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Citicoline (CDP-choline) protects myocardium from ischemia/reperfusion injury via inhibiting mitochondrial permeability transition.
Hernández-Esquivel, Luz; Pavón, Natalia; Buelna-Chontal, Mabel; González-Pacheco, Héctor; Belmont, Javier; Chávez, Edmundo.
Afiliación
  • Hernández-Esquivel L; Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, Mexico, D. F. Mexico.
  • Pavón N; Departamento de Farmacología, Instituto Nacional de Cardiología, Ignacio Chávez, Mexico, D. F. Mexico.
  • Buelna-Chontal M; Departamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología, Ignacio Chávez, Mexico, D. F. Mexico.
  • González-Pacheco H; Unidad Coronaria, Instituto Nacional de Cardiología, Ignacio Chávez, Mexico, D. F. Mexico.
  • Belmont J; Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, Mexico, D. F. Mexico.
  • Chávez E; Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, Mexico, D. F. Mexico. Electronic address: echavez@salud.gob.mx.
Life Sci ; 96(1-2): 53-8, 2014 Feb 06.
Article en En | MEDLINE | ID: mdl-24389400
AIMS: Oxidative stress emerges after reperfusion of an organ following an ischemic period and results in tissue damage. In the heart, an amplified generation of reactive oxygen species and a significant Ca(2+) accumulation cause ventricular arrhythmias and mitochondrial dysfunction. This occurs in consequence of increased non-specific permeability. A number of works have shown that permeability transition is a common substrate that underlies the reperfusion-induced heart injury. The aim of this work was to explore the possibility that CDP-choline may circumvent heart damage and mitochondrial permeability transition. MAIN METHODS: Rats were injected i.p. with CDP-choline at 20 mg/kg body weight. Heart electric behavior was followed during a closure/opening cycle of the left coronary descendent artery. Heart mitochondria were isolated from rats treated with CDP-choline, and their function was evaluated by analyzing Ca(2+) movements, achievement of a high level of the transmembrane potential, and respiratory control. Oxidative stress was estimated following the activity of the enzymes cis-aconitase and superoxide dismutase, as well as the disruption of mitochondrial DNA. KEY FINDINGS: This study shows that CDP-choline avoided ventricular arrhythmias and drop of blood pressure. Results also show that mitochondria, isolated from CDP-choline-treated rats, maintained selective permeability, retained accumulated Ca(2+), an elevated value of transmembrane potential, and a high ratio of respiratory control. Furthermore, activity of cis-aconitase enzyme and mDNA structure were preserved. SIGNIFICANCE: This work introduces CDP-choline as a useful tool to preserve heart function from reperfusion damage by inhibiting mitochondrial permeability transition.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Cardiotónicos / Daño por Reperfusión Miocárdica / Permeabilidad de la Membrana Celular / Citidina Difosfato Colina / Proteínas de Transporte de Membrana Mitocondrial / Miocardio Límite: Animals Idioma: En Revista: Life Sci Año: 2014 Tipo del documento: Article Pais de publicación: Países Bajos
Texto completo
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Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Cardiotónicos / Daño por Reperfusión Miocárdica / Permeabilidad de la Membrana Celular / Citidina Difosfato Colina / Proteínas de Transporte de Membrana Mitocondrial / Miocardio Límite: Animals Idioma: En Revista: Life Sci Año: 2014 Tipo del documento: Article Pais de publicación: Países Bajos