Application of physiologically based modelling and transcriptomics to probe the systems toxicology of aldicarb for Caenorhabditis elegans (Maupas 1900)
The toxicity of aldicarb on movement, life cycle, population growth rate and resource allocation, and the gene expression changes underpinning these effects, were investigated for Caenorhabditis elegans. A clear effect of aldicarb on nematode movement was found suggesting that this pesticide acts as...
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description | The toxicity of aldicarb on movement, life cycle, population growth rate and resource allocation, and the gene expression changes underpinning these effects, were investigated for Caenorhabditis elegans. A clear effect of aldicarb on nematode movement was found suggesting that this pesticide acts as a neurotoxicant. Aldicarb also had an effect on life cycle traits including low concentration life-span extension; high concentration brood size reduction and a high concentration extension of time to first egg. All life-cycle and growth data were integrated into a biology-based model (DEBtox) to characterise aldicarb effects on life-history traits, resource allocation and population growth rate within a single modelling framework. The DEBtox fits described concentration dependent effects on individual traits and population growth rate and indicated that the most probable mechanism of action of the pesticide was an increase in energy demands for somatic and reproductive tissue maintenance. Transcriptomic profiling indicated that aldicarb was associated with changes in amino acid metabolism, DNA structure, fatty acid metabolism and cytochrome P450 mediated xenobiotic metabolism. The changes in the amino acid and fatty acid pathways suggest an effect of aldicarb on protein integrity; while effects on DNA suggests that aldicarb influence DNA morphology or replication. Both these effects have the potential to incur increased costs for structural maintenance of macromolecules. These effects, coupled to the effect on biotransformation enzymes also seen, represent the materialisation of the maintenance costs indicated by DEBtox modelling. |
doi_str_mv | 10.1007/s10646-010-0591-z |
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A clear effect of aldicarb on nematode movement was found suggesting that this pesticide acts as a neurotoxicant. Aldicarb also had an effect on life cycle traits including low concentration life-span extension; high concentration brood size reduction and a high concentration extension of time to first egg. All life-cycle and growth data were integrated into a biology-based model (DEBtox) to characterise aldicarb effects on life-history traits, resource allocation and population growth rate within a single modelling framework. The DEBtox fits described concentration dependent effects on individual traits and population growth rate and indicated that the most probable mechanism of action of the pesticide was an increase in energy demands for somatic and reproductive tissue maintenance. Transcriptomic profiling indicated that aldicarb was associated with changes in amino acid metabolism, DNA structure, fatty acid metabolism and cytochrome P450 mediated xenobiotic metabolism. The changes in the amino acid and fatty acid pathways suggest an effect of aldicarb on protein integrity; while effects on DNA suggests that aldicarb influence DNA morphology or replication. Both these effects have the potential to incur increased costs for structural maintenance of macromolecules. These effects, coupled to the effect on biotransformation enzymes also seen, represent the materialisation of the maintenance costs indicated by DEBtox modelling.</description><identifier>ISSN: 0963-9292</identifier><identifier>EISSN: 1573-3017</identifier><identifier>DOI: 10.1007/s10646-010-0591-z</identifier><identifier>PMID: 21253838</identifier><identifier>CODEN: ECOTEL</identifier><language>eng</language><publisher>Boston: Boston : Springer US</publisher><subject>Acetylcholinesterase ; Acetylcholinesterase - metabolism ; Aldicarb ; Aldicarb - toxicity ; amino acid metabolism ; Amino acids ; Animals ; Biological effects ; Biotransformation ; Caenorhabditis elegans ; Caenorhabditis elegans - drug effects ; Caenorhabditis elegans - genetics ; Caenorhabditis elegans - physiology ; Carbamates ; Cholinesterase Inhibitors ; Cholinesterase Inhibitors - toxicity ; cytochrome P-450 ; DEBtox ; Deoxyribonucleic acid ; DNA ; drug effects ; Earth and Environmental Science ; Ecology ; Ecotoxicology ; eggs ; Environment ; Environmental Management ; enzymes ; fatty acid metabolism ; Fatty acids ; Gene Expression ; Gene Expression - drug effects ; Gene Expression Profiling ; gene expression regulation ; genetics ; Growth rate ; Insecticides ; Insecticides - toxicity ; Investigations ; Life Cycle Stages ; Life Cycle Stages - drug effects ; Life cycles ; Life history ; Life-span ; Maintenance costs ; mechanism of action ; Metabolism ; Modelling ; Models, Biological ; Nematoda ; Nervous System ; Nervous System - drug effects ; pesticidal properties ; Pesticides ; Physiological aspects ; physiology ; Population growth ; protein metabolism ; reproduction ; Resource allocation ; toxicity ; Toxicology ; transcriptomics</subject><ispartof>Ecotoxicology (London), 2011-03, Vol.20 (2), p.397-408</ispartof><rights>The Author(s) 2011</rights><rights>COPYRIGHT 2011 Springer</rights><rights>Springer Science+Business Media, LLC 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c656t-a1825046edc3b382063602f5962c3082a8391aecc364cb9ce8d77efc0d2f48353</citedby><cites>FETCH-LOGICAL-c656t-a1825046edc3b382063602f5962c3082a8391aecc364cb9ce8d77efc0d2f48353</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/s10646-010-0591-z$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10646-010-0591-z$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,777,781,882,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21253838$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wren, Jodie F</creatorcontrib><creatorcontrib>Kille, Peter</creatorcontrib><creatorcontrib>Spurgeon, David J</creatorcontrib><creatorcontrib>Swain, Suresh</creatorcontrib><creatorcontrib>Sturzenbaum, Stephen R</creatorcontrib><creatorcontrib>Jager, Tjalling</creatorcontrib><title>Application of physiologically based modelling and transcriptomics to probe the systems toxicology of aldicarb for Caenorhabditis elegans (Maupas 1900)</title><title>Ecotoxicology (London)</title><addtitle>Ecotoxicology</addtitle><addtitle>Ecotoxicology</addtitle><description>The toxicity of aldicarb on movement, life cycle, population growth rate and resource allocation, and the gene expression changes underpinning these effects, were investigated for Caenorhabditis elegans. A clear effect of aldicarb on nematode movement was found suggesting that this pesticide acts as a neurotoxicant. Aldicarb also had an effect on life cycle traits including low concentration life-span extension; high concentration brood size reduction and a high concentration extension of time to first egg. All life-cycle and growth data were integrated into a biology-based model (DEBtox) to characterise aldicarb effects on life-history traits, resource allocation and population growth rate within a single modelling framework. The DEBtox fits described concentration dependent effects on individual traits and population growth rate and indicated that the most probable mechanism of action of the pesticide was an increase in energy demands for somatic and reproductive tissue maintenance. Transcriptomic profiling indicated that aldicarb was associated with changes in amino acid metabolism, DNA structure, fatty acid metabolism and cytochrome P450 mediated xenobiotic metabolism. The changes in the amino acid and fatty acid pathways suggest an effect of aldicarb on protein integrity; while effects on DNA suggests that aldicarb influence DNA morphology or replication. Both these effects have the potential to incur increased costs for structural maintenance of macromolecules. These effects, coupled to the effect on biotransformation enzymes also seen, represent the materialisation of the maintenance costs indicated by DEBtox modelling.</description><subject>Acetylcholinesterase</subject><subject>Acetylcholinesterase - metabolism</subject><subject>Aldicarb</subject><subject>Aldicarb - toxicity</subject><subject>amino acid metabolism</subject><subject>Amino acids</subject><subject>Animals</subject><subject>Biological effects</subject><subject>Biotransformation</subject><subject>Caenorhabditis elegans</subject><subject>Caenorhabditis elegans - drug effects</subject><subject>Caenorhabditis elegans - genetics</subject><subject>Caenorhabditis elegans - physiology</subject><subject>Carbamates</subject><subject>Cholinesterase Inhibitors</subject><subject>Cholinesterase Inhibitors - toxicity</subject><subject>cytochrome P-450</subject><subject>DEBtox</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>drug effects</subject><subject>Earth and Environmental Science</subject><subject>Ecology</subject><subject>Ecotoxicology</subject><subject>eggs</subject><subject>Environment</subject><subject>Environmental Management</subject><subject>enzymes</subject><subject>fatty acid metabolism</subject><subject>Fatty acids</subject><subject>Gene Expression</subject><subject>Gene Expression - drug effects</subject><subject>Gene Expression Profiling</subject><subject>gene expression regulation</subject><subject>genetics</subject><subject>Growth rate</subject><subject>Insecticides</subject><subject>Insecticides - toxicity</subject><subject>Investigations</subject><subject>Life Cycle Stages</subject><subject>Life Cycle Stages - drug effects</subject><subject>Life cycles</subject><subject>Life history</subject><subject>Life-span</subject><subject>Maintenance costs</subject><subject>mechanism of action</subject><subject>Metabolism</subject><subject>Modelling</subject><subject>Models, Biological</subject><subject>Nematoda</subject><subject>Nervous System</subject><subject>Nervous System - drug effects</subject><subject>pesticidal properties</subject><subject>Pesticides</subject><subject>Physiological aspects</subject><subject>physiology</subject><subject>Population growth</subject><subject>protein metabolism</subject><subject>reproduction</subject><subject>Resource allocation</subject><subject>toxicity</subject><subject>Toxicology</subject><subject>transcriptomics</subject><issn>0963-9292</issn><issn>1573-3017</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><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>eNqFk89u1DAQhyMEokvhAbiARQ-UQ8rYTuz4grRa8U8q4gA9W47jZF0ldrCzqNsX4XVxmlIoQkU5RBp_88kz-SXLnmI4wQD8dcTACpYDhhxKgfPLe9kKl5zmFDC_n61AMJoLIshB9ijGcwAQvICH2QHBpKQVrVbZj_U49laryXqHfIvG7T5a3_su1fp-j2oVTYMG35i-t65DyjVoCspFHew4-cHqiCaPxuBrg6atQXEfJzPMxQurZ9F-1qq-ScJQo9YHtFHG-bBVdWMnG5HpTZeE6PiT2o0qIiwAXj3OHrSqj-bJ9fswO3v39uvmQ376-f3Hzfo016xkU65wRUoomGk0rWlFgFEGpC0FI5pCRVRFBVZGa8oKXQttqoZz02poSFtUtKSH2ZvFO-7qIVmMS9P1cgx2UGEvvbLy9omzW9n575IC5YUgSfDyWhD8t52Jkxxs1Glbyhm_i7JikO6VLvR_suQYM3FFHt9JYs45LigueEJf_IWe-11waWXJhwkV5RV0tECd6o20rvVpFD075ZrjNEfFYaZO_kGlpzHpM3tnWpvqtxrw0qCDjzGY9mZtGOQcULkEVKaAyjmg8jL1PPtz3zcdvxKZALIAMR25zoTfA91lfb40tcpL1QUb5dkXAjj9B6IAIUr6Ewj6-wQ</recordid><startdate>20110301</startdate><enddate>20110301</enddate><creator>Wren, 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of physiologically based modelling and transcriptomics to probe the systems toxicology of aldicarb for Caenorhabditis elegans (Maupas 1900)</title><author>Wren, Jodie F ; Kille, Peter ; Spurgeon, David J ; Swain, Suresh ; Sturzenbaum, Stephen R ; Jager, Tjalling</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c656t-a1825046edc3b382063602f5962c3082a8391aecc364cb9ce8d77efc0d2f48353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Acetylcholinesterase</topic><topic>Acetylcholinesterase - metabolism</topic><topic>Aldicarb</topic><topic>Aldicarb - toxicity</topic><topic>amino acid metabolism</topic><topic>Amino acids</topic><topic>Animals</topic><topic>Biological effects</topic><topic>Biotransformation</topic><topic>Caenorhabditis elegans</topic><topic>Caenorhabditis elegans - drug effects</topic><topic>Caenorhabditis elegans - genetics</topic><topic>Caenorhabditis elegans - physiology</topic><topic>Carbamates</topic><topic>Cholinesterase Inhibitors</topic><topic>Cholinesterase Inhibitors - toxicity</topic><topic>cytochrome P-450</topic><topic>DEBtox</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>drug effects</topic><topic>Earth and Environmental Science</topic><topic>Ecology</topic><topic>Ecotoxicology</topic><topic>eggs</topic><topic>Environment</topic><topic>Environmental Management</topic><topic>enzymes</topic><topic>fatty acid metabolism</topic><topic>Fatty acids</topic><topic>Gene Expression</topic><topic>Gene Expression - drug effects</topic><topic>Gene Expression Profiling</topic><topic>gene expression regulation</topic><topic>genetics</topic><topic>Growth rate</topic><topic>Insecticides</topic><topic>Insecticides - toxicity</topic><topic>Investigations</topic><topic>Life Cycle Stages</topic><topic>Life Cycle Stages - drug effects</topic><topic>Life cycles</topic><topic>Life history</topic><topic>Life-span</topic><topic>Maintenance costs</topic><topic>mechanism of action</topic><topic>Metabolism</topic><topic>Modelling</topic><topic>Models, Biological</topic><topic>Nematoda</topic><topic>Nervous System</topic><topic>Nervous System - drug effects</topic><topic>pesticidal properties</topic><topic>Pesticides</topic><topic>Physiological aspects</topic><topic>physiology</topic><topic>Population growth</topic><topic>protein metabolism</topic><topic>reproduction</topic><topic>Resource allocation</topic><topic>toxicity</topic><topic>Toxicology</topic><topic>transcriptomics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wren, Jodie F</creatorcontrib><creatorcontrib>Kille, Peter</creatorcontrib><creatorcontrib>Spurgeon, David J</creatorcontrib><creatorcontrib>Swain, Suresh</creatorcontrib><creatorcontrib>Sturzenbaum, Stephen R</creatorcontrib><creatorcontrib>Jager, 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(London)</jtitle><stitle>Ecotoxicology</stitle><addtitle>Ecotoxicology</addtitle><date>2011-03-01</date><risdate>2011</risdate><volume>20</volume><issue>2</issue><spage>397</spage><epage>408</epage><pages>397-408</pages><issn>0963-9292</issn><eissn>1573-3017</eissn><coden>ECOTEL</coden><abstract>The toxicity of aldicarb on movement, life cycle, population growth rate and resource allocation, and the gene expression changes underpinning these effects, were investigated for Caenorhabditis elegans. A clear effect of aldicarb on nematode movement was found suggesting that this pesticide acts as a neurotoxicant. Aldicarb also had an effect on life cycle traits including low concentration life-span extension; high concentration brood size reduction and a high concentration extension of time to first egg. All life-cycle and growth data were integrated into a biology-based model (DEBtox) to characterise aldicarb effects on life-history traits, resource allocation and population growth rate within a single modelling framework. The DEBtox fits described concentration dependent effects on individual traits and population growth rate and indicated that the most probable mechanism of action of the pesticide was an increase in energy demands for somatic and reproductive tissue maintenance. Transcriptomic profiling indicated that aldicarb was associated with changes in amino acid metabolism, DNA structure, fatty acid metabolism and cytochrome P450 mediated xenobiotic metabolism. The changes in the amino acid and fatty acid pathways suggest an effect of aldicarb on protein integrity; while effects on DNA suggests that aldicarb influence DNA morphology or replication. Both these effects have the potential to incur increased costs for structural maintenance of macromolecules. These effects, coupled to the effect on biotransformation enzymes also seen, represent the materialisation of the maintenance costs indicated by DEBtox modelling.</abstract><cop>Boston</cop><pub>Boston : Springer US</pub><pmid>21253838</pmid><doi>10.1007/s10646-010-0591-z</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acetylcholinesterase Acetylcholinesterase - metabolism Aldicarb Aldicarb - toxicity amino acid metabolism Amino acids Animals Biological effects Biotransformation Caenorhabditis elegans Caenorhabditis elegans - drug effects Caenorhabditis elegans - genetics Caenorhabditis elegans - physiology Carbamates Cholinesterase Inhibitors Cholinesterase Inhibitors - toxicity cytochrome P-450 DEBtox Deoxyribonucleic acid DNA drug effects Earth and Environmental Science Ecology Ecotoxicology eggs Environment Environmental Management enzymes fatty acid metabolism Fatty acids Gene Expression Gene Expression - drug effects Gene Expression Profiling gene expression regulation genetics Growth rate Insecticides Insecticides - toxicity Investigations Life Cycle Stages Life Cycle Stages - drug effects Life cycles Life history Life-span Maintenance costs mechanism of action Metabolism Modelling Models, Biological Nematoda Nervous System Nervous System - drug effects pesticidal properties Pesticides Physiological aspects physiology Population growth protein metabolism reproduction Resource allocation toxicity Toxicology transcriptomics |
title | Application of physiologically based modelling and transcriptomics to probe the systems toxicology of aldicarb for Caenorhabditis elegans (Maupas 1900) |
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