NO control of mitochondrial function in normal and transformed cells
Autor(a) principal: | |
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Data de Publicação: | 2017 |
Outros Autores: | |
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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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 |
|
_version_ |
1802764123236204544 |