Modulation of brain mitochondrial membrane permeability and synaptosomal Ca2+ transport by dopamine oxidation
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, KJ | - |
dc.contributor.author | Jang, YY | - |
dc.contributor.author | Hang, ES | - |
dc.contributor.author | Lee, CS | - |
dc.date.available | 2019-05-30T10:35:26Z | - |
dc.date.issued | 1999-11 | - |
dc.identifier.issn | 0300-8177 | - |
dc.identifier.issn | 1573-4919 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/25380 | - |
dc.description.abstract | Effects of dopamine on the membrane permeability transition, thioredoxin reductase activity, production of free radicals and oxidation of sulfhydryl groups in brain mitochondria and the Ca2+ uptake by Na+-Ca2+ exchange and sulfhydryl oxidation in brain synaptosomes were examined. The brain mitochondrial swelling and the fall of transmembrane potential were altered by pretreatment of dopamine in a dose dependent manner. Depressive effect of dopamine on mitochondrial swelling was reversed by 10 mu g/ml catalase, and 10 mM DMSO. The activities of thioredoxin reductase in intact or disrupted mitochondria were decreased by dopamine (1-100 mu M), 25 mu M Zn2+ and 50 mu M Mn2+. Dopamine-inhibited enzyme activity was reversed by 10 mu g/ml SOD and 10 mu g/ml catalase. Pretreatment of dopamine decreased Ca2+ transport in synaptosomes, which was restored by 10 mu g/ml SOD and 10 mM DMSO. Dopamine (1-100 mu M) in the medium containing mitochondria produced superoxide anion and hydrogen peroxide, while its effect on nitrite production was very weak. The oxidation of sulfhydryl groups in mitochondria and synaptosomes were enhanced by dopamine with increasing incubation times. Results suggest that dopamine could modulate membrane permeability in mitochondria and calcium transport at nerve terminals, which may be ascribed to the action of free radicals and the loss of reduced sulfhydryl groups. | - |
dc.format.extent | 10 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | KLUWER ACADEMIC PUBL | - |
dc.title | Modulation of brain mitochondrial membrane permeability and synaptosomal Ca2+ transport by dopamine oxidation | - |
dc.type | Article | - |
dc.identifier.doi | 10.1023/A:1007008417342 | - |
dc.identifier.bibliographicCitation | MOLECULAR AND CELLULAR BIOCHEMISTRY, v.201, no.1-2, pp 89 - 98 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000083717300012 | - |
dc.identifier.scopusid | 2-s2.0-0001952035 | - |
dc.citation.endPage | 98 | - |
dc.citation.number | 1-2 | - |
dc.citation.startPage | 89 | - |
dc.citation.title | MOLECULAR AND CELLULAR BIOCHEMISTRY | - |
dc.citation.volume | 201 | - |
dc.type.docType | Article | - |
dc.publisher.location | 네델란드 | - |
dc.subject.keywordAuthor | dopamine | - |
dc.subject.keywordAuthor | brain mitochondria | - |
dc.subject.keywordAuthor | synaptosomes | - |
dc.subject.keywordAuthor | oxidative stress | - |
dc.subject.keywordPlus | RAT-LIVER MITOCHONDRIA | - |
dc.subject.keywordPlus | PARKINSONS-DISEASE | - |
dc.subject.keywordPlus | MONOAMINE-OXIDASE | - |
dc.subject.keywordPlus | FREE-RADICALS | - |
dc.subject.keywordPlus | CELL-DEATH | - |
dc.subject.keywordPlus | STRESS | - |
dc.subject.keywordPlus | GLUTATHIONE | - |
dc.subject.keywordPlus | TRANSITION | - |
dc.subject.keywordPlus | MECHANISM | - |
dc.subject.keywordPlus | INJURY | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
84, Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea (06974)02-820-6194
COPYRIGHT 2019 Chung-Ang University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.