Loading…
Tolerance of neonatal rat brain to acute hyperammonemia
The aim of the present work was to study the effects of hyperammonemia on brain energy metabolism in neonatal rats. Rats were rendered hyperammonemic by ammonium acetate administration. This decreased brain ATP concentrations but enhanced brain ammonia and lactate levels in both adult and neonatal r...
Saved in:
Published in: | Brain research 2003-05, Vol.973 (1), p.31-38 |
---|---|
Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c424t-964d4b32035cddf700127a95d558cc84048e406b3a93e83c67cdda0044ccbc6f3 |
---|---|
cites | cdi_FETCH-LOGICAL-c424t-964d4b32035cddf700127a95d558cc84048e406b3a93e83c67cdda0044ccbc6f3 |
container_end_page | 38 |
container_issue | 1 |
container_start_page | 31 |
container_title | Brain research |
container_volume | 973 |
creator | Garcı́ a, M.Victoria López-Mediavilla, Casilda Juanes de la Peña, Marı́ a C. Medina, José M. |
description | The aim of the present work was to study the effects of hyperammonemia on brain energy metabolism in neonatal rats. Rats were rendered hyperammonemic by ammonium acetate administration. This decreased brain ATP concentrations but enhanced brain ammonia and lactate levels in both adult and neonatal rats. In adult rats, the decrease in brain ATP concentrations was accompanied by a plunge in the respiratory control rate (RCR) of brain mitochondria. However, the ammonia-induced effect on RCR was not observed in neonatal rats, suggesting that the fall in ATP levels observed in neonatal rats would not be due to an impairment of mitochondrial respiratory efficiency. However, in neonatal rats the increase in blood and brain ammonia concentrations did not change brain glutamate concentrations but decreased glutamine contents. These results may be of relevance for the understanding of the resistance of neonatal rats observed in this work to acute ammonia toxicity |
doi_str_mv | 10.1016/S0006-8993(03)02529-0 |
format | article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_18918540</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0006899303025290</els_id><sourcerecordid>18918540</sourcerecordid><originalsourceid>FETCH-LOGICAL-c424t-964d4b32035cddf700127a95d558cc84048e406b3a93e83c67cdda0044ccbc6f3</originalsourceid><addsrcrecordid>eNqFkE1LxDAQhoMouq7-BKUXRQ_VyVfbnEQWv2DBg-s5pGmKkbZZk1bYf2_qFvcoDAwDz8y8PAidYbjBgLPbNwDI0kIIegX0GggnIoU9NMNFTtKMMNhHsz_kCB2H8BlHSgUcoiNMciIEhxnKV64xXnXaJK5OOuM61asm8apPSq9sl_QuUXroTfKxWUewbV1nWqtO0EGtmmBOpz5H748Pq8Vzunx9elncL1PNCOtTkbGKlZQA5bqq6hwgvlaCV5wXWhcMWGEYZCVVgpqC6iyPmAJgTOtSZzWdo8vt3bV3X4MJvWxt0KZpVMw6BIkLgQvOIIJ8C2rvQvCmlmtvW-U3EoMcjclfY3LUISHWaEyOe-fTg6FsTbXbmhRF4GICVNCqqUdZNuw4ljOeQx65uy1noo5va7wM2pootrLe6F5Wzv4T5QfV04a-</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>18918540</pqid></control><display><type>article</type><title>Tolerance of neonatal rat brain to acute hyperammonemia</title><source>Elsevier:Jisc Collections:Elsevier Read and Publish Agreement 2022-2024:Freedom Collection (Reading list)</source><creator>Garcı&#x0301;a, M.Victoria ; López-Mediavilla, Casilda ; Juanes de la Peña, Marı&#x0301;a C. ; Medina, José M.</creator><creatorcontrib>Garcı&#x0301;a, M.Victoria ; López-Mediavilla, Casilda ; Juanes de la Peña, Marı&#x0301;a C. ; Medina, José M.</creatorcontrib><description>The aim of the present work was to study the effects of hyperammonemia on brain energy metabolism in neonatal rats. Rats were rendered hyperammonemic by ammonium acetate administration. This decreased brain ATP concentrations but enhanced brain ammonia and lactate levels in both adult and neonatal rats. In adult rats, the decrease in brain ATP concentrations was accompanied by a plunge in the respiratory control rate (RCR) of brain mitochondria. However, the ammonia-induced effect on RCR was not observed in neonatal rats, suggesting that the fall in ATP levels observed in neonatal rats would not be due to an impairment of mitochondrial respiratory efficiency. However, in neonatal rats the increase in blood and brain ammonia concentrations did not change brain glutamate concentrations but decreased glutamine contents. These results may be of relevance for the understanding of the resistance of neonatal rats observed in this work to acute ammonia toxicity</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/S0006-8993(03)02529-0</identifier><identifier>PMID: 12729950</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Acute Disease ; Adenosine Triphosphate - metabolism ; Age Factors ; Ammonia - metabolism ; Ammonia - toxicity ; Animals ; Animals, Newborn ; Biological and medical sciences ; Brain - drug effects ; Brain - metabolism ; Errors of metabolism ; Female ; Glutamate ; Glutamic Acid - metabolism ; Glutamine ; Hyperammonemia ; Hyperammonemia - chemically induced ; Hyperammonemia - metabolism ; Lactic Acid - metabolism ; Male ; Medical sciences ; Metabolic diseases ; Miscellaneous hereditary metabolic disorders ; Mitochondria ; Neonate ; Rats ; Rats, Wistar</subject><ispartof>Brain research, 2003-05, Vol.973 (1), p.31-38</ispartof><rights>2003 Elsevier Science B.V.</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c424t-964d4b32035cddf700127a95d558cc84048e406b3a93e83c67cdda0044ccbc6f3</citedby><cites>FETCH-LOGICAL-c424t-964d4b32035cddf700127a95d558cc84048e406b3a93e83c67cdda0044ccbc6f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14745707$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12729950$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Garcı&#x0301;a, M.Victoria</creatorcontrib><creatorcontrib>López-Mediavilla, Casilda</creatorcontrib><creatorcontrib>Juanes de la Peña, Marı&#x0301;a C.</creatorcontrib><creatorcontrib>Medina, José M.</creatorcontrib><title>Tolerance of neonatal rat brain to acute hyperammonemia</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>The aim of the present work was to study the effects of hyperammonemia on brain energy metabolism in neonatal rats. Rats were rendered hyperammonemic by ammonium acetate administration. This decreased brain ATP concentrations but enhanced brain ammonia and lactate levels in both adult and neonatal rats. In adult rats, the decrease in brain ATP concentrations was accompanied by a plunge in the respiratory control rate (RCR) of brain mitochondria. However, the ammonia-induced effect on RCR was not observed in neonatal rats, suggesting that the fall in ATP levels observed in neonatal rats would not be due to an impairment of mitochondrial respiratory efficiency. However, in neonatal rats the increase in blood and brain ammonia concentrations did not change brain glutamate concentrations but decreased glutamine contents. These results may be of relevance for the understanding of the resistance of neonatal rats observed in this work to acute ammonia toxicity</description><subject>Acute Disease</subject><subject>Adenosine Triphosphate - metabolism</subject><subject>Age Factors</subject><subject>Ammonia - metabolism</subject><subject>Ammonia - toxicity</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Biological and medical sciences</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Errors of metabolism</subject><subject>Female</subject><subject>Glutamate</subject><subject>Glutamic Acid - metabolism</subject><subject>Glutamine</subject><subject>Hyperammonemia</subject><subject>Hyperammonemia - chemically induced</subject><subject>Hyperammonemia - metabolism</subject><subject>Lactic Acid - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Miscellaneous hereditary metabolic disorders</subject><subject>Mitochondria</subject><subject>Neonate</subject><subject>Rats</subject><subject>Rats, Wistar</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNqFkE1LxDAQhoMouq7-BKUXRQ_VyVfbnEQWv2DBg-s5pGmKkbZZk1bYf2_qFvcoDAwDz8y8PAidYbjBgLPbNwDI0kIIegX0GggnIoU9NMNFTtKMMNhHsz_kCB2H8BlHSgUcoiNMciIEhxnKV64xXnXaJK5OOuM61asm8apPSq9sl_QuUXroTfKxWUewbV1nWqtO0EGtmmBOpz5H748Pq8Vzunx9elncL1PNCOtTkbGKlZQA5bqq6hwgvlaCV5wXWhcMWGEYZCVVgpqC6iyPmAJgTOtSZzWdo8vt3bV3X4MJvWxt0KZpVMw6BIkLgQvOIIJ8C2rvQvCmlmtvW-U3EoMcjclfY3LUISHWaEyOe-fTg6FsTbXbmhRF4GICVNCqqUdZNuw4ljOeQx65uy1noo5va7wM2pootrLe6F5Wzv4T5QfV04a-</recordid><startdate>20030523</startdate><enddate>20030523</enddate><creator>Garcı&#x0301;a, M.Victoria</creator><creator>López-Mediavilla, Casilda</creator><creator>Juanes de la Peña, Marı&#x0301;a C.</creator><creator>Medina, José M.</creator><general>Elsevier B.V</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>20030523</creationdate><title>Tolerance of neonatal rat brain to acute hyperammonemia</title><author>Garcı&#x0301;a, M.Victoria ; López-Mediavilla, Casilda ; Juanes de la Peña, Marı&#x0301;a C. ; Medina, José M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c424t-964d4b32035cddf700127a95d558cc84048e406b3a93e83c67cdda0044ccbc6f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Acute Disease</topic><topic>Adenosine Triphosphate - metabolism</topic><topic>Age Factors</topic><topic>Ammonia - metabolism</topic><topic>Ammonia - toxicity</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Biological and medical sciences</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Errors of metabolism</topic><topic>Female</topic><topic>Glutamate</topic><topic>Glutamic Acid - metabolism</topic><topic>Glutamine</topic><topic>Hyperammonemia</topic><topic>Hyperammonemia - chemically induced</topic><topic>Hyperammonemia - metabolism</topic><topic>Lactic Acid - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Miscellaneous hereditary metabolic disorders</topic><topic>Mitochondria</topic><topic>Neonate</topic><topic>Rats</topic><topic>Rats, Wistar</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Garcı&#x0301;a, M.Victoria</creatorcontrib><creatorcontrib>López-Mediavilla, Casilda</creatorcontrib><creatorcontrib>Juanes de la Peña, Marı&#x0301;a C.</creatorcontrib><creatorcontrib>Medina, José M.</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>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Garcı&#x0301;a, M.Victoria</au><au>López-Mediavilla, Casilda</au><au>Juanes de la Peña, Marı&#x0301;a C.</au><au>Medina, José M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tolerance of neonatal rat brain to acute hyperammonemia</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2003-05-23</date><risdate>2003</risdate><volume>973</volume><issue>1</issue><spage>31</spage><epage>38</epage><pages>31-38</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>The aim of the present work was to study the effects of hyperammonemia on brain energy metabolism in neonatal rats. Rats were rendered hyperammonemic by ammonium acetate administration. This decreased brain ATP concentrations but enhanced brain ammonia and lactate levels in both adult and neonatal rats. In adult rats, the decrease in brain ATP concentrations was accompanied by a plunge in the respiratory control rate (RCR) of brain mitochondria. However, the ammonia-induced effect on RCR was not observed in neonatal rats, suggesting that the fall in ATP levels observed in neonatal rats would not be due to an impairment of mitochondrial respiratory efficiency. However, in neonatal rats the increase in blood and brain ammonia concentrations did not change brain glutamate concentrations but decreased glutamine contents. These results may be of relevance for the understanding of the resistance of neonatal rats observed in this work to acute ammonia toxicity</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>12729950</pmid><doi>10.1016/S0006-8993(03)02529-0</doi><tpages>8</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0006-8993 |
ispartof | Brain research, 2003-05, Vol.973 (1), p.31-38 |
issn | 0006-8993 1872-6240 |
language | eng |
recordid | cdi_proquest_miscellaneous_18918540 |
source | Elsevier:Jisc Collections:Elsevier Read and Publish Agreement 2022-2024:Freedom Collection (Reading list) |
subjects | Acute Disease Adenosine Triphosphate - metabolism Age Factors Ammonia - metabolism Ammonia - toxicity Animals Animals, Newborn Biological and medical sciences Brain - drug effects Brain - metabolism Errors of metabolism Female Glutamate Glutamic Acid - metabolism Glutamine Hyperammonemia Hyperammonemia - chemically induced Hyperammonemia - metabolism Lactic Acid - metabolism Male Medical sciences Metabolic diseases Miscellaneous hereditary metabolic disorders Mitochondria Neonate Rats Rats, Wistar |
title | Tolerance of neonatal rat brain to acute hyperammonemia |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-01T01%3A14%3A32IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Tolerance%20of%20neonatal%20rat%20brain%20to%20acute%20hyperammonemia&rft.jtitle=Brain%20research&rft.au=Garc%C4%B1&%23x0301;a,%20M.Victoria&rft.date=2003-05-23&rft.volume=973&rft.issue=1&rft.spage=31&rft.epage=38&rft.pages=31-38&rft.issn=0006-8993&rft.eissn=1872-6240&rft.coden=BRREAP&rft_id=info:doi/10.1016/S0006-8993(03)02529-0&rft_dat=%3Cproquest_cross%3E18918540%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c424t-964d4b32035cddf700127a95d558cc84048e406b3a93e83c67cdda0044ccbc6f3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=18918540&rft_id=info:pmid/12729950&rfr_iscdi=true |