Effects of cellular redox balance on induction of apoptosis by eicosapentaenoic acid in HT29 colorectal adenocarcinoma cells and rat colon in vivo
BACKGROUND AND AIMS Epidemiological evidence suggests n-3 polyunsaturated lipids may protect against colorectal neoplasia. Consumption of fish oil modulates crypt cytokinetics in humans, and crypt apoptosis in animal models. To explore these effects, we investigated involvement of caspase enzymes an...
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| Veröffentlicht in: | Gut 2001-07, Vol.49 (1), p.97-105 |
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| description | BACKGROUND AND AIMS Epidemiological evidence suggests n-3 polyunsaturated lipids may protect against colorectal neoplasia. Consumption of fish oil modulates crypt cytokinetics in humans, and crypt apoptosis in animal models. To explore these effects, we investigated involvement of caspase enzymes and cellular redox balance in the induction of apoptosis by eicosapentaenoic acid (EPA) in HT29 cells, and in rat colon in vivo. METHODS Survival of HT29 cells grown with EPA in the presence of caspase inhibitors, antioxidants, or buthionine sulphoximine, an inhibitor of glutathione neosynthesis, was determined. The effects of EPA enriched fish oil and glutathione depletion on apoptosis in rat colon were assessed using microdissected crypts. RESULTS Treatment of HT29 cells with EPA reduced viable cell number and activated caspase 3, prior to cell detachment. Antioxidants and caspase inhibitors blocked HT29 cell death whereas glutathione depletion increased it. Rats fed fish oil had higher crypt cell apoptosis than those fed corn oil, and glutathione depletion enhanced this effect. CONCLUSIONS Incorporation of EPA into colonic epithelial cell lipids increases apoptosis. The results of this study, using both an animal and cell line model, support the hypothesis that this effect is mediated via cellular redox tone, and is sensitive to glutathione metabolism. The data suggest a mechanism whereby polyunsaturated fatty acids may influence the susceptibility of colorectal crypt cells to induction or progression of neoplasia. |
| doi_str_mv | 10.1136/gut.49.1.97 |
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| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1728373</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A76905915</galeid><sourcerecordid>A76905915</sourcerecordid><originalsourceid>FETCH-LOGICAL-b605t-7af0c8399a935c8bad5ce5ed601f61f617d5eeb9295ad013f57527fc47fc49813</originalsourceid><addsrcrecordid>eNp9kl1v0zAUhiMEYmNwxT2yGOIGUuwmjuMbpKkaDFGBJo1xaZ34o7gkdrGTavsb_GKctVoLqlAc2fJ59J4Pv1n2nOAJIUX1bjH0k5JPyISzB9kxKas6L6Z1_TA7xpiwnLKSH2VPYlxijOuak8fZESElKQhhx9nvc2O07CPyBkndtkMLAQWt_A1qoAUnNfIOWacG2dt0Shis_Kr30UbU3CJtpY-w0q4H7byVCKRViUcXV1OOpG99SPLQIlApLiFI63wHd7kiAqdQgP6OG7OgtV37p9kjA23Uz7b7Sfbtw_nV7CKff_34aXY2z5sK0z5nYLCsC86BF1TWDSgqNdWqwsRU42KKat3wKaegMCkMZXTKjCzHn9ekOMneb3RXQ9NpJVMPAVqxCraDcCs8WPF3xNkfYuHXgrBpXbAiCbzeCgT_a9CxF52NY2PgtB-iYDglJ1WdwNN_wKUfgkvNJS3GeUVKWibq5YZaQKuFdcanrHKUFGes4phyQhP09gC00E6nCr3TxqbrfTw_gKdP6S693AH-zYaXwccYtLkfB8FidJtIbhMlF0RwlugX-xPcsVt7JeDVFoAooTUhGcrGPc2KM8p3VdrY65v7MISfomIFo-LL9Ux8v_48v-SXhah3g2-65X8L_APHNPoT</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1779961454</pqid></control><display><type>article</type><title>Effects of cellular redox balance on induction of apoptosis by eicosapentaenoic acid in HT29 colorectal adenocarcinoma cells and rat colon in vivo</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Latham, P ; Lund, E K ; Brown, J C ; Johnson, I T</creator><creatorcontrib>Latham, P ; Lund, E K ; Brown, J C ; Johnson, I T</creatorcontrib><description>BACKGROUND AND AIMS Epidemiological evidence suggests n-3 polyunsaturated lipids may protect against colorectal neoplasia. Consumption of fish oil modulates crypt cytokinetics in humans, and crypt apoptosis in animal models. To explore these effects, we investigated involvement of caspase enzymes and cellular redox balance in the induction of apoptosis by eicosapentaenoic acid (EPA) in HT29 cells, and in rat colon in vivo. METHODS Survival of HT29 cells grown with EPA in the presence of caspase inhibitors, antioxidants, or buthionine sulphoximine, an inhibitor of glutathione neosynthesis, was determined. The effects of EPA enriched fish oil and glutathione depletion on apoptosis in rat colon were assessed using microdissected crypts. RESULTS Treatment of HT29 cells with EPA reduced viable cell number and activated caspase 3, prior to cell detachment. Antioxidants and caspase inhibitors blocked HT29 cell death whereas glutathione depletion increased it. Rats fed fish oil had higher crypt cell apoptosis than those fed corn oil, and glutathione depletion enhanced this effect. CONCLUSIONS Incorporation of EPA into colonic epithelial cell lipids increases apoptosis. The results of this study, using both an animal and cell line model, support the hypothesis that this effect is mediated via cellular redox tone, and is sensitive to glutathione metabolism. The data suggest a mechanism whereby polyunsaturated fatty acids may influence the susceptibility of colorectal crypt cells to induction or progression of neoplasia.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>EISSN: 1458-3288</identifier><identifier>DOI: 10.1136/gut.49.1.97</identifier><identifier>PMID: 11413117</identifier><identifier>CODEN: GUTTAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>Animals ; Antioxidants - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - physiology ; Biological and medical sciences ; Buthionine Sulfoximine - pharmacology ; caspase ; Caspase Inhibitors ; Cell death ; Cell Survival ; Colorectal cancer ; Corn Oil - administration & dosage ; Corn Oil - chemistry ; eicosapentaenoic acid ; Eicosapentaenoic Acid - pharmacology ; Enzyme Induction - drug effects ; Enzyme Inhibitors - pharmacology ; Fish oils ; Fish Oils - administration & dosage ; Fish Oils - chemistry ; Gastroenterology. Liver. Pancreas. Abdomen ; glutathione ; Health aspects ; HT29 Cells - drug effects ; HT29 Cells - metabolism ; Humans ; Lipids ; Male ; Medical sciences ; Oxidation-Reduction - drug effects ; Physiological aspects ; Prevention ; rat ; Rats ; Rats as laboratory animals ; Rats, Wistar ; redox ; Rodents ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumor Cells, Cultured ; Tumors</subject><ispartof>Gut, 2001-07, Vol.49 (1), p.97-105</ispartof><rights>British Society of Gastroenterology</rights><rights>2001 INIST-CNRS</rights><rights>COPYRIGHT 2001 BMJ Publishing Group Ltd.</rights><rights>Copyright: 2001 British Society of Gastroenterology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b605t-7af0c8399a935c8bad5ce5ed601f61f617d5eeb9295ad013f57527fc47fc49813</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1728373/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1728373/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,725,778,782,883,27907,27908,53774,53776</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1069759$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11413117$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Latham, P</creatorcontrib><creatorcontrib>Lund, E K</creatorcontrib><creatorcontrib>Brown, J C</creatorcontrib><creatorcontrib>Johnson, I T</creatorcontrib><title>Effects of cellular redox balance on induction of apoptosis by eicosapentaenoic acid in HT29 colorectal adenocarcinoma cells and rat colon in vivo</title><title>Gut</title><addtitle>Gut</addtitle><description>BACKGROUND AND AIMS Epidemiological evidence suggests n-3 polyunsaturated lipids may protect against colorectal neoplasia. Consumption of fish oil modulates crypt cytokinetics in humans, and crypt apoptosis in animal models. To explore these effects, we investigated involvement of caspase enzymes and cellular redox balance in the induction of apoptosis by eicosapentaenoic acid (EPA) in HT29 cells, and in rat colon in vivo. METHODS Survival of HT29 cells grown with EPA in the presence of caspase inhibitors, antioxidants, or buthionine sulphoximine, an inhibitor of glutathione neosynthesis, was determined. The effects of EPA enriched fish oil and glutathione depletion on apoptosis in rat colon were assessed using microdissected crypts. RESULTS Treatment of HT29 cells with EPA reduced viable cell number and activated caspase 3, prior to cell detachment. Antioxidants and caspase inhibitors blocked HT29 cell death whereas glutathione depletion increased it. Rats fed fish oil had higher crypt cell apoptosis than those fed corn oil, and glutathione depletion enhanced this effect. CONCLUSIONS Incorporation of EPA into colonic epithelial cell lipids increases apoptosis. The results of this study, using both an animal and cell line model, support the hypothesis that this effect is mediated via cellular redox tone, and is sensitive to glutathione metabolism. The data suggest a mechanism whereby polyunsaturated fatty acids may influence the susceptibility of colorectal crypt cells to induction or progression of neoplasia.</description><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Buthionine Sulfoximine - pharmacology</subject><subject>caspase</subject><subject>Caspase Inhibitors</subject><subject>Cell death</subject><subject>Cell Survival</subject><subject>Colorectal cancer</subject><subject>Corn Oil - administration & dosage</subject><subject>Corn Oil - chemistry</subject><subject>eicosapentaenoic acid</subject><subject>Eicosapentaenoic Acid - pharmacology</subject><subject>Enzyme Induction - drug effects</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fish oils</subject><subject>Fish Oils - administration & dosage</subject><subject>Fish Oils - chemistry</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>glutathione</subject><subject>Health aspects</subject><subject>HT29 Cells - drug effects</subject><subject>HT29 Cells - metabolism</subject><subject>Humans</subject><subject>Lipids</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Oxidation-Reduction - drug effects</subject><subject>Physiological aspects</subject><subject>Prevention</subject><subject>rat</subject><subject>Rats</subject><subject>Rats as laboratory animals</subject><subject>Rats, Wistar</subject><subject>redox</subject><subject>Rodents</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0017-5749</issn><issn>1468-3288</issn><issn>1458-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kl1v0zAUhiMEYmNwxT2yGOIGUuwmjuMbpKkaDFGBJo1xaZ34o7gkdrGTavsb_GKctVoLqlAc2fJ59J4Pv1n2nOAJIUX1bjH0k5JPyISzB9kxKas6L6Z1_TA7xpiwnLKSH2VPYlxijOuak8fZESElKQhhx9nvc2O07CPyBkndtkMLAQWt_A1qoAUnNfIOWacG2dt0Shis_Kr30UbU3CJtpY-w0q4H7byVCKRViUcXV1OOpG99SPLQIlApLiFI63wHd7kiAqdQgP6OG7OgtV37p9kjA23Uz7b7Sfbtw_nV7CKff_34aXY2z5sK0z5nYLCsC86BF1TWDSgqNdWqwsRU42KKat3wKaegMCkMZXTKjCzHn9ekOMneb3RXQ9NpJVMPAVqxCraDcCs8WPF3xNkfYuHXgrBpXbAiCbzeCgT_a9CxF52NY2PgtB-iYDglJ1WdwNN_wKUfgkvNJS3GeUVKWibq5YZaQKuFdcanrHKUFGes4phyQhP09gC00E6nCr3TxqbrfTw_gKdP6S693AH-zYaXwccYtLkfB8FidJtIbhMlF0RwlugX-xPcsVt7JeDVFoAooTUhGcrGPc2KM8p3VdrY65v7MISfomIFo-LL9Ux8v_48v-SXhah3g2-65X8L_APHNPoT</recordid><startdate>20010701</startdate><enddate>20010701</enddate><creator>Latham, P</creator><creator>Lund, E K</creator><creator>Brown, J C</creator><creator>Johnson, I T</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ</general><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</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>BTHHO</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>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20010701</creationdate><title>Effects of cellular redox balance on induction of apoptosis by eicosapentaenoic acid in HT29 colorectal adenocarcinoma cells and rat colon in vivo</title><author>Latham, P ; Lund, E K ; Brown, J C ; Johnson, I T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b605t-7af0c8399a935c8bad5ce5ed601f61f617d5eeb9295ad013f57527fc47fc49813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Buthionine Sulfoximine - pharmacology</topic><topic>caspase</topic><topic>Caspase Inhibitors</topic><topic>Cell death</topic><topic>Cell Survival</topic><topic>Colorectal cancer</topic><topic>Corn Oil - administration & dosage</topic><topic>Corn Oil - chemistry</topic><topic>eicosapentaenoic acid</topic><topic>Eicosapentaenoic Acid - pharmacology</topic><topic>Enzyme Induction - drug effects</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fish oils</topic><topic>Fish Oils - administration & dosage</topic><topic>Fish Oils - chemistry</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>glutathione</topic><topic>Health aspects</topic><topic>HT29 Cells - drug effects</topic><topic>HT29 Cells - metabolism</topic><topic>Humans</topic><topic>Lipids</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Oxidation-Reduction - drug effects</topic><topic>Physiological aspects</topic><topic>Prevention</topic><topic>rat</topic><topic>Rats</topic><topic>Rats as laboratory animals</topic><topic>Rats, Wistar</topic><topic>redox</topic><topic>Rodents</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. 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Consumption of fish oil modulates crypt cytokinetics in humans, and crypt apoptosis in animal models. To explore these effects, we investigated involvement of caspase enzymes and cellular redox balance in the induction of apoptosis by eicosapentaenoic acid (EPA) in HT29 cells, and in rat colon in vivo. METHODS Survival of HT29 cells grown with EPA in the presence of caspase inhibitors, antioxidants, or buthionine sulphoximine, an inhibitor of glutathione neosynthesis, was determined. The effects of EPA enriched fish oil and glutathione depletion on apoptosis in rat colon were assessed using microdissected crypts. RESULTS Treatment of HT29 cells with EPA reduced viable cell number and activated caspase 3, prior to cell detachment. Antioxidants and caspase inhibitors blocked HT29 cell death whereas glutathione depletion increased it. Rats fed fish oil had higher crypt cell apoptosis than those fed corn oil, and glutathione depletion enhanced this effect. CONCLUSIONS Incorporation of EPA into colonic epithelial cell lipids increases apoptosis. The results of this study, using both an animal and cell line model, support the hypothesis that this effect is mediated via cellular redox tone, and is sensitive to glutathione metabolism. The data suggest a mechanism whereby polyunsaturated fatty acids may influence the susceptibility of colorectal crypt cells to induction or progression of neoplasia.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>11413117</pmid><doi>10.1136/gut.49.1.97</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antioxidants - pharmacology Apoptosis Apoptosis - drug effects Apoptosis - physiology Biological and medical sciences Buthionine Sulfoximine - pharmacology caspase Caspase Inhibitors Cell death Cell Survival Colorectal cancer Corn Oil - administration & dosage Corn Oil - chemistry eicosapentaenoic acid Eicosapentaenoic Acid - pharmacology Enzyme Induction - drug effects Enzyme Inhibitors - pharmacology Fish oils Fish Oils - administration & dosage Fish Oils - chemistry Gastroenterology. Liver. Pancreas. Abdomen glutathione Health aspects HT29 Cells - drug effects HT29 Cells - metabolism Humans Lipids Male Medical sciences Oxidation-Reduction - drug effects Physiological aspects Prevention rat Rats Rats as laboratory animals Rats, Wistar redox Rodents Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumor Cells, Cultured Tumors |
| title | Effects of cellular redox balance on induction of apoptosis by eicosapentaenoic acid in HT29 colorectal adenocarcinoma cells and rat colon in vivo |
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