Hydrogen sulfide modulates sub-cellular susceptibility to oxidative stress induced by myocardial ischemic reperfusion injury.
Chem Biol Interact
; 252: 28-35, 2016 May 25.
Article
em En
| MEDLINE
| ID: mdl-27041072
ABSTRACT
In this study, we compared the impact of H2S pre (HIPC) and post-conditioning (HPOC) on oxidative stress, the prime reason for myocardial ischemia reperfusion injury (I/R), in different compartments of the myocardium, such as the mitochondria beside its subpopulations (interfibrillar (IFM) and subsarcolemmal (SSM) mitochondria) and microsomal fractions in I/R injured rat heart. The results demonstrated that compared to I/R rat heart, HIPC and HPOC treated hearts shows reduced myocardial injury, enhanced antioxidant enzyme activities and reduced the level of TBARS in different cellular compartments. The extent of recovery (measured by TBARS and GSH levels) in subcellular fractions, were in the following descending order microsome > SSM > IFM in both HIPC and HPOC. In summary, oxidative stress mediated mitochondrial dysfunction, one of the primary causes for I/R injury, was partly recovered by HIPC and HPOC treatment, with significant improvement in SSM fraction compared to the IFM.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Cardiotônicos
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Traumatismo por Reperfusão Miocárdica
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Estresse Oxidativo
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Gasotransmissores
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Sulfeto de Hidrogênio
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Mitocôndrias Cardíacas
Limite:
Animals
Idioma:
En
Revista:
Chem Biol Interact
Ano de publicação:
2016
Tipo de documento:
Article
País de afiliação:
Índia