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Disturbances of the Lung Glutathione System in Adult Guinea Pigs Following Neonatal Vitamin C or Cysteine Deficiency
In premature infants receiving parenteral nutrition, oxidative stress is a trigger for the development of bronchopulmonary dysplasia, which is an important factor in the development of adult lung diseases. Neonatal vitamin C and glutathione deficiency is suspected to induce permanent modification of...
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Published in: | Antioxidants 2023-06, Vol.12 (7), p.1361 |
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description | In premature infants receiving parenteral nutrition, oxidative stress is a trigger for the development of bronchopulmonary dysplasia, which is an important factor in the development of adult lung diseases. Neonatal vitamin C and glutathione deficiency is suspected to induce permanent modification of redox metabolism favoring the development of neonatal and adult lung diseases. A total of 64 3-day-old guinea pigs were fed an oral diet that was either complete or deficient in vitamin C (VCD), cysteine (CD) (glutathione-limiting substrate) or both (DD) for 4 days. At 1 week of age, half of the animals were sacrificed while the other started a complete diet until 12 weeks of age. At 1 week, the decrease in lung GSH in all deficient groups was partially explained by the oxidation of liver methionine-adenosyltransferase. mRNA levels of kelch-like ECH-associated protein 1 (
), glutathione-reductase (
) and glutaredoxin-1 (
) were significantly lower only in CD but not in DD. At 12 weeks, glutathione levels were increased in VCD and CD.
,
and
mRNA were increased, while glutathione-reductase and glutaredoxin proteins were lower in CD, favoring a higher glutathionylation status. Both neonatal deficiencies result in a long-term change in glutathione metabolism that could contribute to lung diseases' development. |
doi_str_mv | 10.3390/antiox12071361 |
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), glutathione-reductase (
) and glutaredoxin-1 (
) were significantly lower only in CD but not in DD. At 12 weeks, glutathione levels were increased in VCD and CD.
,
and
mRNA were increased, while glutathione-reductase and glutaredoxin proteins were lower in CD, favoring a higher glutathionylation status. Both neonatal deficiencies result in a long-term change in glutathione metabolism that could contribute to lung diseases' development.</description><identifier>ISSN: 2076-3921</identifier><identifier>EISSN: 2076-3921</identifier><identifier>DOI: 10.3390/antiox12071361</identifier><identifier>PMID: 37507901</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adults ; Ascorbic acid ; bronchopulmonary dysplasia ; Capillary electrophoresis ; Chronic obstructive pulmonary disease ; Cysteine ; developmental origins of health and disease (DOHaD) ; Diet ; Diseases ; Dysplasia ; Ethylenediaminetetraacetic acid ; Evaluation ; Glutaredoxin ; Glutathione ; glutathionylation ; Infants (Newborn) ; Infants (Premature) ; Laboratories ; Lung diseases ; Lungs ; Membranes ; Metabolism ; Methionine ; Monoclonal antibodies ; mRNA ; Neonates ; Nutrition research ; Oxidative stress ; Parenteral nutrition ; Premature birth ; Proteins ; RNA ; Thiols ; thrifty phenotype hypothesis ; Vitamin C ; Vitamin deficiency</subject><ispartof>Antioxidants, 2023-06, Vol.12 (7), p.1361</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c507t-37d0b9b788dd5f651c49db87cc2fc975b2e4c96ea6f5cce24eb49e423d4533c13</cites><orcidid>0000-0002-9860-0279 ; 0000-0002-5910-0300 ; 0000-0002-5785-9110</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2842912668/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2842912668?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,74998</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37507901$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Teixeira, Vitor</creatorcontrib><creatorcontrib>Mohamed, Ibrahim</creatorcontrib><creatorcontrib>Lavoie, Jean-Claude</creatorcontrib><title>Disturbances of the Lung Glutathione System in Adult Guinea Pigs Following Neonatal Vitamin C or Cysteine Deficiency</title><title>Antioxidants</title><addtitle>Antioxidants (Basel)</addtitle><description>In premature infants receiving parenteral nutrition, oxidative stress is a trigger for the development of bronchopulmonary dysplasia, which is an important factor in the development of adult lung diseases. Neonatal vitamin C and glutathione deficiency is suspected to induce permanent modification of redox metabolism favoring the development of neonatal and adult lung diseases. A total of 64 3-day-old guinea pigs were fed an oral diet that was either complete or deficient in vitamin C (VCD), cysteine (CD) (glutathione-limiting substrate) or both (DD) for 4 days. At 1 week of age, half of the animals were sacrificed while the other started a complete diet until 12 weeks of age. At 1 week, the decrease in lung GSH in all deficient groups was partially explained by the oxidation of liver methionine-adenosyltransferase. mRNA levels of kelch-like ECH-associated protein 1 (
), glutathione-reductase (
) and glutaredoxin-1 (
) were significantly lower only in CD but not in DD. At 12 weeks, glutathione levels were increased in VCD and CD.
,
and
mRNA were increased, while glutathione-reductase and glutaredoxin proteins were lower in CD, favoring a higher glutathionylation status. Both neonatal deficiencies result in a long-term change in glutathione metabolism that could contribute to lung diseases' development.</description><subject>Adults</subject><subject>Ascorbic acid</subject><subject>bronchopulmonary dysplasia</subject><subject>Capillary electrophoresis</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Cysteine</subject><subject>developmental origins of health and disease (DOHaD)</subject><subject>Diet</subject><subject>Diseases</subject><subject>Dysplasia</subject><subject>Ethylenediaminetetraacetic acid</subject><subject>Evaluation</subject><subject>Glutaredoxin</subject><subject>Glutathione</subject><subject>glutathionylation</subject><subject>Infants (Newborn)</subject><subject>Infants (Premature)</subject><subject>Laboratories</subject><subject>Lung diseases</subject><subject>Lungs</subject><subject>Membranes</subject><subject>Metabolism</subject><subject>Methionine</subject><subject>Monoclonal antibodies</subject><subject>mRNA</subject><subject>Neonates</subject><subject>Nutrition research</subject><subject>Oxidative stress</subject><subject>Parenteral nutrition</subject><subject>Premature birth</subject><subject>Proteins</subject><subject>RNA</subject><subject>Thiols</subject><subject>thrifty phenotype hypothesis</subject><subject>Vitamin C</subject><subject>Vitamin deficiency</subject><issn>2076-3921</issn><issn>2076-3921</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkk1vEzEQhlcIRKvQK0dkiQuXFH-tvT6hKKWhUgRIfFwtr3c2cbRrF9sL5N_jtKU0qPbBo_E7j2fGU1UvCT5nTOG3xmcXfhOKJWGCPKlOiyXmTFHy9IF9Up2ltMNlKcIarJ5XJ0zWWCpMTqt84VKeYmu8hYRCj_IW0HryG7Qapmzy1gUP6Ms-ZRiR82jRTUNGq8l5MOiz2yR0GYYh_HIl4iMEb7IZ0HeXzVjESxQiWh5iixxdQO-sA2_3L6pnvRkSnN2ds-rb5fuvyw_z9afV1XKxntuSXp4z2eFWtbJpuq7uRU0sV13bSGtpb5WsWwrcKgFG9LW1QDm0XAGnrOM1Y5awWXV1y-2C2enr6EYT9zoYp28cIW60idnZATSjhtU9ttQIya0hjZBdzVtZc9Nw1YjCenfLup7aEToLPkczHEGPb7zb6k34qQlmUvAbwps7Qgw_JkhZjy5ZGAbjIUxJ04ZzrJqm5D6rXv8n3YUp-tKrg4oqQoVo_qk2plTgfB_Kw_YA1QtZF5AQ-KA6f0RVdgejs-V3e1f8jwXYGFKK0N8XSbA-zJ0-nrsS8Opha-7lf6eM_QGwa9Nv</recordid><startdate>20230629</startdate><enddate>20230629</enddate><creator>Teixeira, Vitor</creator><creator>Mohamed, Ibrahim</creator><creator>Lavoie, Jean-Claude</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QR</scope><scope>7T5</scope><scope>7TO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-9860-0279</orcidid><orcidid>https://orcid.org/0000-0002-5910-0300</orcidid><orcidid>https://orcid.org/0000-0002-5785-9110</orcidid></search><sort><creationdate>20230629</creationdate><title>Disturbances of the Lung Glutathione System in Adult Guinea Pigs Following Neonatal Vitamin C or Cysteine Deficiency</title><author>Teixeira, Vitor ; Mohamed, Ibrahim ; Lavoie, Jean-Claude</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-37d0b9b788dd5f651c49db87cc2fc975b2e4c96ea6f5cce24eb49e423d4533c13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Adults</topic><topic>Ascorbic acid</topic><topic>bronchopulmonary dysplasia</topic><topic>Capillary electrophoresis</topic><topic>Chronic obstructive pulmonary disease</topic><topic>Cysteine</topic><topic>developmental origins of health and disease (DOHaD)</topic><topic>Diet</topic><topic>Diseases</topic><topic>Dysplasia</topic><topic>Ethylenediaminetetraacetic acid</topic><topic>Evaluation</topic><topic>Glutaredoxin</topic><topic>Glutathione</topic><topic>glutathionylation</topic><topic>Infants (Newborn)</topic><topic>Infants (Premature)</topic><topic>Laboratories</topic><topic>Lung diseases</topic><topic>Lungs</topic><topic>Membranes</topic><topic>Metabolism</topic><topic>Methionine</topic><topic>Monoclonal antibodies</topic><topic>mRNA</topic><topic>Neonates</topic><topic>Nutrition research</topic><topic>Oxidative stress</topic><topic>Parenteral nutrition</topic><topic>Premature birth</topic><topic>Proteins</topic><topic>RNA</topic><topic>Thiols</topic><topic>thrifty phenotype hypothesis</topic><topic>Vitamin C</topic><topic>Vitamin deficiency</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Teixeira, Vitor</creatorcontrib><creatorcontrib>Mohamed, Ibrahim</creatorcontrib><creatorcontrib>Lavoie, Jean-Claude</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content (ProQuest)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Antioxidants</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Teixeira, Vitor</au><au>Mohamed, Ibrahim</au><au>Lavoie, Jean-Claude</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disturbances of the Lung Glutathione System in Adult Guinea Pigs Following Neonatal Vitamin C or Cysteine Deficiency</atitle><jtitle>Antioxidants</jtitle><addtitle>Antioxidants (Basel)</addtitle><date>2023-06-29</date><risdate>2023</risdate><volume>12</volume><issue>7</issue><spage>1361</spage><pages>1361-</pages><issn>2076-3921</issn><eissn>2076-3921</eissn><abstract>In premature infants receiving parenteral nutrition, oxidative stress is a trigger for the development of bronchopulmonary dysplasia, which is an important factor in the development of adult lung diseases. Neonatal vitamin C and glutathione deficiency is suspected to induce permanent modification of redox metabolism favoring the development of neonatal and adult lung diseases. A total of 64 3-day-old guinea pigs were fed an oral diet that was either complete or deficient in vitamin C (VCD), cysteine (CD) (glutathione-limiting substrate) or both (DD) for 4 days. At 1 week of age, half of the animals were sacrificed while the other started a complete diet until 12 weeks of age. At 1 week, the decrease in lung GSH in all deficient groups was partially explained by the oxidation of liver methionine-adenosyltransferase. mRNA levels of kelch-like ECH-associated protein 1 (
), glutathione-reductase (
) and glutaredoxin-1 (
) were significantly lower only in CD but not in DD. At 12 weeks, glutathione levels were increased in VCD and CD.
,
and
mRNA were increased, while glutathione-reductase and glutaredoxin proteins were lower in CD, favoring a higher glutathionylation status. Both neonatal deficiencies result in a long-term change in glutathione metabolism that could contribute to lung diseases' development.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37507901</pmid><doi>10.3390/antiox12071361</doi><orcidid>https://orcid.org/0000-0002-9860-0279</orcidid><orcidid>https://orcid.org/0000-0002-5910-0300</orcidid><orcidid>https://orcid.org/0000-0002-5785-9110</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adults Ascorbic acid bronchopulmonary dysplasia Capillary electrophoresis Chronic obstructive pulmonary disease Cysteine developmental origins of health and disease (DOHaD) Diet Diseases Dysplasia Ethylenediaminetetraacetic acid Evaluation Glutaredoxin Glutathione glutathionylation Infants (Newborn) Infants (Premature) Laboratories Lung diseases Lungs Membranes Metabolism Methionine Monoclonal antibodies mRNA Neonates Nutrition research Oxidative stress Parenteral nutrition Premature birth Proteins RNA Thiols thrifty phenotype hypothesis Vitamin C Vitamin deficiency |
title | Disturbances of the Lung Glutathione System in Adult Guinea Pigs Following Neonatal Vitamin C or Cysteine Deficiency |
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