Palmitoyl-CoA effect on cytochrome c release, a key process of apoptosis, from liver mitochondria of rat with sucrose diet-induced obesity


Por: Barrios-Maya M.-A., Ruiz-Ramírez A., Quezada H., Céspedes Acuña C.L., El-Hafidi M.

Publicada: 1 ene 2021
Resumen:
Cytochrome c (cyt-c) release from the mitochondria to the cytosol is a key process in the initiation of hepatocyte apoptosis involved in the progression of non-alcoholic fatty liver disease (NAFLD) to fibrosis, cirrhosis and hepatocellular carcinoma. Hepatocyte apoptosis may be related to lipotoxicity due to the accumulation of palmitic acid and palmitoyl-CoA (Pal-CoA). Therefore, the aim of this study is to examine whether Pal-CoA induces cyt-c release from liver mitochondria of sucrose-fed rat (SF). Pal-CoA-induced cyt-c release was sensitive to cyclosporine A indicating the involvement of the mitochondrial membrane permeability transition (mMPT). In addition, cyt-c release from SF mitochondria remains significantly lower than C mitochondria despite the increased rate of H2O2 generation in SF mitochondria. The decreased cyt-c release from SF may be also related to the increased proportion of the palmitic acid-enriched cardiolipin, due to the high availibilty of palmitic acid in SF liver. The enrichment of cardiolipin molecular species with palmitic acid makes cardiolipin more resistant to peroxidation, a mechanism involved in the dissociation of cyt-c from mitochondrial inner membrane. These results suggest that Pal-CoA may participate in the progression of NAFLD to more severe disease through mechanisms involving cyt-c release and mMPT, a key process of apoptosis. © 2021

Filiaciones:
Depto de Biomedicina Cardiovascular, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano No 1, Colonia Sección XVI, Tlalpan, C.D. México CP 14080, Mexico
Laboratorio de Inmunología y Proteómica, Hospital Infantil de México Federico Gómez, Doctor Márquez # 162, Col. DoctoresC.D. México CP 06720, Mexico
Departamento de Ciencias Básicas, Facultad de Ciencias, Universidad del BioBio, Chillan, Chile
ISSN: 02786915
Editorial
Elsevier Ltd, THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND, Reino Unido
Tipo de documento: Article
Volumen: 154 Número:
Páginas:
WOS Id: 000677525200001
ID de PubMed: 34171418

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