Adenosines scavenged hydroxyl radicals and prevented posttraumatic epilepsy
Intracortical injection of iron ions has been used as a model of posttraumatic epilepsy. Oxidation of lipids in neural membranes by reactive oxygen species, especially hydroxyl radicals (OH), is involved in the mechanisms responsible for iron-induced seizures. We examined the scavenging effects of a...
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| Veröffentlicht in: | Free radical biology & medicine 1995-10, Vol.19 (4), p.473-479 |
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| creator | Yokoi, Isao Toma, Junji Liu, Jiankang Kabuto, Hideaki Mori, Akitane |
| description | Intracortical injection of iron ions has been used as a model of posttraumatic epilepsy. Oxidation of lipids in neural membranes by reactive oxygen species, especially hydroxyl radicals (OH), is involved in the mechanisms responsible for iron-induced seizures. We examined the scavenging effects of adenosine (Ado) and 2-chloroadenosine (Cl-Ado) on OH radicals and superoxide (O
2
·-) using an electron spin resonance (ESR) spectrometer, and the occurrence of epileptic discharges in electrocorticogram (ECoG) induced by FeCl
3 injection into the sensorimotor cortex of rats. Though DMPO-O
2
·- spin adducts generated by the hypoxanthine-xanthine oxidase system were not quenched by Ado or Cl-Ado, 5 mM of each showed a quenching effect on DMPO-OH spin adducts (5.3 × 10
16 spins/ml) generated by the Fenton reagent. In ECoG of rats, spike discharges appeared 15–45 min after FeCl
3 injection (500 nmol) into the sensorimotor cortex, and polyspikes and/or ictal patterns were observed 70–90 min after the injection. Cl-Ado (1 mg/kg) or Ado (5 mg/kg) injected intraperitoneally 30 min prior to the FeC1
3 injection suppressed or delayed the occurrence of epileptic discharges induced by FeC1
3. Cl-Ado and Ado may suppress the occurrence of epileptic discharges by scavenging OH and by their anticonvulsant effect. |
| doi_str_mv | 10.1016/0891-5849(95)00050-8 |
| format | Article |
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2
·-) using an electron spin resonance (ESR) spectrometer, and the occurrence of epileptic discharges in electrocorticogram (ECoG) induced by FeCl
3 injection into the sensorimotor cortex of rats. Though DMPO-O
2
·- spin adducts generated by the hypoxanthine-xanthine oxidase system were not quenched by Ado or Cl-Ado, 5 mM of each showed a quenching effect on DMPO-OH spin adducts (5.3 × 10
16 spins/ml) generated by the Fenton reagent. In ECoG of rats, spike discharges appeared 15–45 min after FeCl
3 injection (500 nmol) into the sensorimotor cortex, and polyspikes and/or ictal patterns were observed 70–90 min after the injection. Cl-Ado (1 mg/kg) or Ado (5 mg/kg) injected intraperitoneally 30 min prior to the FeC1
3 injection suppressed or delayed the occurrence of epileptic discharges induced by FeC1
3. Cl-Ado and Ado may suppress the occurrence of epileptic discharges by scavenging OH and by their anticonvulsant effect.</description><identifier>ISSN: 0891-5849</identifier><identifier>EISSN: 1873-4596</identifier><identifier>DOI: 10.1016/0891-5849(95)00050-8</identifier><identifier>PMID: 7590396</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>2-Chloroadenosine ; 2-Chloroadenosine - pharmacology ; 2-Chloroadenosine - therapeutic use ; Adenosine ; Adenosine - pharmacology ; Adenosine - therapeutic use ; Animals ; Chlorides ; Cyclic N-Oxides ; Electroencephalography ; Electron Spin Resonance Spectroscopy ; Epilepsy, Post-Traumatic - chemically induced ; Epilepsy, Post-Traumatic - prevention & control ; Experimental epilepsy ; Ferric Compounds ; Free Radical Scavengers ; Free Radicals ; Hydroxyl Radical - metabolism ; Hydroxyl radical scavenger ; Hypoxanthine ; Hypoxanthines - metabolism ; Iron-induced epilepsy ; Male ; Posttraumatic epilepsy ; Rats ; Rats, Sprague-Dawley ; Spin Labels ; Superoxides - metabolism ; Xanthine Oxidase - metabolism</subject><ispartof>Free radical biology & medicine, 1995-10, Vol.19 (4), p.473-479</ispartof><rights>1995</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c388t-c622c022d86f011abe9ab2473106d575372694b63a7ef77c0cd1434deba1086e3</citedby><cites>FETCH-LOGICAL-c388t-c622c022d86f011abe9ab2473106d575372694b63a7ef77c0cd1434deba1086e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0891-5849(95)00050-8$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27922,27923,45993</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7590396$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yokoi, Isao</creatorcontrib><creatorcontrib>Toma, Junji</creatorcontrib><creatorcontrib>Liu, Jiankang</creatorcontrib><creatorcontrib>Kabuto, Hideaki</creatorcontrib><creatorcontrib>Mori, Akitane</creatorcontrib><title>Adenosines scavenged hydroxyl radicals and prevented posttraumatic epilepsy</title><title>Free radical biology & medicine</title><addtitle>Free Radic Biol Med</addtitle><description>Intracortical injection of iron ions has been used as a model of posttraumatic epilepsy. Oxidation of lipids in neural membranes by reactive oxygen species, especially hydroxyl radicals (OH), is involved in the mechanisms responsible for iron-induced seizures. We examined the scavenging effects of adenosine (Ado) and 2-chloroadenosine (Cl-Ado) on OH radicals and superoxide (O
2
·-) using an electron spin resonance (ESR) spectrometer, and the occurrence of epileptic discharges in electrocorticogram (ECoG) induced by FeCl
3 injection into the sensorimotor cortex of rats. Though DMPO-O
2
·- spin adducts generated by the hypoxanthine-xanthine oxidase system were not quenched by Ado or Cl-Ado, 5 mM of each showed a quenching effect on DMPO-OH spin adducts (5.3 × 10
16 spins/ml) generated by the Fenton reagent. In ECoG of rats, spike discharges appeared 15–45 min after FeCl
3 injection (500 nmol) into the sensorimotor cortex, and polyspikes and/or ictal patterns were observed 70–90 min after the injection. Cl-Ado (1 mg/kg) or Ado (5 mg/kg) injected intraperitoneally 30 min prior to the FeC1
3 injection suppressed or delayed the occurrence of epileptic discharges induced by FeC1
3. Cl-Ado and Ado may suppress the occurrence of epileptic discharges by scavenging OH and by their anticonvulsant effect.</description><subject>2-Chloroadenosine</subject><subject>2-Chloroadenosine - pharmacology</subject><subject>2-Chloroadenosine - therapeutic use</subject><subject>Adenosine</subject><subject>Adenosine - pharmacology</subject><subject>Adenosine - therapeutic use</subject><subject>Animals</subject><subject>Chlorides</subject><subject>Cyclic N-Oxides</subject><subject>Electroencephalography</subject><subject>Electron Spin Resonance Spectroscopy</subject><subject>Epilepsy, Post-Traumatic - chemically induced</subject><subject>Epilepsy, Post-Traumatic - prevention & control</subject><subject>Experimental epilepsy</subject><subject>Ferric Compounds</subject><subject>Free Radical Scavengers</subject><subject>Free Radicals</subject><subject>Hydroxyl Radical - metabolism</subject><subject>Hydroxyl radical scavenger</subject><subject>Hypoxanthine</subject><subject>Hypoxanthines - metabolism</subject><subject>Iron-induced epilepsy</subject><subject>Male</subject><subject>Posttraumatic epilepsy</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Spin Labels</subject><subject>Superoxides - metabolism</subject><subject>Xanthine Oxidase - metabolism</subject><issn>0891-5849</issn><issn>1873-4596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtOwzAQRS0EKqXwByBlhWARsOP4tUGqKl6iEhtYW449AaM0CXZSkb8npVWXrGZxz53RHITOCb4hmPBbLBVJmczVlWLXGGOGU3mApkQKmuZM8UM03SPH6CTGrxHKGZUTNBFMYar4FL3MHdRN9DXEJFqzhvoDXPI5uND8DFUSjPPWVDExtUvaAGPejXnbxK4Lpl-ZztsEWl9BG4dTdFSOLJzt5gy9P9y_LZ7S5evj82K-TC2VskstzzKLs8xJXmJCTAHKFFkuKMHcMcGoyLjKC06NgFIIi60jOc0dFIZgyYHO0OV2bxua7x5ip1c-WqgqU0PTR00EJhkbNcxQvgVtaGIMUOo2-JUJgyZYbxzqjSC9EaQV038OtRxrF7v9fbECty_tpI353TaH8cm1h6Cj9VBbcD6A7bRr_P8HfgGLqoE1</recordid><startdate>19951001</startdate><enddate>19951001</enddate><creator>Yokoi, Isao</creator><creator>Toma, Junji</creator><creator>Liu, Jiankang</creator><creator>Kabuto, Hideaki</creator><creator>Mori, Akitane</creator><general>Elsevier Inc</general><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>7TK</scope></search><sort><creationdate>19951001</creationdate><title>Adenosines scavenged hydroxyl radicals and prevented posttraumatic epilepsy</title><author>Yokoi, Isao ; Toma, Junji ; Liu, Jiankang ; Kabuto, Hideaki ; Mori, Akitane</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-c622c022d86f011abe9ab2473106d575372694b63a7ef77c0cd1434deba1086e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>2-Chloroadenosine</topic><topic>2-Chloroadenosine - pharmacology</topic><topic>2-Chloroadenosine - therapeutic use</topic><topic>Adenosine</topic><topic>Adenosine - pharmacology</topic><topic>Adenosine - therapeutic use</topic><topic>Animals</topic><topic>Chlorides</topic><topic>Cyclic N-Oxides</topic><topic>Electroencephalography</topic><topic>Electron Spin Resonance Spectroscopy</topic><topic>Epilepsy, Post-Traumatic - chemically induced</topic><topic>Epilepsy, Post-Traumatic - prevention & control</topic><topic>Experimental epilepsy</topic><topic>Ferric Compounds</topic><topic>Free Radical Scavengers</topic><topic>Free Radicals</topic><topic>Hydroxyl Radical - metabolism</topic><topic>Hydroxyl radical scavenger</topic><topic>Hypoxanthine</topic><topic>Hypoxanthines - metabolism</topic><topic>Iron-induced epilepsy</topic><topic>Male</topic><topic>Posttraumatic epilepsy</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Spin Labels</topic><topic>Superoxides - metabolism</topic><topic>Xanthine Oxidase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yokoi, Isao</creatorcontrib><creatorcontrib>Toma, Junji</creatorcontrib><creatorcontrib>Liu, Jiankang</creatorcontrib><creatorcontrib>Kabuto, Hideaki</creatorcontrib><creatorcontrib>Mori, Akitane</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Free radical biology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yokoi, Isao</au><au>Toma, Junji</au><au>Liu, Jiankang</au><au>Kabuto, Hideaki</au><au>Mori, Akitane</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adenosines scavenged hydroxyl radicals and prevented posttraumatic epilepsy</atitle><jtitle>Free radical biology & medicine</jtitle><addtitle>Free Radic Biol Med</addtitle><date>1995-10-01</date><risdate>1995</risdate><volume>19</volume><issue>4</issue><spage>473</spage><epage>479</epage><pages>473-479</pages><issn>0891-5849</issn><eissn>1873-4596</eissn><abstract>Intracortical injection of iron ions has been used as a model of posttraumatic epilepsy. Oxidation of lipids in neural membranes by reactive oxygen species, especially hydroxyl radicals (OH), is involved in the mechanisms responsible for iron-induced seizures. We examined the scavenging effects of adenosine (Ado) and 2-chloroadenosine (Cl-Ado) on OH radicals and superoxide (O
2
·-) using an electron spin resonance (ESR) spectrometer, and the occurrence of epileptic discharges in electrocorticogram (ECoG) induced by FeCl
3 injection into the sensorimotor cortex of rats. Though DMPO-O
2
·- spin adducts generated by the hypoxanthine-xanthine oxidase system were not quenched by Ado or Cl-Ado, 5 mM of each showed a quenching effect on DMPO-OH spin adducts (5.3 × 10
16 spins/ml) generated by the Fenton reagent. In ECoG of rats, spike discharges appeared 15–45 min after FeCl
3 injection (500 nmol) into the sensorimotor cortex, and polyspikes and/or ictal patterns were observed 70–90 min after the injection. Cl-Ado (1 mg/kg) or Ado (5 mg/kg) injected intraperitoneally 30 min prior to the FeC1
3 injection suppressed or delayed the occurrence of epileptic discharges induced by FeC1
3. Cl-Ado and Ado may suppress the occurrence of epileptic discharges by scavenging OH and by their anticonvulsant effect.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>7590396</pmid><doi>10.1016/0891-5849(95)00050-8</doi><tpages>7</tpages></addata></record> |
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| subjects | 2-Chloroadenosine 2-Chloroadenosine - pharmacology 2-Chloroadenosine - therapeutic use Adenosine Adenosine - pharmacology Adenosine - therapeutic use Animals Chlorides Cyclic N-Oxides Electroencephalography Electron Spin Resonance Spectroscopy Epilepsy, Post-Traumatic - chemically induced Epilepsy, Post-Traumatic - prevention & control Experimental epilepsy Ferric Compounds Free Radical Scavengers Free Radicals Hydroxyl Radical - metabolism Hydroxyl radical scavenger Hypoxanthine Hypoxanthines - metabolism Iron-induced epilepsy Male Posttraumatic epilepsy Rats Rats, Sprague-Dawley Spin Labels Superoxides - metabolism Xanthine Oxidase - metabolism |
| title | Adenosines scavenged hydroxyl radicals and prevented posttraumatic epilepsy |
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