Sequential events of apoptosis induced by zearalenone in cultured hepatocarcinoma cells
Zearalenone (ZEA) is a fungal metabolite that can contaminate feed and foodstuffs and can cause serious health problems for animals as well as for humans. The present investigation was conducted to determine the chronological succession of the main events that characterise ZEA-induced toxicity in hu...
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| Veröffentlicht in: | Mycotoxin research 2010-08, Vol.26 (3), p.187-197 |
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| creator | Gazzah, Amel Chatti El Golli Bennour, Emna Bouaziz, Chayma Abid, Salwa Ladjimi, Moncef Bacha, Hassen |
| description | Zearalenone (ZEA) is a fungal metabolite that can contaminate feed and foodstuffs and can cause serious health problems for animals as well as for humans. The present investigation was conducted to determine the chronological succession of the main events that characterise ZEA-induced toxicity in human hepatocarcinoma cells. To this aim, we have monitored the effects of ZEA on (1) cell viability, (2) heat-shock protein expression, (3) oxidative damage, (4) DNA fragmentation, (5) the cell cycle and (6) the cell-death-signalling pathway. Our results demonstrated that ZEA reduced cell viability in a time- and dose-dependent manner. When we exposed HepG2 cells to 100 µ
M
ZEA (80% of cells are viable) for different treatment times (2, 4, 8, 24, 30, 48 and 60 h), we demonstrated an induction of Hsp70 protein, an increase in reactive oxygen species (ROS) generation, DNA fragmentation and cell-cycle arrest. These events begin after only 2 h of mycotoxin exposure and are earlier than those implicated in the execution of apoptosis. However, significant apoptotic cell death was observed after at least 30 h of ZEA exposure as a consequence of increased Bax expression, decreased Bcl-2 expression and mitochondrial membrane potential (Δψm)-released cytochrome c and activated caspase-3 and caspase-9. |
| doi_str_mv | 10.1007/s12550-010-0053-8 |
| format | Article |
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M
ZEA (80% of cells are viable) for different treatment times (2, 4, 8, 24, 30, 48 and 60 h), we demonstrated an induction of Hsp70 protein, an increase in reactive oxygen species (ROS) generation, DNA fragmentation and cell-cycle arrest. These events begin after only 2 h of mycotoxin exposure and are earlier than those implicated in the execution of apoptosis. However, significant apoptotic cell death was observed after at least 30 h of ZEA exposure as a consequence of increased Bax expression, decreased Bcl-2 expression and mitochondrial membrane potential (Δψm)-released cytochrome c and activated caspase-3 and caspase-9.</description><identifier>ISSN: 0178-7888</identifier><identifier>EISSN: 1867-1632</identifier><identifier>DOI: 10.1007/s12550-010-0053-8</identifier><identifier>PMID: 23605383</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Apoptosis ; Biomedical and Life Sciences ; Cancer ; Chemistry/Food Science ; Deoxyribonucleic acid ; DNA ; Food contamination & poisoning ; Fungi ; Health problems ; Life Sciences ; Medical Microbiology ; Medicine/Public Health ; Metabolites ; Microbiology ; Mycotoxins ; Original Paper ; Toxicology</subject><ispartof>Mycotoxin research, 2010-08, Vol.26 (3), p.187-197</ispartof><rights>Society for Mycotoxin Research and Springer 2010</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3188-c15e9bd658e7cdc6781a75fa7a36d2a59c4aab80b6fdd313b4fa94c38bd81583</citedby><cites>FETCH-LOGICAL-c3188-c15e9bd658e7cdc6781a75fa7a36d2a59c4aab80b6fdd313b4fa94c38bd81583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12550-010-0053-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12550-010-0053-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23605383$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gazzah, Amel Chatti</creatorcontrib><creatorcontrib>El Golli Bennour, Emna</creatorcontrib><creatorcontrib>Bouaziz, Chayma</creatorcontrib><creatorcontrib>Abid, Salwa</creatorcontrib><creatorcontrib>Ladjimi, Moncef</creatorcontrib><creatorcontrib>Bacha, Hassen</creatorcontrib><title>Sequential events of apoptosis induced by zearalenone in cultured hepatocarcinoma cells</title><title>Mycotoxin research</title><addtitle>Mycotox Res</addtitle><addtitle>Mycotoxin Res</addtitle><description>Zearalenone (ZEA) is a fungal metabolite that can contaminate feed and foodstuffs and can cause serious health problems for animals as well as for humans. The present investigation was conducted to determine the chronological succession of the main events that characterise ZEA-induced toxicity in human hepatocarcinoma cells. To this aim, we have monitored the effects of ZEA on (1) cell viability, (2) heat-shock protein expression, (3) oxidative damage, (4) DNA fragmentation, (5) the cell cycle and (6) the cell-death-signalling pathway. Our results demonstrated that ZEA reduced cell viability in a time- and dose-dependent manner. When we exposed HepG2 cells to 100 µ
M
ZEA (80% of cells are viable) for different treatment times (2, 4, 8, 24, 30, 48 and 60 h), we demonstrated an induction of Hsp70 protein, an increase in reactive oxygen species (ROS) generation, DNA fragmentation and cell-cycle arrest. These events begin after only 2 h of mycotoxin exposure and are earlier than those implicated in the execution of apoptosis. 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M
ZEA (80% of cells are viable) for different treatment times (2, 4, 8, 24, 30, 48 and 60 h), we demonstrated an induction of Hsp70 protein, an increase in reactive oxygen species (ROS) generation, DNA fragmentation and cell-cycle arrest. These events begin after only 2 h of mycotoxin exposure and are earlier than those implicated in the execution of apoptosis. However, significant apoptotic cell death was observed after at least 30 h of ZEA exposure as a consequence of increased Bax expression, decreased Bcl-2 expression and mitochondrial membrane potential (Δψm)-released cytochrome c and activated caspase-3 and caspase-9.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>23605383</pmid><doi>10.1007/s12550-010-0053-8</doi><tpages>11</tpages></addata></record> |
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| source | Springer Nature - Complete Springer Journals |
| subjects | Apoptosis Biomedical and Life Sciences Cancer Chemistry/Food Science Deoxyribonucleic acid DNA Food contamination & poisoning Fungi Health problems Life Sciences Medical Microbiology Medicine/Public Health Metabolites Microbiology Mycotoxins Original Paper Toxicology |
| title | Sequential events of apoptosis induced by zearalenone in cultured hepatocarcinoma cells |
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