Effect of immobilization, cold and cold-restraint stress on liver monooxygenase activity and lipid peroxidation of influenza virus-infected mice.
Identifieur interne : 000987 ( PubMed/Corpus ); précédent : 000986; suivant : 000988Effect of immobilization, cold and cold-restraint stress on liver monooxygenase activity and lipid peroxidation of influenza virus-infected mice.
Auteurs : M. Mileva ; R. Bakalova ; L. Tancheva ; S. GalabovSource :
- Archives of toxicology [ 0340-5761 ] ; 2002.
English descriptors
- KwdEn :
- Aminopyrine N-Demethylase (metabolism), Animals, Cold Temperature (adverse effects), Cytochrome P-450 Enzyme System (metabolism), Immobilization, Influenza A virus, Lipid Peroxidation, Liver (enzymology), Liver (virology), Male, Mice, Mice, Inbred ICR, Orthomyxoviridae Infections (metabolism), Stress, Physiological (etiology), Stress, Physiological (metabolism).
- MESH :
- chemical , metabolism : Aminopyrine N-Demethylase, Cytochrome P-450 Enzyme System.
- adverse effects : Cold Temperature.
- enzymology : Liver.
- etiology : Stress, Physiological.
- metabolism : Orthomyxoviridae Infections, Stress, Physiological.
- virology : Liver.
- Animals, Immobilization, Influenza A virus, Lipid Peroxidation, Male, Mice, Mice, Inbred ICR.
Abstract
The present study provides a direct experimental evidence that the combination of influenza A/Aichi/2/68 (H3N2) infection with different models of "oxidative stress", such as immobilization, cold and cold-restraint, is associated with graduated oxidative disturbances in the liver of mice, despite the absence of virus and inflammation in this tissue. It was found that experimental influenza virus infection is accompanied with a significant increase of lipid peroxidation products, a decrease of natural antioxidants (vitamin E, glutathione) and cytochrome P-450, an inhibition of cytochrome c reductase and liver monooxygenases (analgin- N-demethylase and amidopyrine- N-demethylase). Immobilization and cold stress, applied separately or in combination (cold-restraint), did not influence significantly any of the analysed parameters compared to those of the control group of non-infected mice. Preliminary exposure of mice to immobilization or cold stress and subsequent inoculation of influenza virus resulted in a significant increase of lipid peroxidation products and a significant decrease of vitamin E and reduced glutathione, compared with levels in control (non-infected) animals. Compared to influenza virus-infected and non-stressed animals, the changes in all these parameters were negligible. Immobilization or cold stress, applied in combination with influenza virus infection, partially prevented the suppressive effect of influenza virus on cytochrome P-450 and liver monooxygenases. A tendency towards normalization of these parameters to the control levels was observed. However, after application of cold-restraint plus influenza virus infection, the level of cytochrome P-450 and activity of cytochrome c reductase stayed markedly lower than in infected and non-stressed animals. The activities of liver monooxygenases were slightly increased compared with those of infected and non-stressed animals, but stayed relatively low compared to control (non-infected) mice. Combination of cold-restraint and influenza virus infection resulted in a greater synergistic increase of lipid peroxidation products and a greater synergistic decrease of vitamin E and reduced glutathione compared to controls, as well as to influenza virus-infected and non-stressed animals.
DOI: 10.1007/s00204-001-0306-6
PubMed: 11914779
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pubmed:11914779Le document en format XML
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Galabov</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:11914779</idno><idno type="pmid">11914779</idno><idno type="doi">10.1007/s00204-001-0306-6</idno><idno type="wicri:Area/PubMed/Corpus">000987</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000987</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effect of immobilization, cold and cold-restraint stress on liver monooxygenase activity and lipid peroxidation of influenza virus-infected mice.</title><author><name sortKey="Mileva, M" sort="Mileva, M" uniqKey="Mileva M" first="M" last="Mileva">M. Mileva</name><affiliation><nlm:affiliation>Department of Medical Physics and Biophysics, Medical University, 2 Zdrave Str., Sofia 1431, Bulgaria. mileva@medfac.acad.bg</nlm:affiliation></affiliation></author><author><name sortKey="Bakalova, R" sort="Bakalova, R" uniqKey="Bakalova R" first="R" last="Bakalova">R. Bakalova</name></author><author><name sortKey="Tancheva, L" sort="Tancheva, L" uniqKey="Tancheva L" first="L" last="Tancheva">L. Tancheva</name></author><author><name sortKey="Galabov, S" sort="Galabov, S" uniqKey="Galabov S" first="S" last="Galabov">S. Galabov</name></author></analytic><series><title level="j">Archives of toxicology</title><idno type="ISSN">0340-5761</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aminopyrine N-Demethylase (metabolism)</term><term>Animals</term><term>Cold Temperature (adverse effects)</term><term>Cytochrome P-450 Enzyme System (metabolism)</term><term>Immobilization</term><term>Influenza A virus</term><term>Lipid Peroxidation</term><term>Liver (enzymology)</term><term>Liver (virology)</term><term>Male</term><term>Mice</term><term>Mice, Inbred ICR</term><term>Orthomyxoviridae Infections (metabolism)</term><term>Stress, Physiological (etiology)</term><term>Stress, Physiological (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Aminopyrine N-Demethylase</term><term>Cytochrome P-450 Enzyme System</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Cold Temperature</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Liver</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Stress, Physiological</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Orthomyxoviridae Infections</term><term>Stress, Physiological</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Liver</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Immobilization</term><term>Influenza A virus</term><term>Lipid Peroxidation</term><term>Male</term><term>Mice</term><term>Mice, Inbred ICR</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The present study provides a direct experimental evidence that the combination of influenza A/Aichi/2/68 (H3N2) infection with different models of "oxidative stress", such as immobilization, cold and cold-restraint, is associated with graduated oxidative disturbances in the liver of mice, despite the absence of virus and inflammation in this tissue. It was found that experimental influenza virus infection is accompanied with a significant increase of lipid peroxidation products, a decrease of natural antioxidants (vitamin E, glutathione) and cytochrome P-450, an inhibition of cytochrome c reductase and liver monooxygenases (analgin- N-demethylase and amidopyrine- N-demethylase). Immobilization and cold stress, applied separately or in combination (cold-restraint), did not influence significantly any of the analysed parameters compared to those of the control group of non-infected mice. Preliminary exposure of mice to immobilization or cold stress and subsequent inoculation of influenza virus resulted in a significant increase of lipid peroxidation products and a significant decrease of vitamin E and reduced glutathione, compared with levels in control (non-infected) animals. Compared to influenza virus-infected and non-stressed animals, the changes in all these parameters were negligible. Immobilization or cold stress, applied in combination with influenza virus infection, partially prevented the suppressive effect of influenza virus on cytochrome P-450 and liver monooxygenases. A tendency towards normalization of these parameters to the control levels was observed. However, after application of cold-restraint plus influenza virus infection, the level of cytochrome P-450 and activity of cytochrome c reductase stayed markedly lower than in infected and non-stressed animals. The activities of liver monooxygenases were slightly increased compared with those of infected and non-stressed animals, but stayed relatively low compared to control (non-infected) mice. Combination of cold-restraint and influenza virus infection resulted in a greater synergistic increase of lipid peroxidation products and a greater synergistic decrease of vitamin E and reduced glutathione compared to controls, as well as to influenza virus-infected and non-stressed animals.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">11914779</PMID><DateCompleted><Year>2002</Year><Month>08</Month><Day>02</Day></DateCompleted><DateRevised><Year>2008</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0340-5761</ISSN><JournalIssue CitedMedium="Print"><Volume>76</Volume><Issue>2</Issue><PubDate><Year>2002</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Archives of toxicology</Title><ISOAbbreviation>Arch. Toxicol.</ISOAbbreviation></Journal><ArticleTitle>Effect of immobilization, cold and cold-restraint stress on liver monooxygenase activity and lipid peroxidation of influenza virus-infected mice.</ArticleTitle><Pagination><MedlinePgn>96-103</MedlinePgn></Pagination><Abstract><AbstractText>The present study provides a direct experimental evidence that the combination of influenza A/Aichi/2/68 (H3N2) infection with different models of "oxidative stress", such as immobilization, cold and cold-restraint, is associated with graduated oxidative disturbances in the liver of mice, despite the absence of virus and inflammation in this tissue. It was found that experimental influenza virus infection is accompanied with a significant increase of lipid peroxidation products, a decrease of natural antioxidants (vitamin E, glutathione) and cytochrome P-450, an inhibition of cytochrome c reductase and liver monooxygenases (analgin- N-demethylase and amidopyrine- N-demethylase). Immobilization and cold stress, applied separately or in combination (cold-restraint), did not influence significantly any of the analysed parameters compared to those of the control group of non-infected mice. Preliminary exposure of mice to immobilization or cold stress and subsequent inoculation of influenza virus resulted in a significant increase of lipid peroxidation products and a significant decrease of vitamin E and reduced glutathione, compared with levels in control (non-infected) animals. Compared to influenza virus-infected and non-stressed animals, the changes in all these parameters were negligible. Immobilization or cold stress, applied in combination with influenza virus infection, partially prevented the suppressive effect of influenza virus on cytochrome P-450 and liver monooxygenases. A tendency towards normalization of these parameters to the control levels was observed. However, after application of cold-restraint plus influenza virus infection, the level of cytochrome P-450 and activity of cytochrome c reductase stayed markedly lower than in infected and non-stressed animals. The activities of liver monooxygenases were slightly increased compared with those of infected and non-stressed animals, but stayed relatively low compared to control (non-infected) mice. Combination of cold-restraint and influenza virus infection resulted in a greater synergistic increase of lipid peroxidation products and a greater synergistic decrease of vitamin E and reduced glutathione compared to controls, as well as to influenza virus-infected and non-stressed animals.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mileva</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medical Physics and Biophysics, Medical University, 2 Zdrave Str., Sofia 1431, Bulgaria. mileva@medfac.acad.bg</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bakalova</LastName><ForeName>R</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Tancheva</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Galabov</LastName><ForeName>S</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2002</Year><Month>02</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Arch Toxicol</MedlineTA><NlmUniqueID>0417615</NlmUniqueID><ISSNLinking>0340-5761</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9035-51-2</RegistryNumber><NameOfSubstance UI="D003577">Cytochrome P-450 Enzyme System</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.5.3.-</RegistryNumber><NameOfSubstance UI="D000633">Aminopyrine N-Demethylase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.5.3.-</RegistryNumber><NameOfSubstance UI="C019666">amidopyrine N-demethylase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000633" MajorTopicYN="N">Aminopyrine N-Demethylase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003080" MajorTopicYN="N">Cold Temperature</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003577" MajorTopicYN="N">Cytochrome P-450 Enzyme System</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007103" MajorTopicYN="N">Immobilization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009980" MajorTopicYN="N">Influenza A virus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015227" MajorTopicYN="Y">Lipid Peroxidation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008813" MajorTopicYN="N">Mice, Inbred ICR</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009976" MajorTopicYN="N">Orthomyxoviridae Infections</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013312" MajorTopicYN="N">Stress, Physiological</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2001</Year><Month>05</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2001</Year><Month>11</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>3</Month><Day>27</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>8</Month><Day>3</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>3</Month><Day>27</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">11914779</ArticleId><ArticleId IdType="doi">10.1007/s00204-001-0306-6</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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