Targeting mitochondrial reactive oxygen species-mediated oxidative stress attenuates nicotine-induced cardiac remodeling and dysfunction

Abstract Long-term nicotine intake is associated with an increased risk of myocardial damage and dysfunction. However, it remains unclear whether targeting mitochondrial reactive oxygen species (ROS) prevents nicotine-induced cardiac remodeling and dysfunction. This study investigated the effects of...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Anand Ramalingam, Siti Balkis Budin, Norsyahida Mohd Fauzi, Rebecca H. Ritchie, Satirah Zainalabidin
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/4822e11dae67459f93b0a8a97da64a99
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:4822e11dae67459f93b0a8a97da64a99
record_format	dspace
spelling	oai:doaj.org-article:4822e11dae67459f93b0a8a97da64a992021-12-02T18:34:13ZTargeting mitochondrial reactive oxygen species-mediated oxidative stress attenuates nicotine-induced cardiac remodeling and dysfunction10.1038/s41598-021-93234-42045-2322https://doaj.org/article/4822e11dae67459f93b0a8a97da64a992021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-93234-4https://doaj.org/toc/2045-2322Abstract Long-term nicotine intake is associated with an increased risk of myocardial damage and dysfunction. However, it remains unclear whether targeting mitochondrial reactive oxygen species (ROS) prevents nicotine-induced cardiac remodeling and dysfunction. This study investigated the effects of mitoTEMPO (a mitochondria-targeted antioxidant), and resveratrol (a sirtuin activator) , on nicotine-induced cardiac remodeling and dysfunction. Sprague–Dawley rats were administered 0.6 mg/kg nicotine daily with 0.7 mg/kg mitoTEMPO, 8 mg/kg resveratrol, or vehicle alone for 28 days. At the end of the study, rat hearts were collected to analyze the cardiac structure, mitochondrial ROS level, oxidative stress, and inflammation markers. A subset of rat hearts was perfused ex vivo to determine the cardiac function and myocardial susceptibility to ischemia–reperfusion injury. Nicotine administration significantly augmented mitochondrial ROS level, cardiomyocyte hypertrophy, fibrosis, and inflammation in rat hearts. Nicotine administration also induced left ventricular dysfunction, which was worsened by ischemia–reperfusion in isolated rat hearts. MitoTEMPO and resveratrol both significantly attenuated the adverse cardiac remodeling induced by nicotine, as well as the aggravation of postischemic ventricular dysfunction. Findings from this study show that targeting mitochondrial ROS with mitoTEMPO or resveratrol partially attenuates nicotine-induced cardiac remodeling and dysfunction.Anand RamalingamSiti Balkis BudinNorsyahida Mohd FauziRebecca H. RitchieSatirah ZainalabidinNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Anand Ramalingam Siti Balkis Budin Norsyahida Mohd Fauzi Rebecca H. Ritchie Satirah Zainalabidin Targeting mitochondrial reactive oxygen species-mediated oxidative stress attenuates nicotine-induced cardiac remodeling and dysfunction
description	Abstract Long-term nicotine intake is associated with an increased risk of myocardial damage and dysfunction. However, it remains unclear whether targeting mitochondrial reactive oxygen species (ROS) prevents nicotine-induced cardiac remodeling and dysfunction. This study investigated the effects of mitoTEMPO (a mitochondria-targeted antioxidant), and resveratrol (a sirtuin activator) , on nicotine-induced cardiac remodeling and dysfunction. Sprague–Dawley rats were administered 0.6 mg/kg nicotine daily with 0.7 mg/kg mitoTEMPO, 8 mg/kg resveratrol, or vehicle alone for 28 days. At the end of the study, rat hearts were collected to analyze the cardiac structure, mitochondrial ROS level, oxidative stress, and inflammation markers. A subset of rat hearts was perfused ex vivo to determine the cardiac function and myocardial susceptibility to ischemia–reperfusion injury. Nicotine administration significantly augmented mitochondrial ROS level, cardiomyocyte hypertrophy, fibrosis, and inflammation in rat hearts. Nicotine administration also induced left ventricular dysfunction, which was worsened by ischemia–reperfusion in isolated rat hearts. MitoTEMPO and resveratrol both significantly attenuated the adverse cardiac remodeling induced by nicotine, as well as the aggravation of postischemic ventricular dysfunction. Findings from this study show that targeting mitochondrial ROS with mitoTEMPO or resveratrol partially attenuates nicotine-induced cardiac remodeling and dysfunction.
format	article
author	Anand Ramalingam Siti Balkis Budin Norsyahida Mohd Fauzi Rebecca H. Ritchie Satirah Zainalabidin
author_facet	Anand Ramalingam Siti Balkis Budin Norsyahida Mohd Fauzi Rebecca H. Ritchie Satirah Zainalabidin
author_sort	Anand Ramalingam
title	Targeting mitochondrial reactive oxygen species-mediated oxidative stress attenuates nicotine-induced cardiac remodeling and dysfunction
title_short	Targeting mitochondrial reactive oxygen species-mediated oxidative stress attenuates nicotine-induced cardiac remodeling and dysfunction
title_full	Targeting mitochondrial reactive oxygen species-mediated oxidative stress attenuates nicotine-induced cardiac remodeling and dysfunction
title_fullStr	Targeting mitochondrial reactive oxygen species-mediated oxidative stress attenuates nicotine-induced cardiac remodeling and dysfunction
title_full_unstemmed	Targeting mitochondrial reactive oxygen species-mediated oxidative stress attenuates nicotine-induced cardiac remodeling and dysfunction
title_sort	targeting mitochondrial reactive oxygen species-mediated oxidative stress attenuates nicotine-induced cardiac remodeling and dysfunction
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/4822e11dae67459f93b0a8a97da64a99
work_keys_str_mv	AT anandramalingam targetingmitochondrialreactiveoxygenspeciesmediatedoxidativestressattenuatesnicotineinducedcardiacremodelinganddysfunction AT sitibalkisbudin targetingmitochondrialreactiveoxygenspeciesmediatedoxidativestressattenuatesnicotineinducedcardiacremodelinganddysfunction AT norsyahidamohdfauzi targetingmitochondrialreactiveoxygenspeciesmediatedoxidativestressattenuatesnicotineinducedcardiacremodelinganddysfunction AT rebeccahritchie targetingmitochondrialreactiveoxygenspeciesmediatedoxidativestressattenuatesnicotineinducedcardiacremodelinganddysfunction AT satirahzainalabidin targetingmitochondrialreactiveoxygenspeciesmediatedoxidativestressattenuatesnicotineinducedcardiacremodelinganddysfunction
_version_	1718377856658046976

Targeting mitochondrial reactive oxygen species-mediated oxidative stress attenuates nicotine-induced cardiac remodeling and dysfunction

Ejemplares similares