Sub-toxic Ethanol Exposure Modulates Gene Expression and Enzyme Activity of Antioxidant Systems to Provide Neuroprotection in Hippocampal HT22 Cells.
Identifieur interne : 000414 ( Main/Exploration ); précédent : 000413; suivant : 000415Sub-toxic Ethanol Exposure Modulates Gene Expression and Enzyme Activity of Antioxidant Systems to Provide Neuroprotection in Hippocampal HT22 Cells.
Auteurs : Ver Nica Casa As-Sánchez [Espagne] ; José A. Pérez [Espagne] ; David Quinto-Alemany [Espagne] ; Mario Díaz [Espagne]Source :
- Frontiers in physiology [ 1664-042X ] ; 2016.
Abstract
Ethanol is known to cause severe systemic damage often explained as secondary to oxidative stress. Brain is particularly vulnerable to ethanol-induced reactive oxygen species (ROS) because the high amounts of lipids, and because nerve cell membranes contain high amounts of peroxidable fatty acids. Usually these effects of ethanol are associated to high and/or chronic exposure to ethanol. However, as we show in this manuscript, a low and acute dose of ethanol trigger a completely different response in hippocampal cells. Thus, we have observed that 0.1% ethanol exposure to HT22 cells, a murine hippocampal-derived cell line, increases the transcriptional expression of different genes belonging to the classical, glutathione/glutaredoxin and thioredoxin/peroxiredoxin antioxidant systems, these including Sod1, Sod2, Gpx1, Gclc, and Txnrd1. Paralleling these changes, enzyme activities of total superoxide dismutase (tSOD), catalase, total glutathione peroxidase (tGPx), glutathione-S-reductase (GSR), and total thioredoxin reductase (tTXNRD), were all increased, while the generation of thiobarbituric acid reactive substances (TBARS), as indicators of lipid peroxidation, and glutathione levels remained unaltered. Ethanol exposure did not affect cell viability or cell growing as assessed by real-time cell culture monitoring, indicating that low ethanol doses are not deleterious for hippocampal cells, but rather prevented glutamate-induced excitotoxicity. In summary, we conclude that sub-toxic exposure to ethanol may well be neuroprotective against oxidative insults in hippocampal cells.
DOI: 10.3389/fphys.2016.00312
PubMed: 27512374
PubMed Central: PMC4961714
Affiliations:
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Pérez</name><affiliation wicri:level="1"><nlm:affiliation>Departamento de Bioquímica, Microbiología, Biología Celular y Genética, Universidad de La LagunaTenerife, Spain; Instituto Universitario de Enfermedades Tropicales y Salud Pública de CanariasTenerife, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Departamento de Bioquímica, Microbiología, Biología Celular y Genética, Universidad de La LagunaTenerife, Spain; Instituto Universitario de Enfermedades Tropicales y Salud Pública de CanariasTenerife</wicri:regionArea><wicri:noRegion>Spain; Instituto Universitario de Enfermedades Tropicales y Salud Pública de CanariasTenerife</wicri:noRegion></affiliation></author><author><name sortKey="Quinto Alemany, David" sort="Quinto Alemany, David" uniqKey="Quinto Alemany D" first="David" last="Quinto-Alemany">David Quinto-Alemany</name><affiliation wicri:level="1"><nlm:affiliation>Departamento de Biología Animal, Edafología y Geología, Universidad de La LagunaTenerife, Spain; Unidad Asociada de Investigación ULL-CSIC, "Fisiología y Biofísica de la Membrana Celular en Patologías Neurodegenerativas y Tumorales"Tenerife, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Departamento de Biología Animal, Edafología y Geología, Universidad de La LagunaTenerife, Spain; Unidad Asociada de Investigación ULL-CSIC, "Fisiología y Biofísica de la Membrana Celular en Patologías Neurodegenerativas y Tumorales"Tenerife</wicri:regionArea><wicri:noRegion>"Fisiología y Biofísica de la Membrana Celular en Patologías Neurodegenerativas y Tumorales"Tenerife</wicri:noRegion></affiliation></author><author><name sortKey="Diaz, Mario" sort="Diaz, Mario" uniqKey="Diaz M" first="Mario" last="Díaz">Mario Díaz</name><affiliation wicri:level="1"><nlm:affiliation>Instituto Universitario de Enfermedades Tropicales y Salud Pública de CanariasTenerife, Spain; Departamento de Biología Animal, Edafología y Geología, Universidad de La LagunaTenerife, Spain; Unidad Asociada de Investigación ULL-CSIC, "Fisiología y Biofísica de la Membrana Celular en Patologías Neurodegenerativas y Tumorales"Tenerife, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Instituto Universitario de Enfermedades Tropicales y Salud Pública de CanariasTenerife, Spain; Departamento de Biología Animal, Edafología y Geología, Universidad de La LagunaTenerife, Spain; Unidad Asociada de Investigación ULL-CSIC, "Fisiología y Biofísica de la Membrana Celular en Patologías Neurodegenerativas y Tumorales"Tenerife</wicri:regionArea><wicri:noRegion>"Fisiología y Biofísica de la Membrana Celular en Patologías Neurodegenerativas y Tumorales"Tenerife</wicri:noRegion></affiliation></author></analytic><series><title level="j">Frontiers in physiology</title><idno type="ISSN">1664-042X</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Ethanol is known to cause severe systemic damage often explained as secondary to oxidative stress. Brain is particularly vulnerable to ethanol-induced reactive oxygen species (ROS) because the high amounts of lipids, and because nerve cell membranes contain high amounts of peroxidable fatty acids. Usually these effects of ethanol are associated to high and/or chronic exposure to ethanol. However, as we show in this manuscript, a low and acute dose of ethanol trigger a completely different response in hippocampal cells. Thus, we have observed that 0.1% ethanol exposure to HT22 cells, a murine hippocampal-derived cell line, increases the transcriptional expression of different genes belonging to the classical, glutathione/glutaredoxin and thioredoxin/peroxiredoxin antioxidant systems, these including Sod1, Sod2, Gpx1, Gclc, and Txnrd1. Paralleling these changes, enzyme activities of total superoxide dismutase (tSOD), catalase, total glutathione peroxidase (tGPx), glutathione-S-reductase (GSR), and total thioredoxin reductase (tTXNRD), were all increased, while the generation of thiobarbituric acid reactive substances (TBARS), as indicators of lipid peroxidation, and glutathione levels remained unaltered. Ethanol exposure did not affect cell viability or cell growing as assessed by real-time cell culture monitoring, indicating that low ethanol doses are not deleterious for hippocampal cells, but rather prevented glutamate-induced excitotoxicity. In summary, we conclude that sub-toxic exposure to ethanol may well be neuroprotective against oxidative insults in hippocampal cells. </div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">27512374</PMID><DateCompleted><Year>2016</Year><Month>08</Month><Day>11</Day></DateCompleted><DateRevised><Year>2020</Year><Month>10</Month><Day>01</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-042X</ISSN><JournalIssue CitedMedium="Print"><Volume>7</Volume><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>Frontiers in physiology</Title><ISOAbbreviation>Front Physiol</ISOAbbreviation></Journal><ArticleTitle>Sub-toxic Ethanol Exposure Modulates Gene Expression and Enzyme Activity of Antioxidant Systems to Provide Neuroprotection in Hippocampal HT22 Cells.</ArticleTitle><Pagination><MedlinePgn>312</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fphys.2016.00312</ELocationID><Abstract><AbstractText>Ethanol is known to cause severe systemic damage often explained as secondary to oxidative stress. Brain is particularly vulnerable to ethanol-induced reactive oxygen species (ROS) because the high amounts of lipids, and because nerve cell membranes contain high amounts of peroxidable fatty acids. Usually these effects of ethanol are associated to high and/or chronic exposure to ethanol. However, as we show in this manuscript, a low and acute dose of ethanol trigger a completely different response in hippocampal cells. Thus, we have observed that 0.1% ethanol exposure to HT22 cells, a murine hippocampal-derived cell line, increases the transcriptional expression of different genes belonging to the classical, glutathione/glutaredoxin and thioredoxin/peroxiredoxin antioxidant systems, these including Sod1, Sod2, Gpx1, Gclc, and Txnrd1. Paralleling these changes, enzyme activities of total superoxide dismutase (tSOD), catalase, total glutathione peroxidase (tGPx), glutathione-S-reductase (GSR), and total thioredoxin reductase (tTXNRD), were all increased, while the generation of thiobarbituric acid reactive substances (TBARS), as indicators of lipid peroxidation, and glutathione levels remained unaltered. Ethanol exposure did not affect cell viability or cell growing as assessed by real-time cell culture monitoring, indicating that low ethanol doses are not deleterious for hippocampal cells, but rather prevented glutamate-induced excitotoxicity. In summary, we conclude that sub-toxic exposure to ethanol may well be neuroprotective against oxidative insults in hippocampal cells. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Casañas-Sánchez</LastName><ForeName>Verónica</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Departamento de Bioquímica, Microbiología, Biología Celular y Genética, Universidad de La LagunaTenerife, Spain; Instituto Universitario de Enfermedades Tropicales y Salud Pública de CanariasTenerife, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pérez</LastName><ForeName>José A</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>Departamento de Bioquímica, Microbiología, Biología Celular y Genética, Universidad de La LagunaTenerife, Spain; Instituto Universitario de Enfermedades Tropicales y Salud Pública de CanariasTenerife, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Quinto-Alemany</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Departamento de Biología Animal, Edafología y Geología, Universidad de La LagunaTenerife, Spain; Unidad Asociada de Investigación ULL-CSIC, "Fisiología y Biofísica de la Membrana Celular en Patologías Neurodegenerativas y Tumorales"Tenerife, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Díaz</LastName><ForeName>Mario</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Instituto Universitario de Enfermedades Tropicales y Salud Pública de CanariasTenerife, Spain; Departamento de Biología Animal, Edafología y Geología, Universidad de La LagunaTenerife, Spain; Unidad Asociada de Investigación ULL-CSIC, "Fisiología y Biofísica de la Membrana Celular en Patologías Neurodegenerativas y Tumorales"Tenerife, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>07</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Physiol</MedlineTA><NlmUniqueID>101549006</NlmUniqueID><ISSNLinking>1664-042X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">HT22 cells</Keyword><Keyword MajorTopicYN="N">antioxidant systems</Keyword><Keyword MajorTopicYN="N">ethanol</Keyword><Keyword MajorTopicYN="N">glutathione</Keyword><Keyword MajorTopicYN="N">hippocampal cells</Keyword><Keyword MajorTopicYN="N">superoxide dismutases</Keyword><Keyword MajorTopicYN="N">thioredoxins</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>04</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>07</Month><Day>11</Day></PubMedPubDate><PubMedPubDate 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Pérez</name><name sortKey="Quinto Alemany, David" sort="Quinto Alemany, David" uniqKey="Quinto Alemany D" first="David" last="Quinto-Alemany">David Quinto-Alemany</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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