Vitamin E and β-carotene protect against ethanol combined with ischemia in an embryonic rat hippocampal culture model of fetal alcohol syndrome
Neurodevelopmental damage can occur as a result of in utero exposure to alcohol. Oxidative stress processes are one of many proposed mechanisms thought to contribute to nervous system dysfunction characterized in fetal alcohol syndrome (FAS). Therefore, this study examined neuroprotective effects of...
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| Veröffentlicht in: | Neuroscience letters 1999-03, Vol.263 (2), p.189-192 |
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| creator | Mitchell, J.Jean Paiva, Michael Heaton, Marieta B |
| description | Neurodevelopmental damage can occur as a result of in utero exposure to alcohol. Oxidative stress processes are one of many proposed mechanisms thought to contribute to nervous system dysfunction characterized in fetal alcohol syndrome (FAS). Therefore, this study examined neuroprotective effects of antioxidant supplementation during ethanol (EtOH) treatment (0, 200, 400, 800 or 1600 mg/dl) combined with concomitants of EtOH exposure: acute (2-h) ischemia (aISCH) and chronic (16-h) hypoglycemia (cHG). The antioxidants vitamin E and
β-carotene protected embryonic hippocampal cultures against 0–1600 mg/dl EtOH/aISCH/cHG treatments. In addition, neuronal viability, as measured by MTT ((3,4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide; 5 mg/ml)), was equal to untreated cultures when supplemented with vitamin E or
β-carotene at 0–800 mg/dl or 0–200 mg/dl EtOH/aISCH/cHG, respectively. These in vitro studies mirror potential in utero ethanol-exposed CNS conditions and may lead to therapeutic strategies targeted at attenuating neurodevelopmental FAS-related deficits. |
| doi_str_mv | 10.1016/S0304-3940(99)00144-5 |
| format | Article |
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β-carotene protected embryonic hippocampal cultures against 0–1600 mg/dl EtOH/aISCH/cHG treatments. In addition, neuronal viability, as measured by MTT ((3,4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide; 5 mg/ml)), was equal to untreated cultures when supplemented with vitamin E or
β-carotene at 0–800 mg/dl or 0–200 mg/dl EtOH/aISCH/cHG, respectively. These in vitro studies mirror potential in utero ethanol-exposed CNS conditions and may lead to therapeutic strategies targeted at attenuating neurodevelopmental FAS-related deficits.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/S0304-3940(99)00144-5</identifier><identifier>PMID: 10213167</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Animals ; Antioxidants ; Antioxidants - pharmacology ; beta Carotene - pharmacology ; Biological and medical sciences ; Brain Ischemia ; Cell Survival - drug effects ; Cells, Cultured ; Embryo, Mammalian ; Ethanol ; Ethanol - toxicity ; Fetal Alcohol Spectrum Disorders - physiopathology ; Fetal Alcohol Spectrum Disorders - prevention & control ; Hippocampus ; Hippocampus - cytology ; Hypoglycemia ; Ischemia ; Medical sciences ; Neurons - cytology ; Neurons - drug effects ; Neurons - physiology ; Neuropharmacology ; Neuroprotective agent ; Neuroprotective Agents - pharmacology ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Pharmacology. Drug treatments ; Rats ; Rats, Long-Evans ; Vitamin E - pharmacology ; Vitamin E, β-carotene</subject><ispartof>Neuroscience letters, 1999-03, Vol.263 (2), p.189-192</ispartof><rights>1999 Elsevier Science Ireland Ltd</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-e1b7c18768db09f64f26a27da75230ff3b8315af60b9ad22fdc09a3f147998e13</citedby><cites>FETCH-LOGICAL-c421t-e1b7c18768db09f64f26a27da75230ff3b8315af60b9ad22fdc09a3f147998e13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0304-3940(99)00144-5$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27907,27908,45978</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1742558$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10213167$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mitchell, J.Jean</creatorcontrib><creatorcontrib>Paiva, Michael</creatorcontrib><creatorcontrib>Heaton, Marieta B</creatorcontrib><title>Vitamin E and β-carotene protect against ethanol combined with ischemia in an embryonic rat hippocampal culture model of fetal alcohol syndrome</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Neurodevelopmental damage can occur as a result of in utero exposure to alcohol. Oxidative stress processes are one of many proposed mechanisms thought to contribute to nervous system dysfunction characterized in fetal alcohol syndrome (FAS). Therefore, this study examined neuroprotective effects of antioxidant supplementation during ethanol (EtOH) treatment (0, 200, 400, 800 or 1600 mg/dl) combined with concomitants of EtOH exposure: acute (2-h) ischemia (aISCH) and chronic (16-h) hypoglycemia (cHG). The antioxidants vitamin E and
β-carotene protected embryonic hippocampal cultures against 0–1600 mg/dl EtOH/aISCH/cHG treatments. In addition, neuronal viability, as measured by MTT ((3,4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide; 5 mg/ml)), was equal to untreated cultures when supplemented with vitamin E or
β-carotene at 0–800 mg/dl or 0–200 mg/dl EtOH/aISCH/cHG, respectively. These in vitro studies mirror potential in utero ethanol-exposed CNS conditions and may lead to therapeutic strategies targeted at attenuating neurodevelopmental FAS-related deficits.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>beta Carotene - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Brain Ischemia</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>Embryo, Mammalian</subject><subject>Ethanol</subject><subject>Ethanol - toxicity</subject><subject>Fetal Alcohol Spectrum Disorders - physiopathology</subject><subject>Fetal Alcohol Spectrum Disorders - prevention & control</subject><subject>Hippocampus</subject><subject>Hippocampus - cytology</subject><subject>Hypoglycemia</subject><subject>Ischemia</subject><subject>Medical sciences</subject><subject>Neurons - cytology</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Neuropharmacology</subject><subject>Neuroprotective agent</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Long-Evans</subject><subject>Vitamin E - pharmacology</subject><subject>Vitamin E, β-carotene</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2O1DAQhSMEYpqBI4C8QAgWAduJk3g1QqPhRxqJBT9bq2KXiVFiB9sB9S04CwfhTLinW8COVUml7z273quqh4w-Z5R1L97ThrZ1I1v6VMpnlLK2rcWtaseGnte97PntavcHOavupfSFUiqYaO9WZ4xy1rCu31U_PrkMi_PkioA35NfPWkMMGT2S9TB1JvAZnE-ZYJ7Ah5nosIzOoyHfXZ6IS3rCxQEpHuAJLmPcB-80iZDJ5NY1aFhWKLJtzltEsgSDMwmWWMxlDbMOU3FNe29iWPB-dcfCnPDBaZ5XH19dfbh8U1-_e_328uV1rVvOco1s7HW5tRvMSKXtWss74L2BXvCGWtuMQ8ME2I6OEgzn1mgqobGs7aUckDXn1ZOjbznz64Ypq6WcgvMMHsOWFOsbOkjRFlAcQR1DShGtWqNbIO4Vo-pQhbqpQh1yVlKqmyqUKLpHpwe2cUHzj-qYfQEenwBIGmYbwWuX_nJ9y4UYCnZxxLCk8c1hVEk79BqNi6UeZYL7z09-A7PuqHk</recordid><startdate>19990326</startdate><enddate>19990326</enddate><creator>Mitchell, J.Jean</creator><creator>Paiva, Michael</creator><creator>Heaton, Marieta B</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><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>7TK</scope></search><sort><creationdate>19990326</creationdate><title>Vitamin E and β-carotene protect against ethanol combined with ischemia in an embryonic rat hippocampal culture model of fetal alcohol syndrome</title><author>Mitchell, J.Jean ; Paiva, Michael ; Heaton, Marieta B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-e1b7c18768db09f64f26a27da75230ff3b8315af60b9ad22fdc09a3f147998e13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>beta Carotene - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Brain Ischemia</topic><topic>Cell Survival - drug effects</topic><topic>Cells, Cultured</topic><topic>Embryo, Mammalian</topic><topic>Ethanol</topic><topic>Ethanol - toxicity</topic><topic>Fetal Alcohol Spectrum Disorders - physiopathology</topic><topic>Fetal Alcohol Spectrum Disorders - prevention & control</topic><topic>Hippocampus</topic><topic>Hippocampus - cytology</topic><topic>Hypoglycemia</topic><topic>Ischemia</topic><topic>Medical sciences</topic><topic>Neurons - cytology</topic><topic>Neurons - drug effects</topic><topic>Neurons - physiology</topic><topic>Neuropharmacology</topic><topic>Neuroprotective agent</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Long-Evans</topic><topic>Vitamin E - pharmacology</topic><topic>Vitamin E, β-carotene</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mitchell, J.Jean</creatorcontrib><creatorcontrib>Paiva, Michael</creatorcontrib><creatorcontrib>Heaton, Marieta B</creatorcontrib><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>Neurosciences Abstracts</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mitchell, J.Jean</au><au>Paiva, Michael</au><au>Heaton, Marieta B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vitamin E and β-carotene protect against ethanol combined with ischemia in an embryonic rat hippocampal culture model of fetal alcohol syndrome</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>1999-03-26</date><risdate>1999</risdate><volume>263</volume><issue>2</issue><spage>189</spage><epage>192</epage><pages>189-192</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>Neurodevelopmental damage can occur as a result of in utero exposure to alcohol. Oxidative stress processes are one of many proposed mechanisms thought to contribute to nervous system dysfunction characterized in fetal alcohol syndrome (FAS). Therefore, this study examined neuroprotective effects of antioxidant supplementation during ethanol (EtOH) treatment (0, 200, 400, 800 or 1600 mg/dl) combined with concomitants of EtOH exposure: acute (2-h) ischemia (aISCH) and chronic (16-h) hypoglycemia (cHG). The antioxidants vitamin E and
β-carotene protected embryonic hippocampal cultures against 0–1600 mg/dl EtOH/aISCH/cHG treatments. In addition, neuronal viability, as measured by MTT ((3,4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide; 5 mg/ml)), was equal to untreated cultures when supplemented with vitamin E or
β-carotene at 0–800 mg/dl or 0–200 mg/dl EtOH/aISCH/cHG, respectively. These in vitro studies mirror potential in utero ethanol-exposed CNS conditions and may lead to therapeutic strategies targeted at attenuating neurodevelopmental FAS-related deficits.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>10213167</pmid><doi>10.1016/S0304-3940(99)00144-5</doi><tpages>4</tpages></addata></record> |
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| subjects | Animals Antioxidants Antioxidants - pharmacology beta Carotene - pharmacology Biological and medical sciences Brain Ischemia Cell Survival - drug effects Cells, Cultured Embryo, Mammalian Ethanol Ethanol - toxicity Fetal Alcohol Spectrum Disorders - physiopathology Fetal Alcohol Spectrum Disorders - prevention & control Hippocampus Hippocampus - cytology Hypoglycemia Ischemia Medical sciences Neurons - cytology Neurons - drug effects Neurons - physiology Neuropharmacology Neuroprotective agent Neuroprotective Agents - pharmacology Oxidative Stress - drug effects Oxidative Stress - physiology Pharmacology. Drug treatments Rats Rats, Long-Evans Vitamin E - pharmacology Vitamin E, β-carotene |
| title | Vitamin E and β-carotene protect against ethanol combined with ischemia in an embryonic rat hippocampal culture model of fetal alcohol syndrome |
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