NO control of mitochondrial function in normal and transformed cells

Detalhes bibliográficos
Autor(a) principal: Tengan, Celia H. [UNIFESP]
Data de Publicação: 2017
Outros Autores: Moraes, Carlos T.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://repositorio.unifesp.br/handle/11600/51487
http://dx.doi.org/10.1016/j.bbabio.2017.02.009
Resumo: Nitric oxide (NO) is a signaling molecule with multiple facets and involved in numerous pathological process, including cancer. Among the different pathways where NO has a functionally relevant participation, is the control of mitochondrial respiration and biogenesis. NO is able to inhibit the electron transport chain, mainly at Complex IV, regulating oxygen consumption and ATP generation, but at the same time, can also induce increase in reactive oxygen and nitrogen species. The presence of reactive species can induce oxidative damage or participate in redox signaling. In this review, we discuss how NO affects mitochondrial respiration and mitochondrial biogenesis, and how it influences the development of mitochondrial deficiency and cancer. This article is part of a Special Issue entitled Mitochondria in Cancer, edited by Giuseppe Gasparre, Rodrigue Rossignol and Pierre Sonveaux. (C) 2017 Elsevier B.V. All rights reserved.
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spelling Tengan, Celia H. [UNIFESP]Moraes, Carlos T.2019-08-19T11:50:11Z2019-08-19T11:50:11Z2017Biochimica Et Biophysica Acta-Bioenergetics. Amsterdam, v. 1858, n. 8, p. 573-581, 2017.0005-2728http://repositorio.unifesp.br/handle/11600/51487http://dx.doi.org/10.1016/j.bbabio.2017.02.00910.1016/j.bbabio.2017.02.009WOS:000405763800003Nitric oxide (NO) is a signaling molecule with multiple facets and involved in numerous pathological process, including cancer. Among the different pathways where NO has a functionally relevant participation, is the control of mitochondrial respiration and biogenesis. NO is able to inhibit the electron transport chain, mainly at Complex IV, regulating oxygen consumption and ATP generation, but at the same time, can also induce increase in reactive oxygen and nitrogen species. The presence of reactive species can induce oxidative damage or participate in redox signaling. In this review, we discuss how NO affects mitochondrial respiration and mitochondrial biogenesis, and how it influences the development of mitochondrial deficiency and cancer. This article is part of a Special Issue entitled Mitochondria in Cancer, edited by Giuseppe Gasparre, Rodrigue Rossignol and Pierre Sonveaux. (C) 2017 Elsevier B.V. All rights reserved.Sao Paulo Research Foundation (FAPESP)National Institutes of Health (NIH)Muscular Dystrophy AssociationUniv Fed São Paulo, Escola Paulista Med, Dept Neurol & Neurosurg, R Pedro de Toledo 781,Setimo Andar, BR-04039032 São Paulo, SP, BrazilUniv Miami, Miller Sch Med, Dept Neurol & Cell Biol, 1420 NW 9th Ave,Rm 229, Miami, FL 33136 USAUniv Fed São Paulo, Escola Paulista Med, Dept Neurol & Neurosurg, R Pedro de Toledo 781,Setimo Andar, BR-04039032 São Paulo, SP, BrazilFAPESP: 2007/03134-9NIH: 1R01NS079965NIH: 1R01AG036871NIH: 5R01EY010804NIH: 1R21ES025673MDA: 294407Web of Science573-581engElsevier Science BvNitric oxideNitric oxide synthaseMitochondriaCancerRespiratory chainNO control of mitochondrial function in normal and transformed cellsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/514872022-02-08 12:09:31.733metadata only accessoai:repositorio.unifesp.br:11600/51487Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-02-08T15:09:31Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv NO control of mitochondrial function in normal and transformed cells
title NO control of mitochondrial function in normal and transformed cells
spellingShingle NO control of mitochondrial function in normal and transformed cells
Tengan, Celia H. [UNIFESP]
Nitric oxide
Nitric oxide synthase
Mitochondria
Cancer
Respiratory chain
title_short NO control of mitochondrial function in normal and transformed cells
title_full NO control of mitochondrial function in normal and transformed cells
title_fullStr NO control of mitochondrial function in normal and transformed cells
title_full_unstemmed NO control of mitochondrial function in normal and transformed cells
title_sort NO control of mitochondrial function in normal and transformed cells
author Tengan, Celia H. [UNIFESP]
author_facet Tengan, Celia H. [UNIFESP]
Moraes, Carlos T.
author_role author
author2 Moraes, Carlos T.
author2_role author
dc.contributor.author.fl_str_mv Tengan, Celia H. [UNIFESP]
Moraes, Carlos T.
dc.subject.eng.fl_str_mv Nitric oxide
Nitric oxide synthase
Mitochondria
Cancer
Respiratory chain
topic Nitric oxide
Nitric oxide synthase
Mitochondria
Cancer
Respiratory chain
description Nitric oxide (NO) is a signaling molecule with multiple facets and involved in numerous pathological process, including cancer. Among the different pathways where NO has a functionally relevant participation, is the control of mitochondrial respiration and biogenesis. NO is able to inhibit the electron transport chain, mainly at Complex IV, regulating oxygen consumption and ATP generation, but at the same time, can also induce increase in reactive oxygen and nitrogen species. The presence of reactive species can induce oxidative damage or participate in redox signaling. In this review, we discuss how NO affects mitochondrial respiration and mitochondrial biogenesis, and how it influences the development of mitochondrial deficiency and cancer. This article is part of a Special Issue entitled Mitochondria in Cancer, edited by Giuseppe Gasparre, Rodrigue Rossignol and Pierre Sonveaux. (C) 2017 Elsevier B.V. All rights reserved.
publishDate 2017
dc.date.issued.fl_str_mv 2017
dc.date.accessioned.fl_str_mv 2019-08-19T11:50:11Z
dc.date.available.fl_str_mv 2019-08-19T11:50:11Z
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.citation.fl_str_mv Biochimica Et Biophysica Acta-Bioenergetics. Amsterdam, v. 1858, n. 8, p. 573-581, 2017.
dc.identifier.uri.fl_str_mv http://repositorio.unifesp.br/handle/11600/51487
http://dx.doi.org/10.1016/j.bbabio.2017.02.009
dc.identifier.issn.none.fl_str_mv 0005-2728
dc.identifier.doi.none.fl_str_mv 10.1016/j.bbabio.2017.02.009
dc.identifier.wos.none.fl_str_mv WOS:000405763800003
identifier_str_mv Biochimica Et Biophysica Acta-Bioenergetics. Amsterdam, v. 1858, n. 8, p. 573-581, 2017.
0005-2728
10.1016/j.bbabio.2017.02.009
WOS:000405763800003
url http://repositorio.unifesp.br/handle/11600/51487
http://dx.doi.org/10.1016/j.bbabio.2017.02.009
dc.language.iso.fl_str_mv eng
language eng
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 573-581
dc.publisher.none.fl_str_mv Elsevier Science Bv
publisher.none.fl_str_mv Elsevier Science Bv
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv
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