Psychoactive pharmaceuticals induce fish gene expression profiles associated with human idiopathic autism
Idiopathic autism, caused by genetic susceptibility interacting with unknown environmental triggers, has increased dramatically in the past 25 years. Identifying environmental triggers has been difficult due to poorly understood pathophysiology and subjective definitions of autism. The use of antide...
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| Veröffentlicht in: | PloS one 2012-06, Vol.7 (6), p.e32917 |
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| description | Idiopathic autism, caused by genetic susceptibility interacting with unknown environmental triggers, has increased dramatically in the past 25 years. Identifying environmental triggers has been difficult due to poorly understood pathophysiology and subjective definitions of autism. The use of antidepressants by pregnant women has been associated with autism. These and other unmetabolized psychoactive pharmaceuticals (UPPs) have also been found in drinking water from surface sources, providing another possible exposure route and raising questions about human health consequences. Here, we examined gene expression patterns of fathead minnows treated with a mixture of three psychoactive pharmaceuticals (fluoxetine, venlafaxine & carbamazepine) in dosages intended to be similar to the highest observed conservative estimates of environmental concentrations. We conducted microarray experiments examining brain tissue of fish exposed to individual pharmaceuticals and a mixture of all three. We used gene-class analysis to test for enrichment of gene sets involved with ten human neurological disorders. Only sets associated with idiopathic autism were unambiguously enriched. We found that UPPs induce autism-like gene expression patterns in fish. Our findings suggest a new potential trigger for idiopathic autism in genetically susceptible individuals involving an overlooked source of environmental contamination. |
| doi_str_mv | 10.1371/journal.pone.0032917 |
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C.</contributor><creatorcontrib>Thomas, Michael A ; Klaper, Rebecca D ; Skoulakis, Efthimios M. C.</creatorcontrib><description>Idiopathic autism, caused by genetic susceptibility interacting with unknown environmental triggers, has increased dramatically in the past 25 years. Identifying environmental triggers has been difficult due to poorly understood pathophysiology and subjective definitions of autism. The use of antidepressants by pregnant women has been associated with autism. These and other unmetabolized psychoactive pharmaceuticals (UPPs) have also been found in drinking water from surface sources, providing another possible exposure route and raising questions about human health consequences. Here, we examined gene expression patterns of fathead minnows treated with a mixture of three psychoactive pharmaceuticals (fluoxetine, venlafaxine & carbamazepine) in dosages intended to be similar to the highest observed conservative estimates of environmental concentrations. We conducted microarray experiments examining brain tissue of fish exposed to individual pharmaceuticals and a mixture of all three. We used gene-class analysis to test for enrichment of gene sets involved with ten human neurological disorders. Only sets associated with idiopathic autism were unambiguously enriched. We found that UPPs induce autism-like gene expression patterns in fish. Our findings suggest a new potential trigger for idiopathic autism in genetically susceptible individuals involving an overlooked source of environmental contamination.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0032917</identifier><identifier>PMID: 22701549</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Antidepressants ; Autism ; Autistic Disorder - chemically induced ; Autistic Disorder - genetics ; Autistic Disorder - metabolism ; Behavior ; Biology ; Biosynthesis ; Bipolar disorder ; Brain ; Carbamazepine ; Carbamazepine - toxicity ; Cell Adhesion Molecules - metabolism ; Contamination ; Cyclohexanols - toxicity ; Cyprinidae - genetics ; Cyprinidae - metabolism ; Disease susceptibility ; DNA microarrays ; Drinking water ; Drugs ; Fetuses ; Fish ; Fishes ; Fluoxetine ; Fluoxetine - toxicity ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation - drug effects ; Genes ; Genetic aspects ; Humans ; Medicine ; Mental disorders ; Microarray Analysis ; Multiple sclerosis ; Nerve Tissue Proteins - metabolism ; Nervous system diseases ; Neurological diseases ; Neurological disorders ; Parkinson's disease ; Pharmaceuticals ; Pregnancy ; Pregnant women ; Psychiatry ; Psychotropic Drugs - toxicity ; Receptors, Immunologic - metabolism ; Schizophrenia ; Serotonin ; Venlafaxine ; Venlafaxine Hydrochloride ; Water Pollutants, Chemical - toxicity ; Womens health</subject><ispartof>PloS one, 2012-06, Vol.7 (6), p.e32917</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Thomas, Klaper. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Thomas, Klaper. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6077-6dde4b5805215d68333fe4d055dba8be6e9138b2b804a8d0803fc8f9c62bfa853</citedby><cites>FETCH-LOGICAL-c6077-6dde4b5805215d68333fe4d055dba8be6e9138b2b804a8d0803fc8f9c62bfa853</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/PMC3368908/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368908/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22701549$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Skoulakis, Efthimios M. C.</contributor><creatorcontrib>Thomas, Michael A</creatorcontrib><creatorcontrib>Klaper, Rebecca D</creatorcontrib><title>Psychoactive pharmaceuticals induce fish gene expression profiles associated with human idiopathic autism</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Idiopathic autism, caused by genetic susceptibility interacting with unknown environmental triggers, has increased dramatically in the past 25 years. Identifying environmental triggers has been difficult due to poorly understood pathophysiology and subjective definitions of autism. The use of antidepressants by pregnant women has been associated with autism. These and other unmetabolized psychoactive pharmaceuticals (UPPs) have also been found in drinking water from surface sources, providing another possible exposure route and raising questions about human health consequences. Here, we examined gene expression patterns of fathead minnows treated with a mixture of three psychoactive pharmaceuticals (fluoxetine, venlafaxine & carbamazepine) in dosages intended to be similar to the highest observed conservative estimates of environmental concentrations. We conducted microarray experiments examining brain tissue of fish exposed to individual pharmaceuticals and a mixture of all three. We used gene-class analysis to test for enrichment of gene sets involved with ten human neurological disorders. Only sets associated with idiopathic autism were unambiguously enriched. We found that UPPs induce autism-like gene expression patterns in fish. Our findings suggest a new potential trigger for idiopathic autism in genetically susceptible individuals involving an overlooked source of environmental contamination.</description><subject>Analysis</subject><subject>Animals</subject><subject>Antidepressants</subject><subject>Autism</subject><subject>Autistic Disorder - chemically induced</subject><subject>Autistic Disorder - genetics</subject><subject>Autistic Disorder - metabolism</subject><subject>Behavior</subject><subject>Biology</subject><subject>Biosynthesis</subject><subject>Bipolar disorder</subject><subject>Brain</subject><subject>Carbamazepine</subject><subject>Carbamazepine - toxicity</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Contamination</subject><subject>Cyclohexanols - toxicity</subject><subject>Cyprinidae - genetics</subject><subject>Cyprinidae - metabolism</subject><subject>Disease susceptibility</subject><subject>DNA microarrays</subject><subject>Drinking water</subject><subject>Drugs</subject><subject>Fetuses</subject><subject>Fish</subject><subject>Fishes</subject><subject>Fluoxetine</subject><subject>Fluoxetine - toxicity</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Medicine</subject><subject>Mental disorders</subject><subject>Microarray Analysis</subject><subject>Multiple sclerosis</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nervous system diseases</subject><subject>Neurological diseases</subject><subject>Neurological disorders</subject><subject>Parkinson's disease</subject><subject>Pharmaceuticals</subject><subject>Pregnancy</subject><subject>Pregnant women</subject><subject>Psychiatry</subject><subject>Psychotropic Drugs - toxicity</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Schizophrenia</subject><subject>Serotonin</subject><subject>Venlafaxine</subject><subject>Venlafaxine Hydrochloride</subject><subject>Water Pollutants, Chemical - toxicity</subject><subject>Womens health</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</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><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAYhYso7rr6D0QLguDFjPlo0_RGWBY_BhZW_LoNb5O30wxtU5N23f33ZpzuMgUFyUVC8pyTcHKS5Dkla8oL-nbnJt9Dux5cj2tCOCtp8SA5pSVnK8EIf3i0PkmehLAjJOdSiMfJCWMFoXlWnib2c7jVjQM92mtMhwZ8Bxqn0WpoQ2p7M2lMaxuadIs9pngzeAzBuj4dvKttiyGFEJy2MKJJf9mxSZupgz61xroBxsbqFKJd6J4mj-roic_m-Sz5_uH9t4tPq8urj5uL88uVFqQoVsIYzKpckpzR3AjJOa8xMyTPTQWyQoEl5bJilSQZSEMk4bWWdakFq2qQOT9LXh58h9YFNacUFOUsJ1QKziKxORDGwU4N3nbgb5UDq_5sOL9V4GMCLSqUQAQgMUUFGRheUV1UQlPGak4khej1br5tqjo0GvvRQ7swXZ70tlFbd604F7IkMhq8mg28-zlhGP_x5JnaQnyV7WsXzXRng1bnWVFQmueER2r9FyoOg53VsSf7D1sK3iwEkRnxZtzCFILafP3y_-zVjyX7-ohtENqxCa6NPXB9WILZAdTeheCxvk-OErWv-V0aal9zNdc8yl4cp34vuus1_w1pbfod</recordid><startdate>20120606</startdate><enddate>20120606</enddate><creator>Thomas, Michael A</creator><creator>Klaper, Rebecca D</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120606</creationdate><title>Psychoactive pharmaceuticals induce fish gene expression profiles associated with human idiopathic autism</title><author>Thomas, Michael A ; Klaper, Rebecca D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6077-6dde4b5805215d68333fe4d055dba8be6e9138b2b804a8d0803fc8f9c62bfa853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Antidepressants</topic><topic>Autism</topic><topic>Autistic Disorder - chemically induced</topic><topic>Autistic Disorder - genetics</topic><topic>Autistic Disorder - metabolism</topic><topic>Behavior</topic><topic>Biology</topic><topic>Biosynthesis</topic><topic>Bipolar disorder</topic><topic>Brain</topic><topic>Carbamazepine</topic><topic>Carbamazepine - toxicity</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Contamination</topic><topic>Cyclohexanols - toxicity</topic><topic>Cyprinidae - genetics</topic><topic>Cyprinidae - metabolism</topic><topic>Disease susceptibility</topic><topic>DNA microarrays</topic><topic>Drinking water</topic><topic>Drugs</topic><topic>Fetuses</topic><topic>Fish</topic><topic>Fishes</topic><topic>Fluoxetine</topic><topic>Fluoxetine - toxicity</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Humans</topic><topic>Medicine</topic><topic>Mental disorders</topic><topic>Microarray Analysis</topic><topic>Multiple sclerosis</topic><topic>Nerve Tissue Proteins - 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C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Psychoactive pharmaceuticals induce fish gene expression profiles associated with human idiopathic autism</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-06-06</date><risdate>2012</risdate><volume>7</volume><issue>6</issue><spage>e32917</spage><pages>e32917-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Idiopathic autism, caused by genetic susceptibility interacting with unknown environmental triggers, has increased dramatically in the past 25 years. Identifying environmental triggers has been difficult due to poorly understood pathophysiology and subjective definitions of autism. The use of antidepressants by pregnant women has been associated with autism. These and other unmetabolized psychoactive pharmaceuticals (UPPs) have also been found in drinking water from surface sources, providing another possible exposure route and raising questions about human health consequences. Here, we examined gene expression patterns of fathead minnows treated with a mixture of three psychoactive pharmaceuticals (fluoxetine, venlafaxine & carbamazepine) in dosages intended to be similar to the highest observed conservative estimates of environmental concentrations. We conducted microarray experiments examining brain tissue of fish exposed to individual pharmaceuticals and a mixture of all three. We used gene-class analysis to test for enrichment of gene sets involved with ten human neurological disorders. Only sets associated with idiopathic autism were unambiguously enriched. We found that UPPs induce autism-like gene expression patterns in fish. Our findings suggest a new potential trigger for idiopathic autism in genetically susceptible individuals involving an overlooked source of environmental contamination.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22701549</pmid><doi>10.1371/journal.pone.0032917</doi><tpages>e32917</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Analysis Animals Antidepressants Autism Autistic Disorder - chemically induced Autistic Disorder - genetics Autistic Disorder - metabolism Behavior Biology Biosynthesis Bipolar disorder Brain Carbamazepine Carbamazepine - toxicity Cell Adhesion Molecules - metabolism Contamination Cyclohexanols - toxicity Cyprinidae - genetics Cyprinidae - metabolism Disease susceptibility DNA microarrays Drinking water Drugs Fetuses Fish Fishes Fluoxetine Fluoxetine - toxicity Gene expression Gene Expression Profiling Gene Expression Regulation - drug effects Genes Genetic aspects Humans Medicine Mental disorders Microarray Analysis Multiple sclerosis Nerve Tissue Proteins - metabolism Nervous system diseases Neurological diseases Neurological disorders Parkinson's disease Pharmaceuticals Pregnancy Pregnant women Psychiatry Psychotropic Drugs - toxicity Receptors, Immunologic - metabolism Schizophrenia Serotonin Venlafaxine Venlafaxine Hydrochloride Water Pollutants, Chemical - toxicity Womens health |
| title | Psychoactive pharmaceuticals induce fish gene expression profiles associated with human idiopathic autism |
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