Biochemical Changes in the Central Nervous System of Rats Exposed to 1-Bromopropane for Seven Days
1-Bromopropane is used widely as an alternative to ozone-depleting solvents. The neurotoxic effects of this agent have been described in humans and experimental animals. Here we investigated the underlying mechanisms of the neurotoxic effects of 1-bromopropane by examining the initial biochemical ch...
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| Veröffentlicht in: | Toxicological sciences 2002-05, Vol.67 (1), p.114-120 |
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| creator | Wang, Hailan Ichihara, Gaku Ito, Hidenori Kato, Kanefusa Kitoh, Junzoh Yamada, Tetsuya Yu, Xiaozhong Tsuboi, Seiji Moriyama, Yoshinori Sakatani, Rie Shibata, Eiji Kamijima, Michihiro Itohara, Seiichiro Takeuchi, Yasuhiro |
| description | 1-Bromopropane is used widely as an alternative to ozone-depleting solvents. The neurotoxic effects of this agent have been described in humans and experimental animals. Here we investigated the underlying mechanisms of the neurotoxic effects of 1-bromopropane by examining the initial biochemical changes in the central nervous system. Four groups of 9 Wistar male rats each were exposed to 200, 400, or 800 ppm 1-bromopropane or only fresh air, 8 h per day for 7 days. At the end of the experiment, the cerebrum, cerebellum, brain stem and lumbar enlargement of the spinal cord were dissected out from each rat (n = 8) for biochemical analyses. Morphological examinations of the nervous system were performed in the remaining rat of each group. 1-Bromopropane dose-dependently decreased neurospecific γ-enolase, total glutathione, and nonprotein sulfhydryl groups in the cerebrum and cerebellum. Creatine kinase activity decreased dose-dependently in the brain and spinal cord. Histopathological examination showed swelling of preterminal axons in gracile nucleus and degeneration of myelin in peripheral nerves. Our results of low levels of γ-enolase suggested that 1-bromopropane might primarily cause functional or cellular loss of neurons in the cerebrum and cerebellum. Glutathione depletion or modification to functional proteins containing a sulfhydryl base as a critical site might be the underlying mechanism of 1-bromopropane neurotoxicity. |
| doi_str_mv | 10.1093/toxsci/67.1.114 |
| format | Article |
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The neurotoxic effects of this agent have been described in humans and experimental animals. Here we investigated the underlying mechanisms of the neurotoxic effects of 1-bromopropane by examining the initial biochemical changes in the central nervous system. Four groups of 9 Wistar male rats each were exposed to 200, 400, or 800 ppm 1-bromopropane or only fresh air, 8 h per day for 7 days. At the end of the experiment, the cerebrum, cerebellum, brain stem and lumbar enlargement of the spinal cord were dissected out from each rat (n = 8) for biochemical analyses. Morphological examinations of the nervous system were performed in the remaining rat of each group. 1-Bromopropane dose-dependently decreased neurospecific γ-enolase, total glutathione, and nonprotein sulfhydryl groups in the cerebrum and cerebellum. Creatine kinase activity decreased dose-dependently in the brain and spinal cord. Histopathological examination showed swelling of preterminal axons in gracile nucleus and degeneration of myelin in peripheral nerves. Our results of low levels of γ-enolase suggested that 1-bromopropane might primarily cause functional or cellular loss of neurons in the cerebrum and cerebellum. Glutathione depletion or modification to functional proteins containing a sulfhydryl base as a critical site might be the underlying mechanism of 1-bromopropane neurotoxicity.</description><identifier>ISSN: 1096-6080</identifier><identifier>EISSN: 1096-0929</identifier><identifier>DOI: 10.1093/toxsci/67.1.114</identifier><identifier>PMID: 11961224</identifier><identifier>CODEN: TOSCF2</identifier><language>eng</language><publisher>Cary, NC: Oxford University Press</publisher><subject>1-bromopropane ; Animals ; Biological and medical sciences ; Body Weight - drug effects ; Brain - drug effects ; Brain - metabolism ; Brain - pathology ; Chemical and industrial products toxicology. Toxic occupational diseases ; creatine kinase ; Creatine Kinase - metabolism ; Dose-Response Relationship, Drug ; glutathione ; Glutathione - metabolism ; Hydrocarbons, Brominated - toxicity ; Male ; Medical sciences ; neurotoxicity ; Organ Size - drug effects ; peripheral nerve ; Phosphopyruvate Hydratase - metabolism ; Rats ; Rats, Wistar ; Solvents - toxicity ; Specific Pathogen-Free Organisms ; Spinal Cord - drug effects ; Spinal Cord - metabolism ; Spinal Cord - pathology ; Tibial Nerve - drug effects ; Tibial Nerve - metabolism ; Toxicity Tests ; Toxicology ; Various organic compounds ; γ-enolase</subject><ispartof>Toxicological sciences, 2002-05, Vol.67 (1), p.114-120</ispartof><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c501t-3e78fa20db949e8f31feee9968a911a4b1f8892f469f4ac9df59112f913d68113</citedby><cites>FETCH-LOGICAL-c501t-3e78fa20db949e8f31feee9968a911a4b1f8892f469f4ac9df59112f913d68113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14186555$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11961224$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Hailan</creatorcontrib><creatorcontrib>Ichihara, Gaku</creatorcontrib><creatorcontrib>Ito, Hidenori</creatorcontrib><creatorcontrib>Kato, Kanefusa</creatorcontrib><creatorcontrib>Kitoh, Junzoh</creatorcontrib><creatorcontrib>Yamada, Tetsuya</creatorcontrib><creatorcontrib>Yu, Xiaozhong</creatorcontrib><creatorcontrib>Tsuboi, Seiji</creatorcontrib><creatorcontrib>Moriyama, Yoshinori</creatorcontrib><creatorcontrib>Sakatani, Rie</creatorcontrib><creatorcontrib>Shibata, Eiji</creatorcontrib><creatorcontrib>Kamijima, Michihiro</creatorcontrib><creatorcontrib>Itohara, Seiichiro</creatorcontrib><creatorcontrib>Takeuchi, Yasuhiro</creatorcontrib><title>Biochemical Changes in the Central Nervous System of Rats Exposed to 1-Bromopropane for Seven Days</title><title>Toxicological sciences</title><addtitle>Toxicol. Sci</addtitle><description>1-Bromopropane is used widely as an alternative to ozone-depleting solvents. The neurotoxic effects of this agent have been described in humans and experimental animals. Here we investigated the underlying mechanisms of the neurotoxic effects of 1-bromopropane by examining the initial biochemical changes in the central nervous system. Four groups of 9 Wistar male rats each were exposed to 200, 400, or 800 ppm 1-bromopropane or only fresh air, 8 h per day for 7 days. At the end of the experiment, the cerebrum, cerebellum, brain stem and lumbar enlargement of the spinal cord were dissected out from each rat (n = 8) for biochemical analyses. Morphological examinations of the nervous system were performed in the remaining rat of each group. 1-Bromopropane dose-dependently decreased neurospecific γ-enolase, total glutathione, and nonprotein sulfhydryl groups in the cerebrum and cerebellum. Creatine kinase activity decreased dose-dependently in the brain and spinal cord. Histopathological examination showed swelling of preterminal axons in gracile nucleus and degeneration of myelin in peripheral nerves. Our results of low levels of γ-enolase suggested that 1-bromopropane might primarily cause functional or cellular loss of neurons in the cerebrum and cerebellum. Glutathione depletion or modification to functional proteins containing a sulfhydryl base as a critical site might be the underlying mechanism of 1-bromopropane neurotoxicity.</description><subject>1-bromopropane</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Body Weight - drug effects</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>creatine kinase</subject><subject>Creatine Kinase - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>glutathione</subject><subject>Glutathione - metabolism</subject><subject>Hydrocarbons, Brominated - toxicity</subject><subject>Male</subject><subject>Medical sciences</subject><subject>neurotoxicity</subject><subject>Organ Size - drug effects</subject><subject>peripheral nerve</subject><subject>Phosphopyruvate Hydratase - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Solvents - toxicity</subject><subject>Specific Pathogen-Free Organisms</subject><subject>Spinal Cord - drug effects</subject><subject>Spinal Cord - metabolism</subject><subject>Spinal Cord - pathology</subject><subject>Tibial Nerve - drug effects</subject><subject>Tibial Nerve - metabolism</subject><subject>Toxicity Tests</subject><subject>Toxicology</subject><subject>Various organic compounds</subject><subject>γ-enolase</subject><issn>1096-6080</issn><issn>1096-0929</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMtOwzAQRS0E4r1mh7yBXVpPnLj2EsqjSAUkChJiY7nJmAaauNgpav8eo0awsnV9PHN1CDkB1gOmeL91q1BUfTHoQQ8g2yL7MRYJU6na7u6CSbZHDkL4YAxAMLVL9gCUgDTN9sn0snLFDOuqMHM6nJnmHQOtGtrOkA6xaX2MH9B_u2Wgk3VosabO0ifTBnq9WriAJW0dheTSu9otvFuYBql1nk7wGxt6ZdbhiOxYMw943J2H5OXm-nk4SsaPt3fDi3FS5AzahONAWpOycqoyhdJysIiolJBGAZhsClZKldpMKJuZQpU2j3lqFfBSSAB-SM43c2ONryWGVtdVKHA-j5VifQ0y44JLGcH-Biy8C8Gj1Qtf1cavNTD9q1VvtGox0KCj1vjjtBu9nNZY_vOdxwicdYAJ0aT1pimq8M9lIEWe55FLNlwVVa7-3o3_jMv4INej1zd9A3yST-5vteQ_AfOQhg</recordid><startdate>20020501</startdate><enddate>20020501</enddate><creator>Wang, Hailan</creator><creator>Ichihara, Gaku</creator><creator>Ito, Hidenori</creator><creator>Kato, Kanefusa</creator><creator>Kitoh, Junzoh</creator><creator>Yamada, Tetsuya</creator><creator>Yu, Xiaozhong</creator><creator>Tsuboi, Seiji</creator><creator>Moriyama, Yoshinori</creator><creator>Sakatani, Rie</creator><creator>Shibata, Eiji</creator><creator>Kamijima, Michihiro</creator><creator>Itohara, Seiichiro</creator><creator>Takeuchi, Yasuhiro</creator><general>Oxford University Press</general><scope>BSCLL</scope><scope>IQODW</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>7U7</scope><scope>C1K</scope></search><sort><creationdate>20020501</creationdate><title>Biochemical Changes in the Central Nervous System of Rats Exposed to 1-Bromopropane for Seven Days</title><author>Wang, Hailan ; Ichihara, Gaku ; Ito, Hidenori ; Kato, Kanefusa ; Kitoh, Junzoh ; Yamada, Tetsuya ; Yu, Xiaozhong ; Tsuboi, Seiji ; Moriyama, Yoshinori ; Sakatani, Rie ; Shibata, Eiji ; Kamijima, Michihiro ; Itohara, Seiichiro ; Takeuchi, Yasuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c501t-3e78fa20db949e8f31feee9968a911a4b1f8892f469f4ac9df59112f913d68113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>1-bromopropane</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Body Weight - drug effects</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>creatine kinase</topic><topic>Creatine Kinase - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>glutathione</topic><topic>Glutathione - metabolism</topic><topic>Hydrocarbons, Brominated - toxicity</topic><topic>Male</topic><topic>Medical sciences</topic><topic>neurotoxicity</topic><topic>Organ Size - drug effects</topic><topic>peripheral nerve</topic><topic>Phosphopyruvate Hydratase - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Solvents - toxicity</topic><topic>Specific Pathogen-Free Organisms</topic><topic>Spinal Cord - drug effects</topic><topic>Spinal Cord - metabolism</topic><topic>Spinal Cord - pathology</topic><topic>Tibial Nerve - drug effects</topic><topic>Tibial Nerve - metabolism</topic><topic>Toxicity Tests</topic><topic>Toxicology</topic><topic>Various organic compounds</topic><topic>γ-enolase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Hailan</creatorcontrib><creatorcontrib>Ichihara, Gaku</creatorcontrib><creatorcontrib>Ito, Hidenori</creatorcontrib><creatorcontrib>Kato, Kanefusa</creatorcontrib><creatorcontrib>Kitoh, Junzoh</creatorcontrib><creatorcontrib>Yamada, Tetsuya</creatorcontrib><creatorcontrib>Yu, Xiaozhong</creatorcontrib><creatorcontrib>Tsuboi, Seiji</creatorcontrib><creatorcontrib>Moriyama, Yoshinori</creatorcontrib><creatorcontrib>Sakatani, Rie</creatorcontrib><creatorcontrib>Shibata, Eiji</creatorcontrib><creatorcontrib>Kamijima, Michihiro</creatorcontrib><creatorcontrib>Itohara, Seiichiro</creatorcontrib><creatorcontrib>Takeuchi, Yasuhiro</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Toxicological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Hailan</au><au>Ichihara, Gaku</au><au>Ito, Hidenori</au><au>Kato, Kanefusa</au><au>Kitoh, Junzoh</au><au>Yamada, Tetsuya</au><au>Yu, Xiaozhong</au><au>Tsuboi, Seiji</au><au>Moriyama, Yoshinori</au><au>Sakatani, Rie</au><au>Shibata, Eiji</au><au>Kamijima, Michihiro</au><au>Itohara, Seiichiro</au><au>Takeuchi, Yasuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biochemical Changes in the Central Nervous System of Rats Exposed to 1-Bromopropane for Seven Days</atitle><jtitle>Toxicological sciences</jtitle><addtitle>Toxicol. Sci</addtitle><date>2002-05-01</date><risdate>2002</risdate><volume>67</volume><issue>1</issue><spage>114</spage><epage>120</epage><pages>114-120</pages><issn>1096-6080</issn><eissn>1096-0929</eissn><coden>TOSCF2</coden><abstract>1-Bromopropane is used widely as an alternative to ozone-depleting solvents. The neurotoxic effects of this agent have been described in humans and experimental animals. Here we investigated the underlying mechanisms of the neurotoxic effects of 1-bromopropane by examining the initial biochemical changes in the central nervous system. Four groups of 9 Wistar male rats each were exposed to 200, 400, or 800 ppm 1-bromopropane or only fresh air, 8 h per day for 7 days. At the end of the experiment, the cerebrum, cerebellum, brain stem and lumbar enlargement of the spinal cord were dissected out from each rat (n = 8) for biochemical analyses. Morphological examinations of the nervous system were performed in the remaining rat of each group. 1-Bromopropane dose-dependently decreased neurospecific γ-enolase, total glutathione, and nonprotein sulfhydryl groups in the cerebrum and cerebellum. Creatine kinase activity decreased dose-dependently in the brain and spinal cord. Histopathological examination showed swelling of preterminal axons in gracile nucleus and degeneration of myelin in peripheral nerves. Our results of low levels of γ-enolase suggested that 1-bromopropane might primarily cause functional or cellular loss of neurons in the cerebrum and cerebellum. Glutathione depletion or modification to functional proteins containing a sulfhydryl base as a critical site might be the underlying mechanism of 1-bromopropane neurotoxicity.</abstract><cop>Cary, NC</cop><pub>Oxford University Press</pub><pmid>11961224</pmid><doi>10.1093/toxsci/67.1.114</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-bromopropane Animals Biological and medical sciences Body Weight - drug effects Brain - drug effects Brain - metabolism Brain - pathology Chemical and industrial products toxicology. Toxic occupational diseases creatine kinase Creatine Kinase - metabolism Dose-Response Relationship, Drug glutathione Glutathione - metabolism Hydrocarbons, Brominated - toxicity Male Medical sciences neurotoxicity Organ Size - drug effects peripheral nerve Phosphopyruvate Hydratase - metabolism Rats Rats, Wistar Solvents - toxicity Specific Pathogen-Free Organisms Spinal Cord - drug effects Spinal Cord - metabolism Spinal Cord - pathology Tibial Nerve - drug effects Tibial Nerve - metabolism Toxicity Tests Toxicology Various organic compounds γ-enolase |
| title | Biochemical Changes in the Central Nervous System of Rats Exposed to 1-Bromopropane for Seven Days |
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