Oxidative stress and mitochondrial dysfunction in parafacial respiratory group induced by maternal cigarette smoke exposure in rat offspring.
Identifieur interne : 000199 ( Main/Exploration ); précédent : 000198; suivant : 000200Oxidative stress and mitochondrial dysfunction in parafacial respiratory group induced by maternal cigarette smoke exposure in rat offspring.
Auteurs : Fang Lei [République populaire de Chine] ; Wen Wang [République populaire de Chine] ; Yating Fu [République populaire de Chine] ; Ji Wang [République populaire de Chine] ; Yu Zheng [République populaire de Chine]Source :
- Free radical biology & medicine [ 1873-4596 ] ; 2018.
Descripteurs français
- KwdFr :
- ADN mitochondrial (agonistes), ADN mitochondrial (génétique), ADN mitochondrial (métabolisme), Adénosine triphosphate (antagonistes et inhibiteurs), Adénosine triphosphate (biosynthèse), Animaux (MeSH), Animaux nouveau-nés (MeSH), Catalase (métabolisme), Désoxyguanosine (analogues et dérivés), Désoxyguanosine (métabolisme), Effets différés de l'exposition prénatale à des facteurs de risque (induit chimiquement), Effets différés de l'exposition prénatale à des facteurs de risque (métabolisme), Effets différés de l'exposition prénatale à des facteurs de risque (physiopathologie), Exposition maternelle (MeSH), Femelle (MeSH), Glutathion (métabolisme), Glutathione reductase (métabolisme), Grossesse (MeSH), Malonaldéhyde (agonistes), Malonaldéhyde (métabolisme), Mitochondries (anatomopathologie), Mitochondries (effets des médicaments et des substances chimiques), Mitochondries (métabolisme), Peroxydation lipidique (effets des médicaments et des substances chimiques), Pollution par la fumée de tabac (effets indésirables), Potentiel de membrane mitochondriale (effets des médicaments et des substances chimiques), Poumon (effets des médicaments et des substances chimiques), Poumon (métabolisme), Poumon (physiopathologie), Rat Sprague-Dawley (MeSH), Rats (MeSH), Stress oxydatif (effets des médicaments et des substances chimiques), Substances réactives à l'acide thiobarbiturique (métabolisme), Superoxide dismutase (métabolisme), Tabac (composition chimique), Tabac (toxicité), Tronc cérébral (effets des médicaments et des substances chimiques), Tronc cérébral (métabolisme).
- MESH :
- agonistes : ADN mitochondrial, Malonaldéhyde.
- analogues et dérivés : Désoxyguanosine.
- anatomopathologie : Mitochondries.
- antagonistes et inhibiteurs : Adénosine triphosphate.
- biosynthèse : Adénosine triphosphate.
- composition chimique : Tabac.
- effets des médicaments et des substances chimiques : Mitochondries, Peroxydation lipidique, Potentiel de membrane mitochondriale, Poumon, Stress oxydatif, Tronc cérébral.
- effets indésirables : Pollution par la fumée de tabac.
- génétique : ADN mitochondrial.
- induit chimiquement : Effets différés de l'exposition prénatale à des facteurs de risque.
- métabolisme : ADN mitochondrial, Catalase, Désoxyguanosine, Effets différés de l'exposition prénatale à des facteurs de risque, Glutathion, Glutathione reductase, Malonaldéhyde, Mitochondries, Poumon, Substances réactives à l'acide thiobarbiturique, Superoxide dismutase, Tronc cérébral.
- physiopathologie : Effets différés de l'exposition prénatale à des facteurs de risque, Poumon.
- toxicité : Tabac.
- Animaux, Animaux nouveau-nés, Exposition maternelle, Femelle, Grossesse, Rat Sprague-Dawley, Rats.
English descriptors
- KwdEn :
- 8-Hydroxy-2'-Deoxyguanosine (MeSH), Adenosine Triphosphate (antagonists & inhibitors), Adenosine Triphosphate (biosynthesis), Animals (MeSH), Animals, Newborn (MeSH), Brain Stem (drug effects), Brain Stem (metabolism), Catalase (metabolism), DNA, Mitochondrial (agonists), DNA, Mitochondrial (genetics), DNA, Mitochondrial (metabolism), Deoxyguanosine (analogs & derivatives), Deoxyguanosine (metabolism), Female (MeSH), Glutathione (metabolism), Glutathione Reductase (metabolism), Lipid Peroxidation (drug effects), Lung (drug effects), Lung (metabolism), Lung (physiopathology), Malondialdehyde (agonists), Malondialdehyde (metabolism), Maternal Exposure (MeSH), Membrane Potential, Mitochondrial (drug effects), Mitochondria (drug effects), Mitochondria (metabolism), Mitochondria (pathology), Oxidative Stress (drug effects), Pregnancy (MeSH), Prenatal Exposure Delayed Effects (chemically induced), Prenatal Exposure Delayed Effects (metabolism), Prenatal Exposure Delayed Effects (physiopathology), Rats (MeSH), Rats, Sprague-Dawley (MeSH), Superoxide Dismutase (metabolism), Thiobarbituric Acid Reactive Substances (metabolism), Tobacco (chemistry), Tobacco (toxicity), Tobacco Smoke Pollution (adverse effects).
- MESH :
- chemical , adverse effects : Tobacco Smoke Pollution.
- chemical , agonists : DNA, Mitochondrial, Malondialdehyde.
- chemical , analogs & derivatives : Deoxyguanosine.
- chemical , antagonists & inhibitors : Adenosine Triphosphate.
- chemical , biosynthesis : Adenosine Triphosphate.
- chemical , genetics : DNA, Mitochondrial.
- chemical , metabolism : Catalase, DNA, Mitochondrial, Deoxyguanosine, Glutathione, Glutathione Reductase, Malondialdehyde, Superoxide Dismutase, Thiobarbituric Acid Reactive Substances.
- chemical : 8-Hydroxy-2'-Deoxyguanosine.
- chemically induced : Prenatal Exposure Delayed Effects.
- chemistry : Tobacco.
- drug effects : Brain Stem, Lipid Peroxidation, Lung, Membrane Potential, Mitochondrial, Mitochondria, Oxidative Stress.
- metabolism : Brain Stem, Lung, Mitochondria, Prenatal Exposure Delayed Effects.
- pathology : Mitochondria.
- physiopathology : Lung, Prenatal Exposure Delayed Effects.
- toxicity : Tobacco.
- Animals, Animals, Newborn, Female, Maternal Exposure, Pregnancy, Rats, Rats, Sprague-Dawley.
Abstract
Cigarette smoke (CS) exposure negatively affects neurodevelopment. We established a CS exposure rat model to determine how maternal CS exposure induces oxidative stress and mitochondrial dysfunction in parafacial respiratory group (pFRG) essential to central chemoreceptive regulation of normal breathing. Pregnant rats were exposed to CS during gestational days 1-20, and the offspring were studied on postnatal day 2. Our data showed that maternal CS exposure resulted in elevated accumulation of ROS, which left a footprint on DNA and lipid with increases in 8-hydroxy-2'-deoxyguanosine and malondialdehyde contents. Furthermore, maternal CS exposure induced decreases in manganese superoxide dismutase, catalase and glutathione reductase activities as well as reduction in glutathione content in pFRG in the offspring. Moreover, maternal exposure to CS led to mitochondrial ultrastructure changes, mitochondrial swelling, reduction in ATP generation, loss of mitochondrial membrane potential and increase in mitochondrial DNA copy number. These findings suggest that maternal exposure to CS alters normal development of pFRG that is critical for normal respiratory control.
DOI: 10.1016/j.freeradbiomed.2018.09.003
PubMed: 30193892
Affiliations:
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Electronic address: yzheng@scu.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Physiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, 3-17 Renmin South Road, Chengdu, Sichuan 610041</wicri:regionArea><wicri:noRegion>Sichuan 610041</wicri:noRegion></affiliation></author></analytic><series><title level="j">Free radical biology & medicine</title><idno type="eISSN">1873-4596</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>8-Hydroxy-2'-Deoxyguanosine (MeSH)</term><term>Adenosine Triphosphate (antagonists & inhibitors)</term><term>Adenosine Triphosphate (biosynthesis)</term><term>Animals (MeSH)</term><term>Animals, Newborn (MeSH)</term><term>Brain Stem (drug effects)</term><term>Brain Stem (metabolism)</term><term>Catalase (metabolism)</term><term>DNA, Mitochondrial (agonists)</term><term>DNA, Mitochondrial (genetics)</term><term>DNA, Mitochondrial (metabolism)</term><term>Deoxyguanosine (analogs & derivatives)</term><term>Deoxyguanosine (metabolism)</term><term>Female (MeSH)</term><term>Glutathione (metabolism)</term><term>Glutathione Reductase (metabolism)</term><term>Lipid Peroxidation (drug effects)</term><term>Lung (drug effects)</term><term>Lung (metabolism)</term><term>Lung (physiopathology)</term><term>Malondialdehyde (agonists)</term><term>Malondialdehyde (metabolism)</term><term>Maternal Exposure (MeSH)</term><term>Membrane Potential, Mitochondrial (drug effects)</term><term>Mitochondria (drug effects)</term><term>Mitochondria (metabolism)</term><term>Mitochondria (pathology)</term><term>Oxidative Stress (drug effects)</term><term>Pregnancy (MeSH)</term><term>Prenatal Exposure Delayed Effects (chemically induced)</term><term>Prenatal Exposure Delayed Effects (metabolism)</term><term>Prenatal Exposure Delayed Effects (physiopathology)</term><term>Rats (MeSH)</term><term>Rats, Sprague-Dawley (MeSH)</term><term>Superoxide Dismutase (metabolism)</term><term>Thiobarbituric Acid Reactive Substances (metabolism)</term><term>Tobacco (chemistry)</term><term>Tobacco (toxicity)</term><term>Tobacco Smoke Pollution (adverse effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ADN mitochondrial (agonistes)</term><term>ADN mitochondrial (génétique)</term><term>ADN mitochondrial (métabolisme)</term><term>Adénosine triphosphate (antagonistes et inhibiteurs)</term><term>Adénosine triphosphate (biosynthèse)</term><term>Animaux (MeSH)</term><term>Animaux nouveau-nés (MeSH)</term><term>Catalase (métabolisme)</term><term>Désoxyguanosine (analogues et dérivés)</term><term>Désoxyguanosine (métabolisme)</term><term>Effets différés de l'exposition prénatale à des facteurs de risque (induit chimiquement)</term><term>Effets différés de l'exposition prénatale à des facteurs de risque (métabolisme)</term><term>Effets différés de l'exposition prénatale à des facteurs de risque (physiopathologie)</term><term>Exposition maternelle (MeSH)</term><term>Femelle (MeSH)</term><term>Glutathion (métabolisme)</term><term>Glutathione reductase (métabolisme)</term><term>Grossesse (MeSH)</term><term>Malonaldéhyde (agonistes)</term><term>Malonaldéhyde (métabolisme)</term><term>Mitochondries (anatomopathologie)</term><term>Mitochondries (effets des médicaments et des substances chimiques)</term><term>Mitochondries (métabolisme)</term><term>Peroxydation lipidique (effets des médicaments et des substances chimiques)</term><term>Pollution par la fumée de tabac (effets indésirables)</term><term>Potentiel de membrane mitochondriale (effets des médicaments et des substances chimiques)</term><term>Poumon (effets des médicaments et des substances chimiques)</term><term>Poumon (métabolisme)</term><term>Poumon (physiopathologie)</term><term>Rat Sprague-Dawley (MeSH)</term><term>Rats (MeSH)</term><term>Stress oxydatif (effets des médicaments et des substances chimiques)</term><term>Substances réactives à l'acide thiobarbiturique (métabolisme)</term><term>Superoxide dismutase (métabolisme)</term><term>Tabac (composition chimique)</term><term>Tabac (toxicité)</term><term>Tronc cérébral (effets des médicaments et des substances chimiques)</term><term>Tronc cérébral (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Tobacco Smoke Pollution</term></keywords><keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>DNA, Mitochondrial</term><term>Malondialdehyde</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Deoxyguanosine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Adenosine Triphosphate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Adenosine Triphosphate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA, Mitochondrial</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Catalase</term><term>DNA, Mitochondrial</term><term>Deoxyguanosine</term><term>Glutathione</term><term>Glutathione Reductase</term><term>Malondialdehyde</term><term>Superoxide Dismutase</term><term>Thiobarbituric Acid Reactive Substances</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>8-Hydroxy-2'-Deoxyguanosine</term></keywords><keywords scheme="MESH" qualifier="agonistes" xml:lang="fr"><term>ADN mitochondrial</term><term>Malonaldéhyde</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Désoxyguanosine</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Mitochondries</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Adénosine triphosphate</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Adénosine triphosphate</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Prenatal Exposure Delayed Effects</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Tabac</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Brain Stem</term><term>Lipid Peroxidation</term><term>Lung</term><term>Membrane Potential, Mitochondrial</term><term>Mitochondria</term><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Mitochondries</term><term>Peroxydation lipidique</term><term>Potentiel de membrane mitochondriale</term><term>Poumon</term><term>Stress oxydatif</term><term>Tronc cérébral</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Pollution par la fumée de tabac</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ADN mitochondrial</term></keywords><keywords scheme="MESH" qualifier="induit chimiquement" xml:lang="fr"><term>Effets différés de l'exposition prénatale à des facteurs de risque</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain Stem</term><term>Lung</term><term>Mitochondria</term><term>Prenatal Exposure Delayed Effects</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ADN mitochondrial</term><term>Catalase</term><term>Désoxyguanosine</term><term>Effets différés de l'exposition prénatale à des facteurs de risque</term><term>Glutathion</term><term>Glutathione reductase</term><term>Malonaldéhyde</term><term>Mitochondries</term><term>Poumon</term><term>Substances réactives à l'acide thiobarbiturique</term><term>Superoxide dismutase</term><term>Tronc cérébral</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Effets différés de l'exposition prénatale à des facteurs de risque</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lung</term><term>Prenatal Exposure Delayed Effects</term></keywords><keywords scheme="MESH" qualifier="toxicity" xml:lang="en"><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Tabac</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Animals, Newborn</term><term>Female</term><term>Maternal Exposure</term><term>Pregnancy</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Animaux nouveau-nés</term><term>Exposition maternelle</term><term>Femelle</term><term>Grossesse</term><term>Rat Sprague-Dawley</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cigarette smoke (CS) exposure negatively affects neurodevelopment. We established a CS exposure rat model to determine how maternal CS exposure induces oxidative stress and mitochondrial dysfunction in parafacial respiratory group (pFRG) essential to central chemoreceptive regulation of normal breathing. Pregnant rats were exposed to CS during gestational days 1-20, and the offspring were studied on postnatal day 2. Our data showed that maternal CS exposure resulted in elevated accumulation of ROS, which left a footprint on DNA and lipid with increases in 8-hydroxy-2'-deoxyguanosine and malondialdehyde contents. Furthermore, maternal CS exposure induced decreases in manganese superoxide dismutase, catalase and glutathione reductase activities as well as reduction in glutathione content in pFRG in the offspring. Moreover, maternal exposure to CS led to mitochondrial ultrastructure changes, mitochondrial swelling, reduction in ATP generation, loss of mitochondrial membrane potential and increase in mitochondrial DNA copy number. These findings suggest that maternal exposure to CS alters normal development of pFRG that is critical for normal respiratory control.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30193892</PMID><DateCompleted><Year>2019</Year><Month>09</Month><Day>30</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-4596</ISSN><JournalIssue CitedMedium="Internet"><Volume>129</Volume><PubDate><Year>2018</Year><Month>12</Month></PubDate></JournalIssue><Title>Free radical biology & medicine</Title><ISOAbbreviation>Free Radic Biol Med</ISOAbbreviation></Journal><ArticleTitle>Oxidative stress and mitochondrial dysfunction in parafacial respiratory group induced by maternal cigarette smoke exposure in rat offspring.</ArticleTitle><Pagination><MedlinePgn>169-176</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0891-5849(18)31071-2</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.freeradbiomed.2018.09.003</ELocationID><Abstract><AbstractText>Cigarette smoke (CS) exposure negatively affects neurodevelopment. We established a CS exposure rat model to determine how maternal CS exposure induces oxidative stress and mitochondrial dysfunction in parafacial respiratory group (pFRG) essential to central chemoreceptive regulation of normal breathing. Pregnant rats were exposed to CS during gestational days 1-20, and the offspring were studied on postnatal day 2. Our data showed that maternal CS exposure resulted in elevated accumulation of ROS, which left a footprint on DNA and lipid with increases in 8-hydroxy-2'-deoxyguanosine and malondialdehyde contents. Furthermore, maternal CS exposure induced decreases in manganese superoxide dismutase, catalase and glutathione reductase activities as well as reduction in glutathione content in pFRG in the offspring. Moreover, maternal exposure to CS led to mitochondrial ultrastructure changes, mitochondrial swelling, reduction in ATP generation, loss of mitochondrial membrane potential and increase in mitochondrial DNA copy number. These findings suggest that maternal exposure to CS alters normal development of pFRG that is critical for normal respiratory control.</AbstractText><CopyrightInformation>Copyright © 2018 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lei</LastName><ForeName>Fang</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Physiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, 3-17 Renmin South Road, Chengdu, Sichuan 610041, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Wen</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Physiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, 3-17 Renmin South Road, Chengdu, Sichuan 610041, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fu</LastName><ForeName>Yating</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Physiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, 3-17 Renmin South Road, Chengdu, Sichuan 610041, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Ji</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Physiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, 3-17 Renmin South Road, Chengdu, Sichuan 610041, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zheng</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Physiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, 3-17 Renmin South Road, Chengdu, Sichuan 610041, PR China. Electronic address: yzheng@scu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>09</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Free Radic Biol Med</MedlineTA><NlmUniqueID>8709159</NlmUniqueID><ISSNLinking>0891-5849</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004272">DNA, Mitochondrial</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017392">Thiobarbituric Acid Reactive Substances</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014028">Tobacco Smoke Pollution</NameOfSubstance></Chemical><Chemical><RegistryNumber>4Y8F71G49Q</RegistryNumber><NameOfSubstance UI="D008315">Malondialdehyde</NameOfSubstance></Chemical><Chemical><RegistryNumber>88847-89-6</RegistryNumber><NameOfSubstance UI="D000080242">8-Hydroxy-2'-Deoxyguanosine</NameOfSubstance></Chemical><Chemical><RegistryNumber>8L70Q75FXE</RegistryNumber><NameOfSubstance UI="D000255">Adenosine Triphosphate</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.6</RegistryNumber><NameOfSubstance UI="D002374">Catalase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="D013482">Superoxide Dismutase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.8.1.7</RegistryNumber><NameOfSubstance UI="D005980">Glutathione Reductase</NameOfSubstance></Chemical><Chemical><RegistryNumber>G9481N71RO</RegistryNumber><NameOfSubstance UI="D003849">Deoxyguanosine</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000080242" MajorTopicYN="N">8-Hydroxy-2'-Deoxyguanosine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000255" MajorTopicYN="N">Adenosine Triphosphate</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000831" MajorTopicYN="N">Animals, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001933" MajorTopicYN="N">Brain Stem</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002374" MajorTopicYN="N">Catalase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004272" MajorTopicYN="N">DNA, Mitochondrial</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003849" MajorTopicYN="N">Deoxyguanosine</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005980" MajorTopicYN="N">Glutathione Reductase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015227" MajorTopicYN="N">Lipid Peroxidation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008315" MajorTopicYN="N">Malondialdehyde</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName><QualifierName UI="Q000378" 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MajorTopicYN="N">Prenatal Exposure Delayed Effects</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013482" MajorTopicYN="N">Superoxide Dismutase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017392" MajorTopicYN="N">Thiobarbituric Acid Reactive Substances</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014026" MajorTopicYN="N">Tobacco</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014028" MajorTopicYN="N">Tobacco Smoke Pollution</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Maternal cigarette smoke exposure</Keyword><Keyword MajorTopicYN="Y">Mitochondrial dysfunction</Keyword><Keyword MajorTopicYN="Y">Oxidative stress</Keyword><Keyword MajorTopicYN="Y">Parafacial respiratory group</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>06</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2018</Year><Month>08</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>09</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>9</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>10</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>9</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30193892</ArticleId><ArticleId IdType="pii">S0891-5849(18)31071-2</ArticleId><ArticleId IdType="doi">10.1016/j.freeradbiomed.2018.09.003</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Lei, Fang" sort="Lei, Fang" uniqKey="Lei F" first="Fang" last="Lei">Fang Lei</name></noRegion><name sortKey="Fu, Yating" sort="Fu, Yating" uniqKey="Fu Y" first="Yating" last="Fu">Yating Fu</name><name sortKey="Wang, Ji" sort="Wang, Ji" uniqKey="Wang J" first="Ji" last="Wang">Ji Wang</name><name sortKey="Wang, Wen" sort="Wang, Wen" uniqKey="Wang W" first="Wen" last="Wang">Wen Wang</name><name sortKey="Zheng, Yu" sort="Zheng, Yu" uniqKey="Zheng Y" first="Yu" last="Zheng">Yu Zheng</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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