Reactive oxygen species as a trigger of the infarct-limiting effects of early hypoxic preconditioning rat myocardium

It is believed that reactive oxygen species (ROS) are involved in the performance of this adaptive hepatoprotective effect phenomenon. However, the role of ROS in the signaling mechanism of the early hypoxic preconditioning (early HP) and the contribution of individual types of oxygen radicals in th...

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Autores principales:	A. S. Sementsov, A. V. Krylatov
Formato:	article
Lenguaje:	RU
Publicado:	Scientific Сentre for Family Health and Human Reproduction Problems 2016
Materias:	reactive oxygen species preconditioning hypoxia ischemia heart Science Q
Acceso en línea:	https://doaj.org/article/8f25aeb362b14ca2a6c4f2f9f02e11e5
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spelling	oai:doaj.org-article:8f25aeb362b14ca2a6c4f2f9f02e11e52021-11-23T06:14:34ZReactive oxygen species as a trigger of the infarct-limiting effects of early hypoxic preconditioning rat myocardium2541-94202587-959610.12737/article_590823a507e6d8.99508073https://doaj.org/article/8f25aeb362b14ca2a6c4f2f9f02e11e52016-05-01T00:00:00Zhttps://www.actabiomedica.ru/jour/article/view/204https://doaj.org/toc/2541-9420https://doaj.org/toc/2587-9596It is believed that reactive oxygen species (ROS) are involved in the performance of this adaptive hepatoprotective effect phenomenon. However, the role of ROS in the signaling mechanism of the early hypoxic preconditioning (early HP) and the contribution of individual types of oxygen radicals in the infarct-limiting effect of early HP remains uncertain to the end. Objective was to investigate the role of various types of reactive oxygen species in the signaling mechanism of the infarct-limiting effect of early hypoxic preconditioning. We investigated the role of reactive oxygen species in the signaling mechanism of early HP in vivo. Adaptation of animals was conducted with 6 transient hypoxia-reoxygenation sessions before prolonged ischemia (45 min) and reperfusion (120 min). Low molecular weight antioxidants were administered 15 minutes prior to the HP. We found out that pretreatment with the nonselective antioxidant indirect action of N-(2-mercaptopropionyl)-glycine and "trap" of hydroxyl radicals 1,3-dimethylthiourea completely eliminated the infarct-limiting effect of adaptation. Administration of antioxidants tempol and trolox, as well as the use of N-(2-mercaptopropionyl)-glycine after HP had no effect on the protective effect of adaptation. Consequently, reactive oxygen species, including hydroxyl radical, operate as the trigger function in the signaling mechanism of early HP.A. S. SementsovA. V. KrylatovScientific Сentre for Family Health and Human Reproduction Problemsarticlereactive oxygen speciespreconditioninghypoxiaischemiaheartScienceQRUActa Biomedica Scientifica, Vol 1, Iss 3(2), Pp 128-130 (2016)
institution	DOAJ
collection	DOAJ
language	RU
topic	reactive oxygen species preconditioning hypoxia ischemia heart Science Q
spellingShingle	reactive oxygen species preconditioning hypoxia ischemia heart Science Q A. S. Sementsov A. V. Krylatov Reactive oxygen species as a trigger of the infarct-limiting effects of early hypoxic preconditioning rat myocardium
description	It is believed that reactive oxygen species (ROS) are involved in the performance of this adaptive hepatoprotective effect phenomenon. However, the role of ROS in the signaling mechanism of the early hypoxic preconditioning (early HP) and the contribution of individual types of oxygen radicals in the infarct-limiting effect of early HP remains uncertain to the end. Objective was to investigate the role of various types of reactive oxygen species in the signaling mechanism of the infarct-limiting effect of early hypoxic preconditioning. We investigated the role of reactive oxygen species in the signaling mechanism of early HP in vivo. Adaptation of animals was conducted with 6 transient hypoxia-reoxygenation sessions before prolonged ischemia (45 min) and reperfusion (120 min). Low molecular weight antioxidants were administered 15 minutes prior to the HP. We found out that pretreatment with the nonselective antioxidant indirect action of N-(2-mercaptopropionyl)-glycine and "trap" of hydroxyl radicals 1,3-dimethylthiourea completely eliminated the infarct-limiting effect of adaptation. Administration of antioxidants tempol and trolox, as well as the use of N-(2-mercaptopropionyl)-glycine after HP had no effect on the protective effect of adaptation. Consequently, reactive oxygen species, including hydroxyl radical, operate as the trigger function in the signaling mechanism of early HP.
format	article
author	A. S. Sementsov A. V. Krylatov
author_facet	A. S. Sementsov A. V. Krylatov
author_sort	A. S. Sementsov
title	Reactive oxygen species as a trigger of the infarct-limiting effects of early hypoxic preconditioning rat myocardium
title_short	Reactive oxygen species as a trigger of the infarct-limiting effects of early hypoxic preconditioning rat myocardium
title_full	Reactive oxygen species as a trigger of the infarct-limiting effects of early hypoxic preconditioning rat myocardium
title_fullStr	Reactive oxygen species as a trigger of the infarct-limiting effects of early hypoxic preconditioning rat myocardium
title_full_unstemmed	Reactive oxygen species as a trigger of the infarct-limiting effects of early hypoxic preconditioning rat myocardium
title_sort	reactive oxygen species as a trigger of the infarct-limiting effects of early hypoxic preconditioning rat myocardium
publisher	Scientific Сentre for Family Health and Human Reproduction Problems
publishDate	2016
url	https://doaj.org/article/8f25aeb362b14ca2a6c4f2f9f02e11e5
work_keys_str_mv	AT assementsov reactiveoxygenspeciesasatriggeroftheinfarctlimitingeffectsofearlyhypoxicpreconditioningratmyocardium AT avkrylatov reactiveoxygenspeciesasatriggeroftheinfarctlimitingeffectsofearlyhypoxicpreconditioningratmyocardium
_version_	1718417082400374784

Reactive oxygen species as a trigger of the infarct-limiting effects of early hypoxic preconditioning rat myocardium

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