Isoobtusilactone A-induced apoptosis in human hepatoma Hep G2 cells is mediated via increased NADPH oxidase-derived reactive oxygen species (ROS) production and the mitochondria-associated apoptotic mechanisms
Chemoprevention by the use of naturally occurring substances is becoming a promising strategy to prevent cancer. In this study, the effects of isoobtusilactone A, a novel constituent isolated from the leaves of Cinnamomum kotoense, on the proliferation of human hepatoma Hep G2 cells were studied. Un...
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| creator | Chen, Chung-Yi Liu, Tsan-Zon Chen, Ching-Hsein Wu, Chih-Chung Cheng, Jiin-Tsuey Yiin, Shuenn-Jiun Shih, Ming-Kuei Wu, Mei-Jem Chern, Chi-Liang |
| description | Chemoprevention by the use of naturally occurring substances is becoming a promising strategy to prevent cancer. In this study, the effects of isoobtusilactone A, a novel constituent isolated from the leaves of
Cinnamomum kotoense, on the proliferation of human hepatoma Hep G2 cells were studied. Under our experimental conditions, isoobtusilactone A was found to elicit a concentration-dependent growth impediment (IC
50
=
37.5
μM). The demise of these cells induced by isoobtusilactone A was apoptotic in nature, exhibiting a concentration-dependent increase in sub-G
1 fraction and DNA fragmentation. Subcellular fractionation analysis further revealed that Bax translocation to mitochondria resulted in a rapid release of cytochrome
c, followed by activation of caspase 3 and PARP cleavage, and finally cell death. Isoobtusilactone A-treated cells also displayed transient increase of ROS during the earlier stage of the experiment, followed by the disruption of mitochondrial transmembrane potential (Δ
Ψ
m). The presence of a ROS scavenger (
N-acetyl-
l-cysteine) and an inhibitor of NADPH oxidase (diphenyleneiodonium chloride) blocked ROS production and the subsequent apoptotic cell death. In addition, in order to investigate the acute toxicity of isoobtusilactone A, groups of 5–6-week old Sprague–Dawley rats were subjected to oral administration of 350, or 700
mg/kg
bw isoobtusilactone A four times each week for two weeks. There was no significant difference between control animals and treated animals with respect to the body weight gain, the body weight ratio of liver, spleen and kidney, haematological and clinical chemistry parameters. Taken together, our data suggest that ROS generated through the activation of NADPH oxidase plays an essential role in apoptosis induced by isoobtusilactone A, and the dosages of isoobtusilactone A tested in this study did not cause animal toxicity. |
| doi_str_mv | 10.1016/j.fct.2007.01.008 |
| format | Article |
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Cinnamomum kotoense, on the proliferation of human hepatoma Hep G2 cells were studied. Under our experimental conditions, isoobtusilactone A was found to elicit a concentration-dependent growth impediment (IC
50
=
37.5
μM). The demise of these cells induced by isoobtusilactone A was apoptotic in nature, exhibiting a concentration-dependent increase in sub-G
1 fraction and DNA fragmentation. Subcellular fractionation analysis further revealed that Bax translocation to mitochondria resulted in a rapid release of cytochrome
c, followed by activation of caspase 3 and PARP cleavage, and finally cell death. Isoobtusilactone A-treated cells also displayed transient increase of ROS during the earlier stage of the experiment, followed by the disruption of mitochondrial transmembrane potential (Δ
Ψ
m). The presence of a ROS scavenger (
N-acetyl-
l-cysteine) and an inhibitor of NADPH oxidase (diphenyleneiodonium chloride) blocked ROS production and the subsequent apoptotic cell death. In addition, in order to investigate the acute toxicity of isoobtusilactone A, groups of 5–6-week old Sprague–Dawley rats were subjected to oral administration of 350, or 700
mg/kg
bw isoobtusilactone A four times each week for two weeks. There was no significant difference between control animals and treated animals with respect to the body weight gain, the body weight ratio of liver, spleen and kidney, haematological and clinical chemistry parameters. Taken together, our data suggest that ROS generated through the activation of NADPH oxidase plays an essential role in apoptosis induced by isoobtusilactone A, and the dosages of isoobtusilactone A tested in this study did not cause animal toxicity.</description><identifier>ISSN: 0278-6915</identifier><identifier>EISSN: 1873-6351</identifier><identifier>DOI: 10.1016/j.fct.2007.01.008</identifier><identifier>PMID: 17321026</identifier><identifier>CODEN: FCTOD7</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Administration, Oral ; Alkanes - pharmacology ; Alkanes - therapeutic use ; Animals ; Antineoplastic Agents, Phytogenic - pharmacology ; Antineoplastic Agents, Phytogenic - toxicity ; Apoptosis ; Apoptosis - drug effects ; Bax ; Biological and medical sciences ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Caspase 3 ; Cell Cycle - drug effects ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cinnamomum ; Cinnamomum - chemistry ; Dose-Response Relationship, Drug ; Drug Screening Assays, Antitumor ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Isoobtusilactone A ; Lactones - pharmacology ; Lactones - therapeutic use ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Medical sciences ; Membrane Potentials - drug effects ; Mitochondria, Liver - pathology ; Mitochondrial transmembrane potential (Δ Ψm) ; NADPH Oxidases - metabolism ; Plant Extracts - pharmacology ; Plant Extracts - toxicity ; Rats ; Rats, Sprague-Dawley ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Toxicology ; Tumors</subject><ispartof>Food and chemical toxicology, 2007-07, Vol.45 (7), p.1268-1276</ispartof><rights>2007 Elsevier Ltd</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c393t-e305cefbec5c2606da858eb571f00aa93d3e66321fb758d249b57f73413e309f3</citedby><cites>FETCH-LOGICAL-c393t-e305cefbec5c2606da858eb571f00aa93d3e66321fb758d249b57f73413e309f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0278691507000269$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18829566$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17321026$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Chung-Yi</creatorcontrib><creatorcontrib>Liu, Tsan-Zon</creatorcontrib><creatorcontrib>Chen, Ching-Hsein</creatorcontrib><creatorcontrib>Wu, Chih-Chung</creatorcontrib><creatorcontrib>Cheng, Jiin-Tsuey</creatorcontrib><creatorcontrib>Yiin, Shuenn-Jiun</creatorcontrib><creatorcontrib>Shih, Ming-Kuei</creatorcontrib><creatorcontrib>Wu, Mei-Jem</creatorcontrib><creatorcontrib>Chern, Chi-Liang</creatorcontrib><title>Isoobtusilactone A-induced apoptosis in human hepatoma Hep G2 cells is mediated via increased NADPH oxidase-derived reactive oxygen species (ROS) production and the mitochondria-associated apoptotic mechanisms</title><title>Food and chemical toxicology</title><addtitle>Food Chem Toxicol</addtitle><description>Chemoprevention by the use of naturally occurring substances is becoming a promising strategy to prevent cancer. In this study, the effects of isoobtusilactone A, a novel constituent isolated from the leaves of
Cinnamomum kotoense, on the proliferation of human hepatoma Hep G2 cells were studied. Under our experimental conditions, isoobtusilactone A was found to elicit a concentration-dependent growth impediment (IC
50
=
37.5
μM). The demise of these cells induced by isoobtusilactone A was apoptotic in nature, exhibiting a concentration-dependent increase in sub-G
1 fraction and DNA fragmentation. Subcellular fractionation analysis further revealed that Bax translocation to mitochondria resulted in a rapid release of cytochrome
c, followed by activation of caspase 3 and PARP cleavage, and finally cell death. Isoobtusilactone A-treated cells also displayed transient increase of ROS during the earlier stage of the experiment, followed by the disruption of mitochondrial transmembrane potential (Δ
Ψ
m). The presence of a ROS scavenger (
N-acetyl-
l-cysteine) and an inhibitor of NADPH oxidase (diphenyleneiodonium chloride) blocked ROS production and the subsequent apoptotic cell death. In addition, in order to investigate the acute toxicity of isoobtusilactone A, groups of 5–6-week old Sprague–Dawley rats were subjected to oral administration of 350, or 700
mg/kg
bw isoobtusilactone A four times each week for two weeks. There was no significant difference between control animals and treated animals with respect to the body weight gain, the body weight ratio of liver, spleen and kidney, haematological and clinical chemistry parameters. Taken together, our data suggest that ROS generated through the activation of NADPH oxidase plays an essential role in apoptosis induced by isoobtusilactone A, and the dosages of isoobtusilactone A tested in this study did not cause animal toxicity.</description><subject>Administration, Oral</subject><subject>Alkanes - pharmacology</subject><subject>Alkanes - therapeutic use</subject><subject>Animals</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Antineoplastic Agents, Phytogenic - toxicity</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Bax</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Caspase 3</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cinnamomum</subject><subject>Cinnamomum - chemistry</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Screening Assays, Antitumor</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Isoobtusilactone A</subject><subject>Lactones - pharmacology</subject><subject>Lactones - therapeutic use</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Medical sciences</subject><subject>Membrane Potentials - drug effects</subject><subject>Mitochondria, Liver - pathology</subject><subject>Mitochondrial transmembrane potential (Δ Ψm)</subject><subject>NADPH Oxidases - metabolism</subject><subject>Plant Extracts - pharmacology</subject><subject>Plant Extracts - toxicity</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Toxicology</subject><subject>Tumors</subject><issn>0278-6915</issn><issn>1873-6351</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2P0zAQhiMEYsvCD-CCfAHBIcWOGycRp2qB7UorFvFxtlx7Ql01dvA4Ffsz-UdMlUp742J7PM986H2L4qXgS8GFer9f9jYvK86bJRdLzttHxUK0jSyVrMXjYsGrpi1VJ-qL4hninhMoGvW0uBCNrASv1KL4e4MxbvOE_mBsjgHYuvTBTRYcM2Mcc0SPzAe2mwZDJ4wmx8GwDYzsumIWDgdKIxvAeZOp6OgN4TaBQYq-rD9-3bD4xzsKSwfJH-mXkjbTixL3vyAwHMF6QPb22933d2xMkeZnHwMzwbG8Azb4HO0uBpe8KQ1itPOwecPsLc23OxM8Dvi8eNKbA8KL831Z_Pz86cfVpry9u765Wt-WVnYylyB5baHfgq1tpbhypq1b2NaN6Dk3ppNOglIkU79t6tZVq45yfSNXQlJp18vL4s3cl_b9PQFmPXg86WECxAl1xatO1StOoJhBmyJigl6PyQ8m3WvB9clHvdfkoz75qLnQ5CPVvDo3n7Yk7UPF2TgCXp8Bg9Yc-mSC9fjAtW3V1erEfZg5ICmOHpJGkjqQvT4BDXXR_2eNf6G-v30</recordid><startdate>200707</startdate><enddate>200707</enddate><creator>Chen, Chung-Yi</creator><creator>Liu, Tsan-Zon</creator><creator>Chen, Ching-Hsein</creator><creator>Wu, Chih-Chung</creator><creator>Cheng, Jiin-Tsuey</creator><creator>Yiin, Shuenn-Jiun</creator><creator>Shih, Ming-Kuei</creator><creator>Wu, Mei-Jem</creator><creator>Chern, Chi-Liang</creator><general>Elsevier Ltd</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QH</scope><scope>7TV</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>200707</creationdate><title>Isoobtusilactone A-induced apoptosis in human hepatoma Hep G2 cells is mediated via increased NADPH oxidase-derived reactive oxygen species (ROS) production and the mitochondria-associated apoptotic mechanisms</title><author>Chen, Chung-Yi ; Liu, Tsan-Zon ; Chen, Ching-Hsein ; Wu, Chih-Chung ; Cheng, Jiin-Tsuey ; Yiin, Shuenn-Jiun ; Shih, Ming-Kuei ; Wu, Mei-Jem ; Chern, Chi-Liang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c393t-e305cefbec5c2606da858eb571f00aa93d3e66321fb758d249b57f73413e309f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Administration, Oral</topic><topic>Alkanes - pharmacology</topic><topic>Alkanes - therapeutic use</topic><topic>Animals</topic><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Antineoplastic Agents, Phytogenic - toxicity</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Bax</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Caspase 3</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cinnamomum</topic><topic>Cinnamomum - chemistry</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Screening Assays, Antitumor</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Isoobtusilactone A</topic><topic>Lactones - pharmacology</topic><topic>Lactones - therapeutic use</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Medical sciences</topic><topic>Membrane Potentials - drug effects</topic><topic>Mitochondria, Liver - pathology</topic><topic>Mitochondrial transmembrane potential (Δ Ψm)</topic><topic>NADPH Oxidases - metabolism</topic><topic>Plant Extracts - pharmacology</topic><topic>Plant Extracts - toxicity</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Toxicology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Chung-Yi</creatorcontrib><creatorcontrib>Liu, Tsan-Zon</creatorcontrib><creatorcontrib>Chen, Ching-Hsein</creatorcontrib><creatorcontrib>Wu, Chih-Chung</creatorcontrib><creatorcontrib>Cheng, Jiin-Tsuey</creatorcontrib><creatorcontrib>Yiin, Shuenn-Jiun</creatorcontrib><creatorcontrib>Shih, Ming-Kuei</creatorcontrib><creatorcontrib>Wu, Mei-Jem</creatorcontrib><creatorcontrib>Chern, Chi-Liang</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Aqualine</collection><collection>Pollution Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Food and chemical toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Chung-Yi</au><au>Liu, Tsan-Zon</au><au>Chen, Ching-Hsein</au><au>Wu, Chih-Chung</au><au>Cheng, Jiin-Tsuey</au><au>Yiin, Shuenn-Jiun</au><au>Shih, Ming-Kuei</au><au>Wu, Mei-Jem</au><au>Chern, Chi-Liang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Isoobtusilactone A-induced apoptosis in human hepatoma Hep G2 cells is mediated via increased NADPH oxidase-derived reactive oxygen species (ROS) production and the mitochondria-associated apoptotic mechanisms</atitle><jtitle>Food and chemical toxicology</jtitle><addtitle>Food Chem Toxicol</addtitle><date>2007-07</date><risdate>2007</risdate><volume>45</volume><issue>7</issue><spage>1268</spage><epage>1276</epage><pages>1268-1276</pages><issn>0278-6915</issn><eissn>1873-6351</eissn><coden>FCTOD7</coden><abstract>Chemoprevention by the use of naturally occurring substances is becoming a promising strategy to prevent cancer. In this study, the effects of isoobtusilactone A, a novel constituent isolated from the leaves of
Cinnamomum kotoense, on the proliferation of human hepatoma Hep G2 cells were studied. Under our experimental conditions, isoobtusilactone A was found to elicit a concentration-dependent growth impediment (IC
50
=
37.5
μM). The demise of these cells induced by isoobtusilactone A was apoptotic in nature, exhibiting a concentration-dependent increase in sub-G
1 fraction and DNA fragmentation. Subcellular fractionation analysis further revealed that Bax translocation to mitochondria resulted in a rapid release of cytochrome
c, followed by activation of caspase 3 and PARP cleavage, and finally cell death. Isoobtusilactone A-treated cells also displayed transient increase of ROS during the earlier stage of the experiment, followed by the disruption of mitochondrial transmembrane potential (Δ
Ψ
m). The presence of a ROS scavenger (
N-acetyl-
l-cysteine) and an inhibitor of NADPH oxidase (diphenyleneiodonium chloride) blocked ROS production and the subsequent apoptotic cell death. In addition, in order to investigate the acute toxicity of isoobtusilactone A, groups of 5–6-week old Sprague–Dawley rats were subjected to oral administration of 350, or 700
mg/kg
bw isoobtusilactone A four times each week for two weeks. There was no significant difference between control animals and treated animals with respect to the body weight gain, the body weight ratio of liver, spleen and kidney, haematological and clinical chemistry parameters. Taken together, our data suggest that ROS generated through the activation of NADPH oxidase plays an essential role in apoptosis induced by isoobtusilactone A, and the dosages of isoobtusilactone A tested in this study did not cause animal toxicity.</abstract><cop>Oxford</cop><cop>New York, NY</cop><pub>Elsevier Ltd</pub><pmid>17321026</pmid><doi>10.1016/j.fct.2007.01.008</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0278-6915 |
| ispartof | Food and chemical toxicology, 2007-07, Vol.45 (7), p.1268-1276 |
| issn | 0278-6915 1873-6351 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Administration, Oral Alkanes - pharmacology Alkanes - therapeutic use Animals Antineoplastic Agents, Phytogenic - pharmacology Antineoplastic Agents, Phytogenic - toxicity Apoptosis Apoptosis - drug effects Bax Biological and medical sciences Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Caspase 3 Cell Cycle - drug effects Cell Line, Tumor Cell Proliferation - drug effects Cinnamomum Cinnamomum - chemistry Dose-Response Relationship, Drug Drug Screening Assays, Antitumor Gastroenterology. Liver. Pancreas. Abdomen Humans Isoobtusilactone A Lactones - pharmacology Lactones - therapeutic use Liver Neoplasms - metabolism Liver Neoplasms - pathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Medical sciences Membrane Potentials - drug effects Mitochondria, Liver - pathology Mitochondrial transmembrane potential (Δ Ψm) NADPH Oxidases - metabolism Plant Extracts - pharmacology Plant Extracts - toxicity Rats Rats, Sprague-Dawley Reactive oxygen species Reactive Oxygen Species - metabolism Toxicology Tumors |
| title | Isoobtusilactone A-induced apoptosis in human hepatoma Hep G2 cells is mediated via increased NADPH oxidase-derived reactive oxygen species (ROS) production and the mitochondria-associated apoptotic mechanisms |
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