Mechanism of Liver Injury in Mice Caused by Lanthanoids
It has been proven that higher dose of lanthanoid (Ln) can induce liver toxicities, but the mechanisms and the molecular pathogenesis are still unclear. In this study, LaCl3, CeCl3, and NdCl3 at a higher dose of 20 mg/kg body weight was injected into the abdominal cavity of ICR mice for 14 consecuti...
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| Veröffentlicht in: | Biological trace element research 2011-06, Vol.140 (3), p.317-329 |
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| creator | Fei, Min Li, Na Ze, Yuguan Liu, Jie Wang, Sisi Gong, Xiuaolan Duan, Yanmei Zhao, Xiaoyang Wang, Han Hong, Fashui |
| description | It has been proven that higher dose of lanthanoid (Ln) can induce liver toxicities, but the mechanisms and the molecular pathogenesis are still unclear. In this study, LaCl3, CeCl3, and NdCl3 at a higher dose of 20 mg/kg body weight was injected into the abdominal cavity of ICR mice for 14 consecutive days, and the inflammatory responses of liver of mice were investigated by histopathological test, real-time quantitative reverse transcription polymerase chain reaction (RT–PCR), and enzyme-linked immunosorbent assay (ELISA) methods. The results showed the significant accumulation of Ln in the liver results in liver histopathological changes and, therefore, liver malfunctions. The real-time quantitative RT–PCR and ELISA analyses showed that Ln could significantly alter the mRNA and protein expressions of several inflammatory cytokines, including nucleic factor-κB, macrophage migration inhibitory factor, tumor necrosis factor-α, interleukin-1β, interleukin-6, cross-reaction protein, interleukin-4, and interleukin-10. Our results also implied that the inflammatory responses and liver injury likely are caused by 4f shell and alterable valence properties of Ln-induced liver toxicity. |
| doi_str_mv | 10.1007/s12011-010-8698-x |
| format | Article |
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In this study, LaCl3, CeCl3, and NdCl3 at a higher dose of 20 mg/kg body weight was injected into the abdominal cavity of ICR mice for 14 consecutive days, and the inflammatory responses of liver of mice were investigated by histopathological test, real-time quantitative reverse transcription polymerase chain reaction (RT–PCR), and enzyme-linked immunosorbent assay (ELISA) methods. The results showed the significant accumulation of Ln in the liver results in liver histopathological changes and, therefore, liver malfunctions. The real-time quantitative RT–PCR and ELISA analyses showed that Ln could significantly alter the mRNA and protein expressions of several inflammatory cytokines, including nucleic factor-κB, macrophage migration inhibitory factor, tumor necrosis factor-α, interleukin-1β, interleukin-6, cross-reaction protein, interleukin-4, and interleukin-10. Our results also implied that the inflammatory responses and liver injury likely are caused by 4f shell and alterable valence properties of Ln-induced liver toxicity.</description><identifier>ISSN: 0163-4984</identifier><identifier>EISSN: 1559-0720</identifier><identifier>DOI: 10.1007/s12011-010-8698-x</identifier><identifier>PMID: 20407842</identifier><language>eng</language><publisher>New York: Springer-Verlag</publisher><subject>abdominal cavity ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biotechnology ; Body weight ; Cerium - toxicity ; cross reaction ; Enzyme-Linked Immunosorbent Assay ; hepatotoxicity ; histopathology ; inflammation ; interleukin-10 ; Interleukin-10 - genetics ; Interleukin-10 - metabolism ; interleukin-1beta ; Interleukin-1beta - genetics ; Interleukin-1beta - metabolism ; interleukin-4 ; Interleukin-4 - genetics ; Interleukin-4 - metabolism ; interleukin-6 ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Intramolecular Oxidoreductases - genetics ; Intramolecular Oxidoreductases - metabolism ; Lanthanoid Series Elements - toxicity ; Lanthanum - toxicity ; Life Sciences ; Liver ; Liver - drug effects ; Liver - metabolism ; macrophage migration inhibitory factors ; Macrophage Migration-Inhibitory Factors - genetics ; Macrophage Migration-Inhibitory Factors - metabolism ; Male ; messenger RNA ; Mice ; Neodymium - toxicity ; NF-kappa B - genetics ; NF-kappa B - metabolism ; Nutrition ; Oncology ; pathogenesis ; protein synthesis ; Reverse Transcriptase Polymerase Chain Reaction ; Rodents ; tumor necrosis factor-alpha ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Biological trace element research, 2011-06, Vol.140 (3), p.317-329</ispartof><rights>Springer Science+Business Media, LLC 2010</rights><rights>Springer Science+Business Media, LLC 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c394t-38a4819e0af09770b82af25b4aadb23c7efbcee0d0095fd9114c3800a2d40d8c3</citedby><cites>FETCH-LOGICAL-c394t-38a4819e0af09770b82af25b4aadb23c7efbcee0d0095fd9114c3800a2d40d8c3</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/s12011-010-8698-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12011-010-8698-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20407842$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fei, Min</creatorcontrib><creatorcontrib>Li, Na</creatorcontrib><creatorcontrib>Ze, Yuguan</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Wang, Sisi</creatorcontrib><creatorcontrib>Gong, Xiuaolan</creatorcontrib><creatorcontrib>Duan, Yanmei</creatorcontrib><creatorcontrib>Zhao, Xiaoyang</creatorcontrib><creatorcontrib>Wang, Han</creatorcontrib><creatorcontrib>Hong, Fashui</creatorcontrib><title>Mechanism of Liver Injury in Mice Caused by Lanthanoids</title><title>Biological trace element research</title><addtitle>Biol Trace Elem Res</addtitle><addtitle>Biol Trace Elem Res</addtitle><description>It has been proven that higher dose of lanthanoid (Ln) can induce liver toxicities, but the mechanisms and the molecular pathogenesis are still unclear. In this study, LaCl3, CeCl3, and NdCl3 at a higher dose of 20 mg/kg body weight was injected into the abdominal cavity of ICR mice for 14 consecutive days, and the inflammatory responses of liver of mice were investigated by histopathological test, real-time quantitative reverse transcription polymerase chain reaction (RT–PCR), and enzyme-linked immunosorbent assay (ELISA) methods. The results showed the significant accumulation of Ln in the liver results in liver histopathological changes and, therefore, liver malfunctions. The real-time quantitative RT–PCR and ELISA analyses showed that Ln could significantly alter the mRNA and protein expressions of several inflammatory cytokines, including nucleic factor-κB, macrophage migration inhibitory factor, tumor necrosis factor-α, interleukin-1β, interleukin-6, cross-reaction protein, interleukin-4, and interleukin-10. Our results also implied that the inflammatory responses and liver injury likely are caused by 4f shell and alterable valence properties of Ln-induced liver toxicity.</description><subject>abdominal cavity</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biotechnology</subject><subject>Body weight</subject><subject>Cerium - toxicity</subject><subject>cross reaction</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>hepatotoxicity</subject><subject>histopathology</subject><subject>inflammation</subject><subject>interleukin-10</subject><subject>Interleukin-10 - genetics</subject><subject>Interleukin-10 - metabolism</subject><subject>interleukin-1beta</subject><subject>Interleukin-1beta - genetics</subject><subject>Interleukin-1beta - metabolism</subject><subject>interleukin-4</subject><subject>Interleukin-4 - genetics</subject><subject>Interleukin-4 - metabolism</subject><subject>interleukin-6</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Intramolecular Oxidoreductases - genetics</subject><subject>Intramolecular Oxidoreductases - metabolism</subject><subject>Lanthanoid Series Elements - toxicity</subject><subject>Lanthanum - toxicity</subject><subject>Life Sciences</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>macrophage migration inhibitory factors</subject><subject>Macrophage Migration-Inhibitory Factors - genetics</subject><subject>Macrophage Migration-Inhibitory Factors - metabolism</subject><subject>Male</subject><subject>messenger RNA</subject><subject>Mice</subject><subject>Neodymium - toxicity</subject><subject>NF-kappa B - genetics</subject><subject>NF-kappa B - metabolism</subject><subject>Nutrition</subject><subject>Oncology</subject><subject>pathogenesis</subject><subject>protein synthesis</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Rodents</subject><subject>tumor necrosis factor-alpha</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - 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research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fei, Min</au><au>Li, Na</au><au>Ze, Yuguan</au><au>Liu, Jie</au><au>Wang, Sisi</au><au>Gong, Xiuaolan</au><au>Duan, Yanmei</au><au>Zhao, Xiaoyang</au><au>Wang, Han</au><au>Hong, Fashui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanism of Liver Injury in Mice Caused by Lanthanoids</atitle><jtitle>Biological trace element research</jtitle><stitle>Biol Trace Elem Res</stitle><addtitle>Biol Trace Elem Res</addtitle><date>2011-06-01</date><risdate>2011</risdate><volume>140</volume><issue>3</issue><spage>317</spage><epage>329</epage><pages>317-329</pages><issn>0163-4984</issn><eissn>1559-0720</eissn><abstract>It has been proven that higher dose of lanthanoid (Ln) can induce liver toxicities, but the mechanisms and the molecular pathogenesis are still unclear. In this study, LaCl3, CeCl3, and NdCl3 at a higher dose of 20 mg/kg body weight was injected into the abdominal cavity of ICR mice for 14 consecutive days, and the inflammatory responses of liver of mice were investigated by histopathological test, real-time quantitative reverse transcription polymerase chain reaction (RT–PCR), and enzyme-linked immunosorbent assay (ELISA) methods. The results showed the significant accumulation of Ln in the liver results in liver histopathological changes and, therefore, liver malfunctions. The real-time quantitative RT–PCR and ELISA analyses showed that Ln could significantly alter the mRNA and protein expressions of several inflammatory cytokines, including nucleic factor-κB, macrophage migration inhibitory factor, tumor necrosis factor-α, interleukin-1β, interleukin-6, cross-reaction protein, interleukin-4, and interleukin-10. Our results also implied that the inflammatory responses and liver injury likely are caused by 4f shell and alterable valence properties of Ln-induced liver toxicity.</abstract><cop>New York</cop><pub>Springer-Verlag</pub><pmid>20407842</pmid><doi>10.1007/s12011-010-8698-x</doi><tpages>13</tpages></addata></record> |
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| subjects | abdominal cavity Animals Biochemistry Biomedical and Life Sciences Biotechnology Body weight Cerium - toxicity cross reaction Enzyme-Linked Immunosorbent Assay hepatotoxicity histopathology inflammation interleukin-10 Interleukin-10 - genetics Interleukin-10 - metabolism interleukin-1beta Interleukin-1beta - genetics Interleukin-1beta - metabolism interleukin-4 Interleukin-4 - genetics Interleukin-4 - metabolism interleukin-6 Interleukin-6 - genetics Interleukin-6 - metabolism Intramolecular Oxidoreductases - genetics Intramolecular Oxidoreductases - metabolism Lanthanoid Series Elements - toxicity Lanthanum - toxicity Life Sciences Liver Liver - drug effects Liver - metabolism macrophage migration inhibitory factors Macrophage Migration-Inhibitory Factors - genetics Macrophage Migration-Inhibitory Factors - metabolism Male messenger RNA Mice Neodymium - toxicity NF-kappa B - genetics NF-kappa B - metabolism Nutrition Oncology pathogenesis protein synthesis Reverse Transcriptase Polymerase Chain Reaction Rodents tumor necrosis factor-alpha Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism |
| title | Mechanism of Liver Injury in Mice Caused by Lanthanoids |
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