Typical neurobehavioral methods and transcriptome analysis reveal the neurotoxicity and mechanisms of di(2-ethylhexyl) phthalate on pubertal male ICR mice with type 2 diabetes mellitus
In the present study, the neurotoxicity and mechanisms of di-(2-ethylhexyl) phthalate (DEHP) exposure on pubertal normal (P-normal) and pubertal type 2 diabetes mellitus (P-T2DM) mice were investigated by typical neurobehavioral methods and transcriptome analysis. Pubertal male ICR mice were orally...
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| Veröffentlicht in: | Archives of toxicology 2020-04, Vol.94 (4), p.1279-1302 |
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| creator | Feng, Weiwei Liu, Yongchao Ding, Yangyang Mao, Guanghua Zhao, Ting Chen, Kun Qiu, Xuchun Xu, Tong Zhao, XiaoFeng Wu, Xiangyang Yang, Liuqing |
| description | In the present study, the neurotoxicity and mechanisms of di-(2-ethylhexyl) phthalate (DEHP) exposure on pubertal normal (P-normal) and pubertal type 2 diabetes mellitus (P-T2DM) mice were investigated by typical neurobehavioral methods and transcriptome analysis. Pubertal male ICR mice were orally exposed to DEHP (0.18, 1.8, 18 and 180 mg/kg/d) for 3 weeks. In Open field test, DEHP significantly increased the time in central area staying and decreased the total distance and clockwise (CW) rotation of P-normal and P-T2DM mice. Morris water maze showed that DEHP significantly increased the latency in locating platform and decreased the original platform quadrant and residence time in target quadrant of P-normal and P-T2DM mice. Transcriptome analysis results revealed the effects of DEHP exposure on neural signaling pathway including biogenic amines neurotransmitters, nerve receptors, neurobiological processes, etc. Enzyme-linked immunosorbent assay (ELISA) and western blotting results showed that DEHP significantly decreased the contents of 5-HT, cAMP, GABA and Ca
2+
, the levels of CREB, phosphorylation of PKA, ERK1/2 and CREB, increased the levels of CaM and phosphorylation of CaMKII in P-normal and P-T2DM mice. Factorial analysis results showed that P-T2DM mice were more sensitive than those of P-normal mice. The potential neurotoxicity mechanism of DEHP may be synergistically mediated by the cAMP–PKA–ERK1/2–CREB signaling and the Ca
2+
signaling pathway.
Article highlights
DEHP can cause neurotoxicity in P-normal and P-T2DM mice.
P-T2DM mice were more sensitive to DEHP than P-normal mice.
Transcriptome analysis revealed genes associated with nervous system.
DEHP may be synergistically mediated by the cAMP–PKA–ERK1/2–CREB signaling and the Ca
2+
signaling pathway. |
| doi_str_mv | 10.1007/s00204-020-02683-9 |
| format | Article |
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2+
, the levels of CREB, phosphorylation of PKA, ERK1/2 and CREB, increased the levels of CaM and phosphorylation of CaMKII in P-normal and P-T2DM mice. Factorial analysis results showed that P-T2DM mice were more sensitive than those of P-normal mice. The potential neurotoxicity mechanism of DEHP may be synergistically mediated by the cAMP–PKA–ERK1/2–CREB signaling and the Ca
2+
signaling pathway.
Article highlights
DEHP can cause neurotoxicity in P-normal and P-T2DM mice.
P-T2DM mice were more sensitive to DEHP than P-normal mice.
Transcriptome analysis revealed genes associated with nervous system.
DEHP may be synergistically mediated by the cAMP–PKA–ERK1/2–CREB signaling and the Ca
2+
signaling pathway.</description><identifier>ISSN: 0340-5761</identifier><identifier>EISSN: 1432-0738</identifier><identifier>DOI: 10.1007/s00204-020-02683-9</identifier><identifier>PMID: 32303808</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Amines ; Animals ; Biogenic amines ; Biomedical and Life Sciences ; Biomedicine ; Ca2+/calmodulin-dependent protein kinase II ; Calcium ions ; Calcium signalling ; Cyclic AMP response element-binding protein ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 ; Diethylhexyl Phthalate - toxicity ; Endocrine Disruptors - toxicity ; Environmental Health ; Enzyme-linked immunosorbent assay ; Exposure ; Factorial analysis ; Field tests ; Gene expression ; Gene Expression Profiling ; Kinases ; Latency ; Life Sciences & Biomedicine ; Male ; Mice ; Mice, Inbred ICR ; Nervous system ; Nervous System - drug effects ; Nervous System - metabolism ; Neurotoxicity ; Neurotoxicity Syndromes ; Neurotransmitters ; Occupational Medicine/Industrial Medicine ; Open-field behavior ; Organ Toxicity and Mechanisms ; Pharmacology/Toxicology ; Phosphorylation ; Phthalates ; Phthalic Acids ; Protein kinase A ; Science & Technology ; Signal transduction ; Signaling ; Toxicology ; Western blotting ; γ-Aminobutyric acid</subject><ispartof>Archives of toxicology, 2020-04, Vol.94 (4), p.1279-1302</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020</rights><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>22</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000532990200015</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c375t-9cffa609ec7bd602d0091d911fc1bb453f014c5e533477e50e505b160de5a53a3</citedby><cites>FETCH-LOGICAL-c375t-9cffa609ec7bd602d0091d911fc1bb453f014c5e533477e50e505b160de5a53a3</cites><orcidid>0000-0002-3856-5539 ; 0000-0002-1974-1824</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00204-020-02683-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00204-020-02683-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,782,786,27931,27932,28255,41495,42564,51326</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32303808$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Feng, Weiwei</creatorcontrib><creatorcontrib>Liu, Yongchao</creatorcontrib><creatorcontrib>Ding, Yangyang</creatorcontrib><creatorcontrib>Mao, Guanghua</creatorcontrib><creatorcontrib>Zhao, Ting</creatorcontrib><creatorcontrib>Chen, Kun</creatorcontrib><creatorcontrib>Qiu, Xuchun</creatorcontrib><creatorcontrib>Xu, Tong</creatorcontrib><creatorcontrib>Zhao, XiaoFeng</creatorcontrib><creatorcontrib>Wu, Xiangyang</creatorcontrib><creatorcontrib>Yang, Liuqing</creatorcontrib><title>Typical neurobehavioral methods and transcriptome analysis reveal the neurotoxicity and mechanisms of di(2-ethylhexyl) phthalate on pubertal male ICR mice with type 2 diabetes mellitus</title><title>Archives of toxicology</title><addtitle>Arch Toxicol</addtitle><addtitle>ARCH TOXICOL</addtitle><addtitle>Arch Toxicol</addtitle><description>In the present study, the neurotoxicity and mechanisms of di-(2-ethylhexyl) phthalate (DEHP) exposure on pubertal normal (P-normal) and pubertal type 2 diabetes mellitus (P-T2DM) mice were investigated by typical neurobehavioral methods and transcriptome analysis. Pubertal male ICR mice were orally exposed to DEHP (0.18, 1.8, 18 and 180 mg/kg/d) for 3 weeks. In Open field test, DEHP significantly increased the time in central area staying and decreased the total distance and clockwise (CW) rotation of P-normal and P-T2DM mice. Morris water maze showed that DEHP significantly increased the latency in locating platform and decreased the original platform quadrant and residence time in target quadrant of P-normal and P-T2DM mice. Transcriptome analysis results revealed the effects of DEHP exposure on neural signaling pathway including biogenic amines neurotransmitters, nerve receptors, neurobiological processes, etc. Enzyme-linked immunosorbent assay (ELISA) and western blotting results showed that DEHP significantly decreased the contents of 5-HT, cAMP, GABA and Ca
2+
, the levels of CREB, phosphorylation of PKA, ERK1/2 and CREB, increased the levels of CaM and phosphorylation of CaMKII in P-normal and P-T2DM mice. Factorial analysis results showed that P-T2DM mice were more sensitive than those of P-normal mice. The potential neurotoxicity mechanism of DEHP may be synergistically mediated by the cAMP–PKA–ERK1/2–CREB signaling and the Ca
2+
signaling pathway.
Article highlights
DEHP can cause neurotoxicity in P-normal and P-T2DM mice.
P-T2DM mice were more sensitive to DEHP than P-normal mice.
Transcriptome analysis revealed genes associated with nervous system.
DEHP may be synergistically mediated by the cAMP–PKA–ERK1/2–CREB signaling and the Ca
2+
signaling pathway.</description><subject>Amines</subject><subject>Animals</subject><subject>Biogenic amines</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Ca2+/calmodulin-dependent protein kinase II</subject><subject>Calcium ions</subject><subject>Calcium signalling</subject><subject>Cyclic AMP response element-binding protein</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2</subject><subject>Diethylhexyl Phthalate - toxicity</subject><subject>Endocrine Disruptors - toxicity</subject><subject>Environmental Health</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Exposure</subject><subject>Factorial analysis</subject><subject>Field tests</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Kinases</subject><subject>Latency</subject><subject>Life Sciences & Biomedicine</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>Nervous system</subject><subject>Nervous System - drug effects</subject><subject>Nervous System - metabolism</subject><subject>Neurotoxicity</subject><subject>Neurotoxicity Syndromes</subject><subject>Neurotransmitters</subject><subject>Occupational Medicine/Industrial Medicine</subject><subject>Open-field behavior</subject><subject>Organ Toxicity and Mechanisms</subject><subject>Pharmacology/Toxicology</subject><subject>Phosphorylation</subject><subject>Phthalates</subject><subject>Phthalic Acids</subject><subject>Protein kinase A</subject><subject>Science & Technology</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Toxicology</subject><subject>Western blotting</subject><subject>γ-Aminobutyric acid</subject><issn>0340-5761</issn><issn>1432-0738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AOWDO</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkV1r1zAUxoso7u_0C3ghAW8UqZ4kTV8uR_FlMBBkXpc0PbUZbVOTdFu_mR_P81_nvBMhOSHh9zwnyZMkLzm85wDFhwAgIEup0MxLmVaPkgPPpEihkOXj5AAyg1QVOT9JnoVwBcBFWcmnyYkUEmQJ5SH5dbkt1uiRzbh61-Kgr63ztJ8wDq4LTM8di17PwXi7RDchnehxCzYwj9dIZBxwV0d3a42N251mQjPo2YYpMNezzr4RKTlu44C32_iWLUMc9KgjMjezZW3Rx2NTPSI7r7-xyRpkNzYOLG4LMkEGusWIgXzH0cY1PE-e9HoM-OJ-PU2-f_p4WX9JL75-Pq_PLlIjCxXTyvS9zqFCU7RdDqIDqHhXcd4b3raZkj3wzChUUmZFgQpoqJbn0KHSSmp5mrzefRfvfq4YYnPlVk9fEBqRgSgpCVURJXbKeBeCx75ZvJ203xoOzTGsZg-rodLchdUcRa_urdd2wu5B8icdAt7twA22rg_G4mzwAQPqLEVVkSUlq4gu_5-ubdTRurl26xxJKndpIHz-gf7vI_9x_9_tC8QJ</recordid><startdate>20200401</startdate><enddate>20200401</enddate><creator>Feng, Weiwei</creator><creator>Liu, Yongchao</creator><creator>Ding, Yangyang</creator><creator>Mao, Guanghua</creator><creator>Zhao, Ting</creator><creator>Chen, Kun</creator><creator>Qiu, Xuchun</creator><creator>Xu, Tong</creator><creator>Zhao, XiaoFeng</creator><creator>Wu, Xiangyang</creator><creator>Yang, Liuqing</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature</general><general>Springer Nature B.V</general><scope>AOWDO</scope><scope>BLEPL</scope><scope>DTL</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>7T2</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><orcidid>https://orcid.org/0000-0002-3856-5539</orcidid><orcidid>https://orcid.org/0000-0002-1974-1824</orcidid></search><sort><creationdate>20200401</creationdate><title>Typical neurobehavioral methods and transcriptome analysis reveal the neurotoxicity and mechanisms of di(2-ethylhexyl) phthalate on pubertal male ICR mice with type 2 diabetes mellitus</title><author>Feng, Weiwei ; Liu, Yongchao ; Ding, Yangyang ; Mao, Guanghua ; Zhao, Ting ; Chen, Kun ; Qiu, Xuchun ; Xu, Tong ; Zhao, XiaoFeng ; Wu, Xiangyang ; Yang, Liuqing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-9cffa609ec7bd602d0091d911fc1bb453f014c5e533477e50e505b160de5a53a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Amines</topic><topic>Animals</topic><topic>Biogenic amines</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Ca2+/calmodulin-dependent protein kinase II</topic><topic>Calcium ions</topic><topic>Calcium signalling</topic><topic>Cyclic AMP response element-binding protein</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2</topic><topic>Diethylhexyl Phthalate - toxicity</topic><topic>Endocrine Disruptors - toxicity</topic><topic>Environmental Health</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Exposure</topic><topic>Factorial analysis</topic><topic>Field tests</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Kinases</topic><topic>Latency</topic><topic>Life Sciences & Biomedicine</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>Nervous system</topic><topic>Nervous System - drug effects</topic><topic>Nervous System - metabolism</topic><topic>Neurotoxicity</topic><topic>Neurotoxicity Syndromes</topic><topic>Neurotransmitters</topic><topic>Occupational Medicine/Industrial Medicine</topic><topic>Open-field behavior</topic><topic>Organ Toxicity and Mechanisms</topic><topic>Pharmacology/Toxicology</topic><topic>Phosphorylation</topic><topic>Phthalates</topic><topic>Phthalic Acids</topic><topic>Protein kinase A</topic><topic>Science & Technology</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Toxicology</topic><topic>Western blotting</topic><topic>γ-Aminobutyric acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Feng, Weiwei</creatorcontrib><creatorcontrib>Liu, Yongchao</creatorcontrib><creatorcontrib>Ding, Yangyang</creatorcontrib><creatorcontrib>Mao, Guanghua</creatorcontrib><creatorcontrib>Zhao, Ting</creatorcontrib><creatorcontrib>Chen, Kun</creatorcontrib><creatorcontrib>Qiu, Xuchun</creatorcontrib><creatorcontrib>Xu, Tong</creatorcontrib><creatorcontrib>Zhao, XiaoFeng</creatorcontrib><creatorcontrib>Wu, Xiangyang</creatorcontrib><creatorcontrib>Yang, Liuqing</creatorcontrib><collection>Web of Science - Science Citation Index Expanded - 2020</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Environmental Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><jtitle>Archives of toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Feng, Weiwei</au><au>Liu, Yongchao</au><au>Ding, Yangyang</au><au>Mao, Guanghua</au><au>Zhao, Ting</au><au>Chen, Kun</au><au>Qiu, Xuchun</au><au>Xu, Tong</au><au>Zhao, XiaoFeng</au><au>Wu, Xiangyang</au><au>Yang, Liuqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Typical neurobehavioral methods and transcriptome analysis reveal the neurotoxicity and mechanisms of di(2-ethylhexyl) phthalate on pubertal male ICR mice with type 2 diabetes mellitus</atitle><jtitle>Archives of toxicology</jtitle><stitle>Arch Toxicol</stitle><stitle>ARCH TOXICOL</stitle><addtitle>Arch Toxicol</addtitle><date>2020-04-01</date><risdate>2020</risdate><volume>94</volume><issue>4</issue><spage>1279</spage><epage>1302</epage><pages>1279-1302</pages><issn>0340-5761</issn><eissn>1432-0738</eissn><abstract>In the present study, the neurotoxicity and mechanisms of di-(2-ethylhexyl) phthalate (DEHP) exposure on pubertal normal (P-normal) and pubertal type 2 diabetes mellitus (P-T2DM) mice were investigated by typical neurobehavioral methods and transcriptome analysis. Pubertal male ICR mice were orally exposed to DEHP (0.18, 1.8, 18 and 180 mg/kg/d) for 3 weeks. In Open field test, DEHP significantly increased the time in central area staying and decreased the total distance and clockwise (CW) rotation of P-normal and P-T2DM mice. Morris water maze showed that DEHP significantly increased the latency in locating platform and decreased the original platform quadrant and residence time in target quadrant of P-normal and P-T2DM mice. Transcriptome analysis results revealed the effects of DEHP exposure on neural signaling pathway including biogenic amines neurotransmitters, nerve receptors, neurobiological processes, etc. Enzyme-linked immunosorbent assay (ELISA) and western blotting results showed that DEHP significantly decreased the contents of 5-HT, cAMP, GABA and Ca
2+
, the levels of CREB, phosphorylation of PKA, ERK1/2 and CREB, increased the levels of CaM and phosphorylation of CaMKII in P-normal and P-T2DM mice. Factorial analysis results showed that P-T2DM mice were more sensitive than those of P-normal mice. The potential neurotoxicity mechanism of DEHP may be synergistically mediated by the cAMP–PKA–ERK1/2–CREB signaling and the Ca
2+
signaling pathway.
Article highlights
DEHP can cause neurotoxicity in P-normal and P-T2DM mice.
P-T2DM mice were more sensitive to DEHP than P-normal mice.
Transcriptome analysis revealed genes associated with nervous system.
DEHP may be synergistically mediated by the cAMP–PKA–ERK1/2–CREB signaling and the Ca
2+
signaling pathway.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>32303808</pmid><doi>10.1007/s00204-020-02683-9</doi><tpages>24</tpages><orcidid>https://orcid.org/0000-0002-3856-5539</orcidid><orcidid>https://orcid.org/0000-0002-1974-1824</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0340-5761 |
| ispartof | Archives of toxicology, 2020-04, Vol.94 (4), p.1279-1302 |
| issn | 0340-5761 1432-0738 |
| language | eng |
| recordid | cdi_pubmed_primary_32303808 |
| source | MEDLINE; SpringerNature Journals; Web of Science - Science Citation Index Expanded - 2020<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /> |
| subjects | Amines Animals Biogenic amines Biomedical and Life Sciences Biomedicine Ca2+/calmodulin-dependent protein kinase II Calcium ions Calcium signalling Cyclic AMP response element-binding protein Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 Diethylhexyl Phthalate - toxicity Endocrine Disruptors - toxicity Environmental Health Enzyme-linked immunosorbent assay Exposure Factorial analysis Field tests Gene expression Gene Expression Profiling Kinases Latency Life Sciences & Biomedicine Male Mice Mice, Inbred ICR Nervous system Nervous System - drug effects Nervous System - metabolism Neurotoxicity Neurotoxicity Syndromes Neurotransmitters Occupational Medicine/Industrial Medicine Open-field behavior Organ Toxicity and Mechanisms Pharmacology/Toxicology Phosphorylation Phthalates Phthalic Acids Protein kinase A Science & Technology Signal transduction Signaling Toxicology Western blotting γ-Aminobutyric acid |
| title | Typical neurobehavioral methods and transcriptome analysis reveal the neurotoxicity and mechanisms of di(2-ethylhexyl) phthalate on pubertal male ICR mice with type 2 diabetes mellitus |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-08T10%3A36%3A41IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Typical%20neurobehavioral%20methods%20and%20transcriptome%20analysis%20reveal%20the%20neurotoxicity%20and%20mechanisms%20of%20di(2-ethylhexyl)%20phthalate%20on%20pubertal%20male%20ICR%20mice%20with%20type%202%20diabetes%20mellitus&rft.jtitle=Archives%20of%20toxicology&rft.au=Feng,%20Weiwei&rft.date=2020-04-01&rft.volume=94&rft.issue=4&rft.spage=1279&rft.epage=1302&rft.pages=1279-1302&rft.issn=0340-5761&rft.eissn=1432-0738&rft_id=info:doi/10.1007/s00204-020-02683-9&rft_dat=%3Cproquest_pubme%3E2402810059%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2402810059&rft_id=info:pmid/32303808&rfr_iscdi=true |