H2O2 release from the very long chain acyl-CoA dehydrogenase.
Redox Biol
; 4: 375-80, 2015.
Article
en En
| MEDLINE
| ID: mdl-25728796
Enhanced mitochondrial generation of oxidants, including hydrogen peroxide (H2O2), is related to a large number of pathological conditions, including diet-induced obesity and steatohepatosis. Indeed, we have previously shown that high fat diets increase the generation of H2O2 in liver mitochondria energized by activated fatty acids. Here, we further study fatty-acid induced H2O2 release in liver mitochondria, and determine the characteristics that regulate it. We find that this production of H2O2 is independent of mitochondrial inner membrane integrity and insensitive to purine nucleotides. On the other hand, palmitate-induced H2O2 production is strongly enhanced by high fat diets and is pH-sensitive, with a peak at a matrix pH of ~8.5. Using recombinantly expressed human very long chain acyl-CoA dehydrogenase, we are able to demonstrate that palmitate-induced H2O2 release may be ascribed to the activity of this enzyme alone, acting as an oxidase. Our results add to a number of findings indicating that sources outside of the electron transport chain can generate significant, physiopathologically relevant, amounts of oxidants in mitochondria.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Mitocondrias Hepáticas
/
Acil-CoA Deshidrogenasa de Cadena Larga
/
Dieta Alta en Grasa
/
Peróxido de Hidrógeno
Límite:
Animals
Idioma:
En
Revista:
Redox Biol
Año:
2015
Tipo del documento:
Article
País de afiliación:
Brasil
Pais de publicación:
Países Bajos