Sleep deprivation reduces total plasma homocysteine levels in rats

Detalhes bibliográficos
Autor(a) principal: Oliveira, A. C. de [UNIFESP]
Data de Publicação: 2002
Outros Autores: D'Almeida, V [UNIFESP], Hipolide, D. C. [UNIFESP], Nobrega, J. N., Tufik, Sergio [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://repositorio.unifesp.br/handle/11600/26761
http://dx.doi.org/10.1139/Y02-018
Resumo: Hyperhomocysteinemia has been associated with pathological and stressful conditions and is a risk factor for cardiovascular disease. Since sleep deprivation is a stressful condition that is associated with disruption of various physiological processes, we investigated whether it would also be associated with increases in plasma homocysteine levels. Further, since hyperhomocysteinemia may promote oxidative stress, and we had previously found evidence of oxidative stress in brain following sleep deprivation, we also searched for evidence of systemic oxidative stress by measuring glutathione and thiobarbituric acid reactive substance levels. Rats were sleep deprived for 96 h using the platform technique. A group was killed after sleep deprivation and another two groups were allowed to undergo sleep recovery for 24 or 48 h. Contrary to expectation, plasma homocysteine was reduced in sleep-deprived rats as compared with the control group and did not revert to normal levels after 24 or 48 h of sleep recovery. A trend was observed towards decreased glutathione and increased thiobarbituric acid reactive substance levels in sleep-deprived rats. It is possible that the observed decreases in homocysteine levels may represent a self-correcting response to depleted glutathione in sleep-deprived animals, which would contribute to the attenuation of the deleterious effects of sleep deprivation.
id UFSP_f8f6e64ba664507370ca39669a08bc2c
oai_identifier_str oai:repositorio.unifesp.br:11600/26761
network_acronym_str UFSP
network_name_str Repositório Institucional da UNIFESP
repository_id_str 3465
spelling Oliveira, A. C. de [UNIFESP]D'Almeida, V [UNIFESP]Hipolide, D. C. [UNIFESP]Nobrega, J. N.Tufik, Sergio [UNIFESP]Universidade Federal de São Paulo (UNIFESP)Ctr Addict & Mental Hlth2016-01-24T12:33:15Z2016-01-24T12:33:15Z2002-03-01Canadian Journal of Physiology and Pharmacology. Ottawa: Natl Research Council Canada, v. 80, n. 3, p. 193-197, 2002.0008-4212http://repositorio.unifesp.br/handle/11600/26761http://dx.doi.org/10.1139/Y02-01810.1139/Y02-018WOS:000174559700003Hyperhomocysteinemia has been associated with pathological and stressful conditions and is a risk factor for cardiovascular disease. Since sleep deprivation is a stressful condition that is associated with disruption of various physiological processes, we investigated whether it would also be associated with increases in plasma homocysteine levels. Further, since hyperhomocysteinemia may promote oxidative stress, and we had previously found evidence of oxidative stress in brain following sleep deprivation, we also searched for evidence of systemic oxidative stress by measuring glutathione and thiobarbituric acid reactive substance levels. Rats were sleep deprived for 96 h using the platform technique. A group was killed after sleep deprivation and another two groups were allowed to undergo sleep recovery for 24 or 48 h. Contrary to expectation, plasma homocysteine was reduced in sleep-deprived rats as compared with the control group and did not revert to normal levels after 24 or 48 h of sleep recovery. A trend was observed towards decreased glutathione and increased thiobarbituric acid reactive substance levels in sleep-deprived rats. It is possible that the observed decreases in homocysteine levels may represent a self-correcting response to depleted glutathione in sleep-deprived animals, which would contribute to the attenuation of the deleterious effects of sleep deprivation.Universidade Federal de São Paulo, Escola Paulista Med, Dept Psychobiol, São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Pediat, São Paulo, BrazilCtr Addict & Mental Hlth, Toronto, ON M5S 2S1, CanadaUniversidade Federal de São Paulo, Escola Paulista Med, Dept Psychobiol, São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Pediat, São Paulo, BrazilWeb of Science193-197engNatl Research Council CanadaCanadian Journal of Physiology and Pharmacologysleep deprivationhomocysteineoxidative stressglutathioneratsSleep deprivation reduces total plasma homocysteine levels in ratsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/267612022-06-02 09:20:42.483metadata only accessoai:repositorio.unifesp.br:11600/26761Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:15:02.374745Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv Sleep deprivation reduces total plasma homocysteine levels in rats
title Sleep deprivation reduces total plasma homocysteine levels in rats
spellingShingle Sleep deprivation reduces total plasma homocysteine levels in rats
Oliveira, A. C. de [UNIFESP]
sleep deprivation
homocysteine
oxidative stress
glutathione
rats
title_short Sleep deprivation reduces total plasma homocysteine levels in rats
title_full Sleep deprivation reduces total plasma homocysteine levels in rats
title_fullStr Sleep deprivation reduces total plasma homocysteine levels in rats
title_full_unstemmed Sleep deprivation reduces total plasma homocysteine levels in rats
title_sort Sleep deprivation reduces total plasma homocysteine levels in rats
author Oliveira, A. C. de [UNIFESP]
author_facet Oliveira, A. C. de [UNIFESP]
D'Almeida, V [UNIFESP]
Hipolide, D. C. [UNIFESP]
Nobrega, J. N.
Tufik, Sergio [UNIFESP]
author_role author
author2 D'Almeida, V [UNIFESP]
Hipolide, D. C. [UNIFESP]
Nobrega, J. N.
Tufik, Sergio [UNIFESP]
author2_role author
author
author
author
dc.contributor.institution.none.fl_str_mv Universidade Federal de São Paulo (UNIFESP)
Ctr Addict & Mental Hlth
dc.contributor.author.fl_str_mv Oliveira, A. C. de [UNIFESP]
D'Almeida, V [UNIFESP]
Hipolide, D. C. [UNIFESP]
Nobrega, J. N.
Tufik, Sergio [UNIFESP]
dc.subject.eng.fl_str_mv sleep deprivation
homocysteine
oxidative stress
glutathione
rats
topic sleep deprivation
homocysteine
oxidative stress
glutathione
rats
description Hyperhomocysteinemia has been associated with pathological and stressful conditions and is a risk factor for cardiovascular disease. Since sleep deprivation is a stressful condition that is associated with disruption of various physiological processes, we investigated whether it would also be associated with increases in plasma homocysteine levels. Further, since hyperhomocysteinemia may promote oxidative stress, and we had previously found evidence of oxidative stress in brain following sleep deprivation, we also searched for evidence of systemic oxidative stress by measuring glutathione and thiobarbituric acid reactive substance levels. Rats were sleep deprived for 96 h using the platform technique. A group was killed after sleep deprivation and another two groups were allowed to undergo sleep recovery for 24 or 48 h. Contrary to expectation, plasma homocysteine was reduced in sleep-deprived rats as compared with the control group and did not revert to normal levels after 24 or 48 h of sleep recovery. A trend was observed towards decreased glutathione and increased thiobarbituric acid reactive substance levels in sleep-deprived rats. It is possible that the observed decreases in homocysteine levels may represent a self-correcting response to depleted glutathione in sleep-deprived animals, which would contribute to the attenuation of the deleterious effects of sleep deprivation.
publishDate 2002
dc.date.issued.fl_str_mv 2002-03-01
dc.date.accessioned.fl_str_mv 2016-01-24T12:33:15Z
dc.date.available.fl_str_mv 2016-01-24T12:33:15Z
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 Canadian Journal of Physiology and Pharmacology. Ottawa: Natl Research Council Canada, v. 80, n. 3, p. 193-197, 2002.
dc.identifier.uri.fl_str_mv http://repositorio.unifesp.br/handle/11600/26761
http://dx.doi.org/10.1139/Y02-018
dc.identifier.issn.none.fl_str_mv 0008-4212
dc.identifier.doi.none.fl_str_mv 10.1139/Y02-018
dc.identifier.wos.none.fl_str_mv WOS:000174559700003
identifier_str_mv Canadian Journal of Physiology and Pharmacology. Ottawa: Natl Research Council Canada, v. 80, n. 3, p. 193-197, 2002.
0008-4212
10.1139/Y02-018
WOS:000174559700003
url http://repositorio.unifesp.br/handle/11600/26761
http://dx.doi.org/10.1139/Y02-018
dc.language.iso.fl_str_mv eng
language eng
dc.relation.ispartof.none.fl_str_mv Canadian Journal of Physiology and Pharmacology
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 193-197
dc.publisher.none.fl_str_mv Natl Research Council Canada
publisher.none.fl_str_mv Natl Research Council Canada
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_ 1783460267913379840