Effects of calmodulin antagonists on the active Ca2+ uptake by rat liver mitochondria
Autor(a) principal: | |
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Data de Publicação: | 1983 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10316/13031 https://doi.org/10.1042/bj2140929 |
Resumo: | The mechanism of Ca2+ transport by rat liver mitochondria was investigated with respect to the possible involvement of calmodulin in this process. We studied the action of exogenous calmodulin isolated from brain tissue on the Ca2+-transport system, as well as the effect of two types of calmodulin antagonists; the phenothiazine drugs trifluoperazine and chlorpromazine and the more specific substance compound 48/80. Our results show that Ca2+ transport by mitochondria and mitochondrial ATPase activity are insensitive to exogenous calmodulin, although they can be inhibited by the phenothiazines. Since no effect of compound 48/80 was observed, we believe that the phenothiazines act through a mechanism that does not involve calmodulin. This is in accord with our inability to locate significant quantities of calmodulin in mitochondria by radioimmunoassay analysis. Our results further show that trifluoperazine and chlorpromazine also inhibit the electron-carrier system of the respiratory chain, and this effect may mediate their inhibitory action on Ca2+ transport when it is energized by respiration instead of ATP hydrolysis |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Effects of calmodulin antagonists on the active Ca2+ uptake by rat liver mitochondriaThe mechanism of Ca2+ transport by rat liver mitochondria was investigated with respect to the possible involvement of calmodulin in this process. We studied the action of exogenous calmodulin isolated from brain tissue on the Ca2+-transport system, as well as the effect of two types of calmodulin antagonists; the phenothiazine drugs trifluoperazine and chlorpromazine and the more specific substance compound 48/80. Our results show that Ca2+ transport by mitochondria and mitochondrial ATPase activity are insensitive to exogenous calmodulin, although they can be inhibited by the phenothiazines. Since no effect of compound 48/80 was observed, we believe that the phenothiazines act through a mechanism that does not involve calmodulin. This is in accord with our inability to locate significant quantities of calmodulin in mitochondria by radioimmunoassay analysis. Our results further show that trifluoperazine and chlorpromazine also inhibit the electron-carrier system of the respiratory chain, and this effect may mediate their inhibitory action on Ca2+ transport when it is energized by respiration instead of ATP hydrolysisPortland Press1983-09-15info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://hdl.handle.net/10316/13031http://hdl.handle.net/10316/13031https://doi.org/10.1042/bj2140929engBiochemical Journal. 214:3 (1983) 929–9350306-3283Vale, M. G. P.Moreno, A. J. M.Carvalho, A. P.info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2021-11-05T10:55:19Zoai:estudogeral.uc.pt:10316/13031Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T20:55:53.764277Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
Effects of calmodulin antagonists on the active Ca2+ uptake by rat liver mitochondria |
title |
Effects of calmodulin antagonists on the active Ca2+ uptake by rat liver mitochondria |
spellingShingle |
Effects of calmodulin antagonists on the active Ca2+ uptake by rat liver mitochondria Vale, M. G. P. |
title_short |
Effects of calmodulin antagonists on the active Ca2+ uptake by rat liver mitochondria |
title_full |
Effects of calmodulin antagonists on the active Ca2+ uptake by rat liver mitochondria |
title_fullStr |
Effects of calmodulin antagonists on the active Ca2+ uptake by rat liver mitochondria |
title_full_unstemmed |
Effects of calmodulin antagonists on the active Ca2+ uptake by rat liver mitochondria |
title_sort |
Effects of calmodulin antagonists on the active Ca2+ uptake by rat liver mitochondria |
author |
Vale, M. G. P. |
author_facet |
Vale, M. G. P. Moreno, A. J. M. Carvalho, A. P. |
author_role |
author |
author2 |
Moreno, A. J. M. Carvalho, A. P. |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
Vale, M. G. P. Moreno, A. J. M. Carvalho, A. P. |
description |
The mechanism of Ca2+ transport by rat liver mitochondria was investigated with respect to the possible involvement of calmodulin in this process. We studied the action of exogenous calmodulin isolated from brain tissue on the Ca2+-transport system, as well as the effect of two types of calmodulin antagonists; the phenothiazine drugs trifluoperazine and chlorpromazine and the more specific substance compound 48/80. Our results show that Ca2+ transport by mitochondria and mitochondrial ATPase activity are insensitive to exogenous calmodulin, although they can be inhibited by the phenothiazines. Since no effect of compound 48/80 was observed, we believe that the phenothiazines act through a mechanism that does not involve calmodulin. This is in accord with our inability to locate significant quantities of calmodulin in mitochondria by radioimmunoassay analysis. Our results further show that trifluoperazine and chlorpromazine also inhibit the electron-carrier system of the respiratory chain, and this effect may mediate their inhibitory action on Ca2+ transport when it is energized by respiration instead of ATP hydrolysis |
publishDate |
1983 |
dc.date.none.fl_str_mv |
1983-09-15 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10316/13031 http://hdl.handle.net/10316/13031 https://doi.org/10.1042/bj2140929 |
url |
http://hdl.handle.net/10316/13031 https://doi.org/10.1042/bj2140929 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Biochemical Journal. 214:3 (1983) 929–935 0306-3283 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.publisher.none.fl_str_mv |
Portland Press |
publisher.none.fl_str_mv |
Portland Press |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
instname_str |
Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
instacron_str |
RCAAP |
institution |
RCAAP |
reponame_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
collection |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
repository.name.fl_str_mv |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
repository.mail.fl_str_mv |
|
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1799133844892286976 |