Cardiotoxicity ; Cell Biology ; Cell Culture ; Cell death ; Chemosensitization ; Chemotherapy ; Diabetes mellitus ; Electron transport ; Electron transport chain ; Gene expression ; Glucose metabolism ; Glycolysis ; Hepatocytes ; Hepatotoxicity ; Immunology ; Intracellular ; Life Sciences ; Liver ; Metformin ; Mitochondria ; Mitochondrial DNA ; NAD ; NADH ; NADH-ubiquinone oxidoreductase ; Neurotoxicity ; Original ; original-article ; Promyeloid leukemia ; Reactive oxygen species ; Toxicity</subject><ispartof>Cell death & disease, 2017-11, Vol.8 (11), p.e3159-e3159</ispartof><rights>The Author(s) 2017</rights><rights>Copyright Nature Publishing Group Nov 2017</rights><rights>Copyright © 2017 The Author(s) 2017 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c524t-722d2f320cdda7dcd69f0d46f4b15a87feebd2104c54fa1e914e9206e53cf8113</citedby><cites>FETCH-LOGICAL-c524t-722d2f320cdda7dcd69f0d46f4b15a87feebd2104c54fa1e914e9206e53cf8113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5775401/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5775401/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29095437$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ling, Sunbin</creatorcontrib><creatorcontrib>Shan, Qiaonan</creatorcontrib><creatorcontrib>Liu, Peng</creatorcontrib><creatorcontrib>Feng, Tingting</creatorcontrib><creatorcontrib>Zhang, Xuanyu</creatorcontrib><creatorcontrib>Xiang, Penghui</creatorcontrib><creatorcontrib>Chen, Kangchen</creatorcontrib><creatorcontrib>Xie, Haiyang</creatorcontrib><creatorcontrib>Song, Penghong</creatorcontrib><creatorcontrib>Zhou, Lin</creatorcontrib><creatorcontrib>Liu, Jimin</creatorcontrib><creatorcontrib>Zheng, Shusen</creatorcontrib><creatorcontrib>Xu, Xiao</creatorcontrib><title>Metformin ameliorates arsenic trioxide hepatotoxicity via inhibiting mitochondrial complex I</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Arsenic trioxide (ATO) is a well-accepted chemotherapy agent in managing promyelocytic leukemia. ATO often causes severe health hazards such as hepatotoxicity, dermatosis, neurotoxicity, nephrotoxicity and cardiotoxicity. The production of reactive oxygen species, (ROS) play a significant role in ATO-induced hepatotoxicity. The oral hypoglycemic drug, metformin, is considered to be a potential novel agent for chemoprevention in the treatment of cancer. Moreover, metformin has also been shown to have hepatoprotective effects. In the present study, we demonstrated that metformin protected normal hepatocytes from ATO-induced apoptotic cell death
in vitro
and
in vivo
. Gene expression screening revealed that glucose metabolism might be related to the metformin-induced protective effect on ATO-treated AML12 cells. The metformin-promoted or induced glycolysis was not responsible for the protection of AML12 cells from ATO-induced apoptotic cell death. Instead, metformin increased the intracellular NADH/NAD+ ratio by inhibiting mitochondrial respiratory chain complex I, further decreasing the intracellular ROS induced by ATO. Treatment with low glucose or rotenone, a mitochondrial respiratory chain complex I inhibitor, also protected AML12 cells from ATO-induced apoptotic cell death. We show for the first time that metformin protects the hepatocyte from ATO by regulating the mitochondrial function. With its properties of chemoprevention, chemosensitization and the amelioration of liver damage, metformin has great prospects for clinical application other than type 2 diabetes mellitus (T2DM).</description><subject>13/1</subject><subject>13/31</subject><subject>38</subject><subject>38/39</subject><subject>38/47</subject><subject>631/80/82/23</subject><subject>64</subject><subject>64/60</subject><subject>692/4022/1585</subject><subject>692/700/565/1436</subject><subject>692/700/565/2194</subject><subject>96</subject><subject>Antibodies</subject><subject>Antidiabetics</subject><subject>Apoptosis</subject><subject>Arsenic</subject><subject>Arsenic trioxide</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer</subject><subject>Cardiotoxicity</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell death</subject><subject>Chemosensitization</subject><subject>Chemotherapy</subject><subject>Diabetes mellitus</subject><subject>Electron transport</subject><subject>Electron transport chain</subject><subject>Gene expression</subject><subject>Glucose metabolism</subject><subject>Glycolysis</subject><subject>Hepatocytes</subject><subject>Hepatotoxicity</subject><subject>Immunology</subject><subject>Intracellular</subject><subject>Life Sciences</subject><subject>Liver</subject><subject>Metformin</subject><subject>Mitochondria</subject><subject>Mitochondrial DNA</subject><subject>NAD</subject><subject>NADH</subject><subject>NADH-ubiquinone oxidoreductase</subject><subject>Neurotoxicity</subject><subject>Original</subject><subject>original-article</subject><subject>Promyeloid leukemia</subject><subject>Reactive oxygen species</subject><subject>Toxicity</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptUcFqGzEQFaWlDqmvORZBz7YlreTdvRRKaJNAQi7tLSBkaWSP2ZVcSQ7233dtJ8GB6jIa5s17M_MIueJsylnVzKxzmKeC8XoqG_GBXAgm-UQ2Tfvx7D8i45zXbHhVxYSafyYj0bJWyaq-IE8PUHxMPQZqeugwJlMgU5MyBLS0JIw7dEBXsDElliGxWPb0GQ3FsMIFFgxL2mOJdhWDS2g6amO_6WBH776QT950GcYv8ZL8-fXz9_Xt5P7x5u76x_3EKiHLpBbCCV8JNuxjamfdvPXMybmXC65MU3uAhROcSaukNxxaLqEVbA6qsr7hvLok30-8m-2iB2chlGQ6vUnYm7TX0aB-Xwm40sv4rFVdK8kOBN9eCFL8u4Vc9DpuUxhm1rxVjap5e5SZnlA2xZwT-DcFzvTBEH00RB8M0YMhQ8PX87ne4K_nHwCzEyAPpbCEdKb7f8p_cI6aZA</recordid><startdate>20171102</startdate><enddate>20171102</enddate><creator>Ling, 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Group</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20171102</creationdate><title>Metformin ameliorates arsenic trioxide hepatotoxicity via inhibiting mitochondrial complex I</title><author>Ling, Sunbin ; Shan, Qiaonan ; Liu, Peng ; Feng, Tingting ; Zhang, Xuanyu ; Xiang, Penghui ; Chen, Kangchen ; Xie, Haiyang ; Song, Penghong ; Zhou, Lin ; Liu, Jimin ; Zheng, Shusen ; Xu, Xiao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c524t-722d2f320cdda7dcd69f0d46f4b15a87feebd2104c54fa1e914e9206e53cf8113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>13/1</topic><topic>13/31</topic><topic>38</topic><topic>38/39</topic><topic>38/47</topic><topic>631/80/82/23</topic><topic>64</topic><topic>64/60</topic><topic>692/4022/1585</topic><topic>692/700/565/1436</topic><topic>692/700/565/2194</topic><topic>96</topic><topic>Antibodies</topic><topic>Antidiabetics</topic><topic>Apoptosis</topic><topic>Arsenic</topic><topic>Arsenic trioxide</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cancer</topic><topic>Cardiotoxicity</topic><topic>Cell Biology</topic><topic>Cell Culture</topic><topic>Cell death</topic><topic>Chemosensitization</topic><topic>Chemotherapy</topic><topic>Diabetes mellitus</topic><topic>Electron transport</topic><topic>Electron transport chain</topic><topic>Gene expression</topic><topic>Glucose metabolism</topic><topic>Glycolysis</topic><topic>Hepatocytes</topic><topic>Hepatotoxicity</topic><topic>Immunology</topic><topic>Intracellular</topic><topic>Life Sciences</topic><topic>Liver</topic><topic>Metformin</topic><topic>Mitochondria</topic><topic>Mitochondrial DNA</topic><topic>NAD</topic><topic>NADH</topic><topic>NADH-ubiquinone oxidoreductase</topic><topic>Neurotoxicity</topic><topic>Original</topic><topic>original-article</topic><topic>Promyeloid leukemia</topic><topic>Reactive oxygen species</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ling, Sunbin</creatorcontrib><creatorcontrib>Shan, Qiaonan</creatorcontrib><creatorcontrib>Liu, Peng</creatorcontrib><creatorcontrib>Feng, 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Edition)</collection><collection>ProQuest Science Journals</collection><collection>ProQuest Biological Science Journals</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ling, Sunbin</au><au>Shan, Qiaonan</au><au>Liu, Peng</au><au>Feng, Tingting</au><au>Zhang, Xuanyu</au><au>Xiang, Penghui</au><au>Chen, Kangchen</au><au>Xie, Haiyang</au><au>Song, Penghong</au><au>Zhou, Lin</au><au>Liu, Jimin</au><au>Zheng, Shusen</au><au>Xu, Xiao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metformin ameliorates arsenic trioxide hepatotoxicity via inhibiting mitochondrial complex I</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2017-11-02</date><risdate>2017</risdate><volume>8</volume><issue>11</issue><spage>e3159</spage><epage>e3159</epage><pages>e3159-e3159</pages><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Arsenic trioxide (ATO) is a well-accepted chemotherapy agent in managing promyelocytic leukemia. ATO often causes severe health hazards such as hepatotoxicity, dermatosis, neurotoxicity, nephrotoxicity and cardiotoxicity. The production of reactive oxygen species, (ROS) play a significant role in ATO-induced hepatotoxicity. The oral hypoglycemic drug, metformin, is considered to be a potential novel agent for chemoprevention in the treatment of cancer. Moreover, metformin has also been shown to have hepatoprotective effects. In the present study, we demonstrated that metformin protected normal hepatocytes from ATO-induced apoptotic cell death
in vitro
and
in vivo
. Gene expression screening revealed that glucose metabolism might be related to the metformin-induced protective effect on ATO-treated AML12 cells. The metformin-promoted or induced glycolysis was not responsible for the protection of AML12 cells from ATO-induced apoptotic cell death. Instead, metformin increased the intracellular NADH/NAD+ ratio by inhibiting mitochondrial respiratory chain complex I, further decreasing the intracellular ROS induced by ATO. Treatment with low glucose or rotenone, a mitochondrial respiratory chain complex I inhibitor, also protected AML12 cells from ATO-induced apoptotic cell death. We show for the first time that metformin protects the hepatocyte from ATO by regulating the mitochondrial function. With its properties of chemoprevention, chemosensitization and the amelioration of liver damage, metformin has great prospects for clinical application other than type 2 diabetes mellitus (T2DM).</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29095437</pmid><doi>10.1038/cddis.2017.482</doi><oa>free_for_read</oa></addata></record> |
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subjects | 13/1 13/31 38 38/39 38/47 631/80/82/23 64 64/60 692/4022/1585 692/700/565/1436 692/700/565/2194 96 Antibodies Antidiabetics Apoptosis Arsenic Arsenic trioxide Biochemistry Biomedical and Life Sciences Cancer Cardiotoxicity Cell Biology Cell Culture Cell death Chemosensitization Chemotherapy Diabetes mellitus Electron transport Electron transport chain Gene expression Glucose metabolism Glycolysis Hepatocytes Hepatotoxicity Immunology Intracellular Life Sciences Liver Metformin Mitochondria Mitochondrial DNA NAD NADH NADH-ubiquinone oxidoreductase Neurotoxicity Original original-article Promyeloid leukemia Reactive oxygen species Toxicity |
title | Metformin ameliorates arsenic trioxide hepatotoxicity via inhibiting mitochondrial complex I |
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