Nonylphenol induces pancreatic damage in rats through mitochondrial dysfunction and oxidative stress
The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants. Due to its hydrophobicity and long half-life, NP can easily accumulate in living organisms, including humans, where it displays a ser...
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| Veröffentlicht in: | Toxicology research (Cambridge) 2017-05, Vol.6 (3), p.353-36 |
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| creator | Li, Xueji Zhou, Liting Ni, Yiping Wang, Aiqing Hu, Mingjiang Lin, Yao Hong, Chengjiao Wan, Jianmei Chen, Bin Fang, Lijun Tong, Jian Tong, Xing Tao, Shasha Tian, Hailin |
| description | The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants. Due to its hydrophobicity and long half-life, NP can easily accumulate in living organisms, including humans, where it displays a series of toxic effects. It has been widely reported that NP affects male reproduction. In addition, there is increasing evidence suggesting that NP is detrimental to various organs, including the pancreas. This study investigated the adverse effects of NP exposure on the pancreas. Sprague-Dawley rats were treated with different doses of NP for 90 consecutive days. The data suggested that the body weights of the rats treated with NP decreased, and the highest dose of NP treatment (180 mg kg
−1
) dramatically increased water consumption by rats. Meanwhile, H&E staining and immunohistochemistry indicated that islets in the pancreases shrunk when the rats were treated with the indicated doses of NP. TUNEL staining demonstrated that NP exposure up-regulated the level of apoptosis in the pancreases in a dose-dependent manner. Besides this, NP exposure inhibited the secretion of insulin and disrupted glucose tolerance. The levels of reactive oxygen species (ROS) and intracellular calcium ([Ca
2+
]
i
) in the islets were up-regulated in the groups of rats treated with NP, but the levels of Mitochondrial Membrane Potential (MMP) were down-regulated. These results suggest that NP-induced pancreatic damage in rats occurs through mitochondrial dysfunction and oxidative stress, which causes disruption of glucose tolerance and decrease in insulin secretion.
The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants. |
| doi_str_mv | 10.1039/c6tx00450d |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_1901761434</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1901761434</sourcerecordid><originalsourceid>FETCH-LOGICAL-c487t-50eb7993e7b0a84e88892877b3074c699378267f2e76f2fa7a43eab58b6b24163</originalsourceid><addsrcrecordid>eNp9ks1vFCEYhydGY5vai3cNxosxWX0HGGAuTcyqtUmjl5r0RhhgdmhmYASm6f73YrdutYdy4U2ehx8fL1X1soYPNZD2o2b5BoA2YJ5Uh7gUK9oQ8XRf48uD6jilKyiDA2akeV4dEIAWGqCHlfke_HacB-vDiJw3i7YJzcrraFV2Ghk1qY0tBEWVE8pDDMtmQJPLQQ_Bm-jUiMw29YvX2QWPlDco3DhTVl9blHK0Kb2onvVqTPb4bj6qfn79crH-tjr_cXq2_nS-0lTwvGrAdrxtieUdKEGtEKLFgvOOAKeaFcIFZrzHlrMe94orSqzqGtGxDtOakaPqZJc7L91kjbY-RzXKObpJxa0Mysn_iXeD3IRryYBh0tYl4N1dQAy_FpuynFzSdhyVt2FJEoNguBH4dq_H1bqFmrOaElrUtw_Uq7BEX16iBNYgMGAgxXq_s3QMKUXb789dg_zTarlmF5e3rf5c5Nf_3nSv_m1sEV7thJj0nt7_lcLfPMblbHryG8Q0uk0</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2010820203</pqid></control><display><type>article</type><title>Nonylphenol induces pancreatic damage in rats through mitochondrial dysfunction and oxidative stress</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>Royal Society Of Chemistry Journals 2008-</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Li, Xueji ; Zhou, Liting ; Ni, Yiping ; Wang, Aiqing ; Hu, Mingjiang ; Lin, Yao ; Hong, Chengjiao ; Wan, Jianmei ; Chen, Bin ; Fang, Lijun ; Tong, Jian ; Tong, Xing ; Tao, Shasha ; Tian, Hailin</creator><creatorcontrib>Li, Xueji ; Zhou, Liting ; Ni, Yiping ; Wang, Aiqing ; Hu, Mingjiang ; Lin, Yao ; Hong, Chengjiao ; Wan, Jianmei ; Chen, Bin ; Fang, Lijun ; Tong, Jian ; Tong, Xing ; Tao, Shasha ; Tian, Hailin</creatorcontrib><description>The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants. Due to its hydrophobicity and long half-life, NP can easily accumulate in living organisms, including humans, where it displays a series of toxic effects. It has been widely reported that NP affects male reproduction. In addition, there is increasing evidence suggesting that NP is detrimental to various organs, including the pancreas. This study investigated the adverse effects of NP exposure on the pancreas. Sprague-Dawley rats were treated with different doses of NP for 90 consecutive days. The data suggested that the body weights of the rats treated with NP decreased, and the highest dose of NP treatment (180 mg kg
−1
) dramatically increased water consumption by rats. Meanwhile, H&E staining and immunohistochemistry indicated that islets in the pancreases shrunk when the rats were treated with the indicated doses of NP. TUNEL staining demonstrated that NP exposure up-regulated the level of apoptosis in the pancreases in a dose-dependent manner. Besides this, NP exposure inhibited the secretion of insulin and disrupted glucose tolerance. The levels of reactive oxygen species (ROS) and intracellular calcium ([Ca
2+
]
i
) in the islets were up-regulated in the groups of rats treated with NP, but the levels of Mitochondrial Membrane Potential (MMP) were down-regulated. These results suggest that NP-induced pancreatic damage in rats occurs through mitochondrial dysfunction and oxidative stress, which causes disruption of glucose tolerance and decrease in insulin secretion.
The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants.</description><identifier>ISSN: 2045-452X</identifier><identifier>EISSN: 2045-4538</identifier><identifier>DOI: 10.1039/c6tx00450d</identifier><identifier>PMID: 30090504</identifier><language>eng</language><publisher>England: Royal Society of Chemistry</publisher><subject>Apoptosis ; Bioaccumulation ; Calcium ; Calcium (intracellular) ; Calcium ions ; Chemistry ; Contaminants ; Endocrine disruptors ; Exposure ; Glucose ; Glucose tolerance ; Hydrophobicity ; Immunohistochemistry ; Insulin ; Insulin secretion ; Membrane potential ; Mitochondria ; Nonylphenol ; Organs ; Oxidative stress ; Pancreas ; Rats ; Reactive oxygen species ; Rodents ; Staining ; Toxicity ; Water consumption</subject><ispartof>Toxicology research (Cambridge), 2017-05, Vol.6 (3), p.353-36</ispartof><rights>Copyright Royal Society of Chemistry 2017</rights><rights>This journal is © The Royal Society of Chemistry 2017 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-50eb7993e7b0a84e88892877b3074c699378267f2e76f2fa7a43eab58b6b24163</citedby><cites>FETCH-LOGICAL-c487t-50eb7993e7b0a84e88892877b3074c699378267f2e76f2fa7a43eab58b6b24163</cites><orcidid>0000-0002-6765-3829</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6062391/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6062391/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30090504$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Xueji</creatorcontrib><creatorcontrib>Zhou, Liting</creatorcontrib><creatorcontrib>Ni, Yiping</creatorcontrib><creatorcontrib>Wang, Aiqing</creatorcontrib><creatorcontrib>Hu, Mingjiang</creatorcontrib><creatorcontrib>Lin, Yao</creatorcontrib><creatorcontrib>Hong, Chengjiao</creatorcontrib><creatorcontrib>Wan, Jianmei</creatorcontrib><creatorcontrib>Chen, Bin</creatorcontrib><creatorcontrib>Fang, Lijun</creatorcontrib><creatorcontrib>Tong, Jian</creatorcontrib><creatorcontrib>Tong, Xing</creatorcontrib><creatorcontrib>Tao, Shasha</creatorcontrib><creatorcontrib>Tian, Hailin</creatorcontrib><title>Nonylphenol induces pancreatic damage in rats through mitochondrial dysfunction and oxidative stress</title><title>Toxicology research (Cambridge)</title><addtitle>Toxicol Res (Camb)</addtitle><description>The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants. Due to its hydrophobicity and long half-life, NP can easily accumulate in living organisms, including humans, where it displays a series of toxic effects. It has been widely reported that NP affects male reproduction. In addition, there is increasing evidence suggesting that NP is detrimental to various organs, including the pancreas. This study investigated the adverse effects of NP exposure on the pancreas. Sprague-Dawley rats were treated with different doses of NP for 90 consecutive days. The data suggested that the body weights of the rats treated with NP decreased, and the highest dose of NP treatment (180 mg kg
−1
) dramatically increased water consumption by rats. Meanwhile, H&E staining and immunohistochemistry indicated that islets in the pancreases shrunk when the rats were treated with the indicated doses of NP. TUNEL staining demonstrated that NP exposure up-regulated the level of apoptosis in the pancreases in a dose-dependent manner. Besides this, NP exposure inhibited the secretion of insulin and disrupted glucose tolerance. The levels of reactive oxygen species (ROS) and intracellular calcium ([Ca
2+
]
i
) in the islets were up-regulated in the groups of rats treated with NP, but the levels of Mitochondrial Membrane Potential (MMP) were down-regulated. These results suggest that NP-induced pancreatic damage in rats occurs through mitochondrial dysfunction and oxidative stress, which causes disruption of glucose tolerance and decrease in insulin secretion.
The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants.</description><subject>Apoptosis</subject><subject>Bioaccumulation</subject><subject>Calcium</subject><subject>Calcium (intracellular)</subject><subject>Calcium ions</subject><subject>Chemistry</subject><subject>Contaminants</subject><subject>Endocrine disruptors</subject><subject>Exposure</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>Hydrophobicity</subject><subject>Immunohistochemistry</subject><subject>Insulin</subject><subject>Insulin secretion</subject><subject>Membrane potential</subject><subject>Mitochondria</subject><subject>Nonylphenol</subject><subject>Organs</subject><subject>Oxidative stress</subject><subject>Pancreas</subject><subject>Rats</subject><subject>Reactive oxygen species</subject><subject>Rodents</subject><subject>Staining</subject><subject>Toxicity</subject><subject>Water consumption</subject><issn>2045-452X</issn><issn>2045-4538</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp9ks1vFCEYhydGY5vai3cNxosxWX0HGGAuTcyqtUmjl5r0RhhgdmhmYASm6f73YrdutYdy4U2ehx8fL1X1soYPNZD2o2b5BoA2YJ5Uh7gUK9oQ8XRf48uD6jilKyiDA2akeV4dEIAWGqCHlfke_HacB-vDiJw3i7YJzcrraFV2Ghk1qY0tBEWVE8pDDMtmQJPLQQ_Bm-jUiMw29YvX2QWPlDco3DhTVl9blHK0Kb2onvVqTPb4bj6qfn79crH-tjr_cXq2_nS-0lTwvGrAdrxtieUdKEGtEKLFgvOOAKeaFcIFZrzHlrMe94orSqzqGtGxDtOakaPqZJc7L91kjbY-RzXKObpJxa0Mysn_iXeD3IRryYBh0tYl4N1dQAy_FpuynFzSdhyVt2FJEoNguBH4dq_H1bqFmrOaElrUtw_Uq7BEX16iBNYgMGAgxXq_s3QMKUXb789dg_zTarlmF5e3rf5c5Nf_3nSv_m1sEV7thJj0nt7_lcLfPMblbHryG8Q0uk0</recordid><startdate>20170501</startdate><enddate>20170501</enddate><creator>Li, Xueji</creator><creator>Zhou, Liting</creator><creator>Ni, Yiping</creator><creator>Wang, Aiqing</creator><creator>Hu, Mingjiang</creator><creator>Lin, Yao</creator><creator>Hong, Chengjiao</creator><creator>Wan, Jianmei</creator><creator>Chen, Bin</creator><creator>Fang, Lijun</creator><creator>Tong, Jian</creator><creator>Tong, Xing</creator><creator>Tao, Shasha</creator><creator>Tian, Hailin</creator><general>Royal Society of Chemistry</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6765-3829</orcidid></search><sort><creationdate>20170501</creationdate><title>Nonylphenol induces pancreatic damage in rats through mitochondrial dysfunction and oxidative stress</title><author>Li, Xueji ; Zhou, Liting ; Ni, Yiping ; Wang, Aiqing ; Hu, Mingjiang ; Lin, Yao ; Hong, Chengjiao ; Wan, Jianmei ; Chen, Bin ; Fang, Lijun ; Tong, Jian ; Tong, Xing ; Tao, Shasha ; Tian, Hailin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c487t-50eb7993e7b0a84e88892877b3074c699378267f2e76f2fa7a43eab58b6b24163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Apoptosis</topic><topic>Bioaccumulation</topic><topic>Calcium</topic><topic>Calcium (intracellular)</topic><topic>Calcium ions</topic><topic>Chemistry</topic><topic>Contaminants</topic><topic>Endocrine disruptors</topic><topic>Exposure</topic><topic>Glucose</topic><topic>Glucose tolerance</topic><topic>Hydrophobicity</topic><topic>Immunohistochemistry</topic><topic>Insulin</topic><topic>Insulin secretion</topic><topic>Membrane potential</topic><topic>Mitochondria</topic><topic>Nonylphenol</topic><topic>Organs</topic><topic>Oxidative stress</topic><topic>Pancreas</topic><topic>Rats</topic><topic>Reactive oxygen species</topic><topic>Rodents</topic><topic>Staining</topic><topic>Toxicity</topic><topic>Water consumption</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Xueji</creatorcontrib><creatorcontrib>Zhou, Liting</creatorcontrib><creatorcontrib>Ni, Yiping</creatorcontrib><creatorcontrib>Wang, Aiqing</creatorcontrib><creatorcontrib>Hu, Mingjiang</creatorcontrib><creatorcontrib>Lin, Yao</creatorcontrib><creatorcontrib>Hong, Chengjiao</creatorcontrib><creatorcontrib>Wan, Jianmei</creatorcontrib><creatorcontrib>Chen, Bin</creatorcontrib><creatorcontrib>Fang, Lijun</creatorcontrib><creatorcontrib>Tong, Jian</creatorcontrib><creatorcontrib>Tong, Xing</creatorcontrib><creatorcontrib>Tao, Shasha</creatorcontrib><creatorcontrib>Tian, Hailin</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Toxicology research (Cambridge)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Xueji</au><au>Zhou, Liting</au><au>Ni, Yiping</au><au>Wang, Aiqing</au><au>Hu, Mingjiang</au><au>Lin, Yao</au><au>Hong, Chengjiao</au><au>Wan, Jianmei</au><au>Chen, Bin</au><au>Fang, Lijun</au><au>Tong, Jian</au><au>Tong, Xing</au><au>Tao, Shasha</au><au>Tian, Hailin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nonylphenol induces pancreatic damage in rats through mitochondrial dysfunction and oxidative stress</atitle><jtitle>Toxicology research (Cambridge)</jtitle><addtitle>Toxicol Res (Camb)</addtitle><date>2017-05-01</date><risdate>2017</risdate><volume>6</volume><issue>3</issue><spage>353</spage><epage>36</epage><pages>353-36</pages><issn>2045-452X</issn><eissn>2045-4538</eissn><abstract>The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants. Due to its hydrophobicity and long half-life, NP can easily accumulate in living organisms, including humans, where it displays a series of toxic effects. It has been widely reported that NP affects male reproduction. In addition, there is increasing evidence suggesting that NP is detrimental to various organs, including the pancreas. This study investigated the adverse effects of NP exposure on the pancreas. Sprague-Dawley rats were treated with different doses of NP for 90 consecutive days. The data suggested that the body weights of the rats treated with NP decreased, and the highest dose of NP treatment (180 mg kg
−1
) dramatically increased water consumption by rats. Meanwhile, H&E staining and immunohistochemistry indicated that islets in the pancreases shrunk when the rats were treated with the indicated doses of NP. TUNEL staining demonstrated that NP exposure up-regulated the level of apoptosis in the pancreases in a dose-dependent manner. Besides this, NP exposure inhibited the secretion of insulin and disrupted glucose tolerance. The levels of reactive oxygen species (ROS) and intracellular calcium ([Ca
2+
]
i
) in the islets were up-regulated in the groups of rats treated with NP, but the levels of Mitochondrial Membrane Potential (MMP) were down-regulated. These results suggest that NP-induced pancreatic damage in rats occurs through mitochondrial dysfunction and oxidative stress, which causes disruption of glucose tolerance and decrease in insulin secretion.
The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants.</abstract><cop>England</cop><pub>Royal Society of Chemistry</pub><pmid>30090504</pmid><doi>10.1039/c6tx00450d</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-6765-3829</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); Royal Society Of Chemistry Journals 2008-; PubMed Central; Alma/SFX Local Collection |
| subjects | Apoptosis Bioaccumulation Calcium Calcium (intracellular) Calcium ions Chemistry Contaminants Endocrine disruptors Exposure Glucose Glucose tolerance Hydrophobicity Immunohistochemistry Insulin Insulin secretion Membrane potential Mitochondria Nonylphenol Organs Oxidative stress Pancreas Rats Reactive oxygen species Rodents Staining Toxicity Water consumption |
| title | Nonylphenol induces pancreatic damage in rats through mitochondrial dysfunction and oxidative stress |
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