H 2 O 2 release from the very long chain acyl-CoA dehydrogenase

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Abstract

Enhanced mitochondrial generation of oxidants, including hydrogen peroxide (H 2 O 2 ), 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 H 2 O 2 in liver mitochondria energized by activated fatty acids. Here, we further study fatty-acid induced H 2 O 2 release in liver mitochondria, and determine the characteristics that regulate it. We find that this production of H 2 O 2 is independent of mitochondrial inner membrane integrity and insensitive to purine nucleotides. On the other hand, palmitate-induced H 2 O 2 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 H 2 O 2 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.

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APA

Kakimoto, P. A. H. B., Tamaki, F. K., Cardoso, A. R., Marana, S. R., & Kowaltowski, A. J. (2015). H 2 O 2 release from the very long chain acyl-CoA dehydrogenase. Redox Biology, 4, 375–380. https://doi.org/10.1016/j.redox.2015.02.003

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