Ochratoxin A induces apoptosis in neuronal cells
The mycotoxin ochratoxin A (OTA), which is produced by Aspergillus and Penicillium subspecies, is a frequently present contaminant of food and feedstuffs. OTA exhibits a wide range of toxic activities including nephro- and hepatotoxicity. However, little is known regarding potential neurotoxic effec...
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| Veröffentlicht in: | Genes & nutrition 2009-03, Vol.4 (1), p.41-48 |
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| creator | Zhang, Xiangnan Boesch-Saadatmandi, Christine Lou, Yijia Wolffram, Siegfried Huebbe, Patricia Rimbach, Gerald |
| description | The mycotoxin ochratoxin A (OTA), which is produced by Aspergillus and Penicillium subspecies, is a frequently present contaminant of food and feedstuffs. OTA exhibits a wide range of toxic activities including nephro- and hepatotoxicity. However, little is known regarding potential neurotoxic effects of OTA. In the present study primary neurons as well as SH-SY5Y neuronal cells were incubated with increasing concentrations of OTA (0.1-2.5 mumol/L). OTA treatment resulted in a dose-dependent increase in cytotoxicity in both neuronal cell types. Caspase-9 and caspase-3 were activated in response to OTA treatment. Furthermore, caspase inhibitors were effective in partly counteracting OTA induced neurocytotoxicity. OTA induced apoptosis was accompanied by a loss of mitochondria membrane potential. Overall, present data indicated that OTA is neurotoxic at relatively low concentrations. OTA induced neurotoxicity seems to be, at least party, mediated by apoptosis. OTA may contribute to the pathogenesis of neurodegenerative diseases (e.g. Alzheimer's and Parkinson's disease) in which apoptotic processes are centrally involved. |
| doi_str_mv | 10.1007/s12263-008-0109-y |
| format | Article |
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OTA exhibits a wide range of toxic activities including nephro- and hepatotoxicity. However, little is known regarding potential neurotoxic effects of OTA. In the present study primary neurons as well as SH-SY5Y neuronal cells were incubated with increasing concentrations of OTA (0.1-2.5 mumol/L). OTA treatment resulted in a dose-dependent increase in cytotoxicity in both neuronal cell types. Caspase-9 and caspase-3 were activated in response to OTA treatment. Furthermore, caspase inhibitors were effective in partly counteracting OTA induced neurocytotoxicity. OTA induced apoptosis was accompanied by a loss of mitochondria membrane potential. Overall, present data indicated that OTA is neurotoxic at relatively low concentrations. OTA induced neurotoxicity seems to be, at least party, mediated by apoptosis. OTA may contribute to the pathogenesis of neurodegenerative diseases (e.g. Alzheimer's and Parkinson's disease) in which apoptotic processes are centrally involved.</description><identifier>ISSN: 1555-8932</identifier><identifier>EISSN: 1865-3499</identifier><identifier>DOI: 10.1007/s12263-008-0109-y</identifier><identifier>PMID: 19148691</identifier><language>eng</language><publisher>Germany: Springer-Verlag</publisher><subject>apoptosis ; Aspergillus ; caspase-3 ; caspase-9 ; cytotoxicity ; dose response ; enzyme inhibitors ; membrane potential ; neurons ; neurotoxicity ; ochratoxin A ; Parkinson disease ; pathogenesis ; Penicillium ; Research Paper</subject><ispartof>Genes & nutrition, 2009-03, Vol.4 (1), p.41-48</ispartof><rights>Springer-Verlag 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-4113809581f5af761752f87868e0b213a936d0a5f71e165624f9a0f1935854f23</citedby><cites>FETCH-LOGICAL-c497t-4113809581f5af761752f87868e0b213a936d0a5f71e165624f9a0f1935854f23</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/PMC2654052/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2654052/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19148691$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Xiangnan</creatorcontrib><creatorcontrib>Boesch-Saadatmandi, Christine</creatorcontrib><creatorcontrib>Lou, Yijia</creatorcontrib><creatorcontrib>Wolffram, Siegfried</creatorcontrib><creatorcontrib>Huebbe, Patricia</creatorcontrib><creatorcontrib>Rimbach, Gerald</creatorcontrib><title>Ochratoxin A induces apoptosis in neuronal cells</title><title>Genes & nutrition</title><addtitle>Genes Nutr</addtitle><description>The mycotoxin ochratoxin A (OTA), which is produced by Aspergillus and Penicillium subspecies, is a frequently present contaminant of food and feedstuffs. OTA exhibits a wide range of toxic activities including nephro- and hepatotoxicity. However, little is known regarding potential neurotoxic effects of OTA. In the present study primary neurons as well as SH-SY5Y neuronal cells were incubated with increasing concentrations of OTA (0.1-2.5 mumol/L). OTA treatment resulted in a dose-dependent increase in cytotoxicity in both neuronal cell types. Caspase-9 and caspase-3 were activated in response to OTA treatment. Furthermore, caspase inhibitors were effective in partly counteracting OTA induced neurocytotoxicity. OTA induced apoptosis was accompanied by a loss of mitochondria membrane potential. Overall, present data indicated that OTA is neurotoxic at relatively low concentrations. OTA induced neurotoxicity seems to be, at least party, mediated by apoptosis. OTA may contribute to the pathogenesis of neurodegenerative diseases (e.g. Alzheimer's and Parkinson's disease) in which apoptotic processes are centrally involved.</description><subject>apoptosis</subject><subject>Aspergillus</subject><subject>caspase-3</subject><subject>caspase-9</subject><subject>cytotoxicity</subject><subject>dose response</subject><subject>enzyme inhibitors</subject><subject>membrane potential</subject><subject>neurons</subject><subject>neurotoxicity</subject><subject>ochratoxin A</subject><subject>Parkinson disease</subject><subject>pathogenesis</subject><subject>Penicillium</subject><subject>Research Paper</subject><issn>1555-8932</issn><issn>1865-3499</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNpVkE1PwzAMhiMEYmPwA7igHrkE7KRJkwvSNPElTdoFzlHWJayoa0bSIvbvabWJj5Mt2-9r-yHkEuEGAYrbhIxJTgEUBQRNd0dkjEoKynOtj_tcCEGV5mxEzlJ6BxCaczglI9SYK6lxTGBRrqNtw1fVZNOsalZd6VJmt2HbhlSlvpI1rouhsXVWurpO5-TE2zq5i0OckNeH-5fZE50vHp9n0zktc120NEfkCrRQ6IX1hcRCMK8KJZWDJUNuNZcrsMIX6FAKyXKvLXjUXCiRe8Yn5G7vu-2WG7cqXdNGW5ttrDY27kywlfnfaaq1eQufhkmRgxgMrg8GMXx0LrVmU6XhBdu40CXDQHAlue7DhOB-tIwhpej8zxoEM5A2e9KmJ20G0mbXa67-3verOKDl3486eJ4</recordid><startdate>20090301</startdate><enddate>20090301</enddate><creator>Zhang, Xiangnan</creator><creator>Boesch-Saadatmandi, Christine</creator><creator>Lou, Yijia</creator><creator>Wolffram, Siegfried</creator><creator>Huebbe, Patricia</creator><creator>Rimbach, Gerald</creator><general>Springer-Verlag</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20090301</creationdate><title>Ochratoxin A induces apoptosis in neuronal cells</title><author>Zhang, Xiangnan ; Boesch-Saadatmandi, Christine ; Lou, Yijia ; Wolffram, Siegfried ; Huebbe, Patricia ; Rimbach, Gerald</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c497t-4113809581f5af761752f87868e0b213a936d0a5f71e165624f9a0f1935854f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>apoptosis</topic><topic>Aspergillus</topic><topic>caspase-3</topic><topic>caspase-9</topic><topic>cytotoxicity</topic><topic>dose response</topic><topic>enzyme inhibitors</topic><topic>membrane potential</topic><topic>neurons</topic><topic>neurotoxicity</topic><topic>ochratoxin A</topic><topic>Parkinson disease</topic><topic>pathogenesis</topic><topic>Penicillium</topic><topic>Research Paper</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Xiangnan</creatorcontrib><creatorcontrib>Boesch-Saadatmandi, Christine</creatorcontrib><creatorcontrib>Lou, Yijia</creatorcontrib><creatorcontrib>Wolffram, Siegfried</creatorcontrib><creatorcontrib>Huebbe, Patricia</creatorcontrib><creatorcontrib>Rimbach, Gerald</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes & nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Xiangnan</au><au>Boesch-Saadatmandi, Christine</au><au>Lou, Yijia</au><au>Wolffram, Siegfried</au><au>Huebbe, Patricia</au><au>Rimbach, Gerald</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ochratoxin A induces apoptosis in neuronal cells</atitle><jtitle>Genes & nutrition</jtitle><addtitle>Genes Nutr</addtitle><date>2009-03-01</date><risdate>2009</risdate><volume>4</volume><issue>1</issue><spage>41</spage><epage>48</epage><pages>41-48</pages><issn>1555-8932</issn><eissn>1865-3499</eissn><abstract>The mycotoxin ochratoxin A (OTA), which is produced by Aspergillus and Penicillium subspecies, is a frequently present contaminant of food and feedstuffs. OTA exhibits a wide range of toxic activities including nephro- and hepatotoxicity. However, little is known regarding potential neurotoxic effects of OTA. In the present study primary neurons as well as SH-SY5Y neuronal cells were incubated with increasing concentrations of OTA (0.1-2.5 mumol/L). OTA treatment resulted in a dose-dependent increase in cytotoxicity in both neuronal cell types. Caspase-9 and caspase-3 were activated in response to OTA treatment. Furthermore, caspase inhibitors were effective in partly counteracting OTA induced neurocytotoxicity. OTA induced apoptosis was accompanied by a loss of mitochondria membrane potential. Overall, present data indicated that OTA is neurotoxic at relatively low concentrations. OTA induced neurotoxicity seems to be, at least party, mediated by apoptosis. OTA may contribute to the pathogenesis of neurodegenerative diseases (e.g. Alzheimer's and Parkinson's disease) in which apoptotic processes are centrally involved.</abstract><cop>Germany</cop><pub>Springer-Verlag</pub><pmid>19148691</pmid><doi>10.1007/s12263-008-0109-y</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | apoptosis Aspergillus caspase-3 caspase-9 cytotoxicity dose response enzyme inhibitors membrane potential neurons neurotoxicity ochratoxin A Parkinson disease pathogenesis Penicillium Research Paper |
| title | Ochratoxin A induces apoptosis in neuronal cells |
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