کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5519726 1544413 2016 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Changes in energy metabolism due to acute rotenone-induced mitochondrial complex I dysfunction - An in vivo large animal model
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیوفیزیک
پیش نمایش صفحه اول مقاله
Changes in energy metabolism due to acute rotenone-induced mitochondrial complex I dysfunction - An in vivo large animal model
چکیده انگلیسی


- A large animal model of acute mitochondrial complex I dysfunction is described.
- Rotenone infusion causes a switch from mitochondrial metabolism to glycolysis.
- TCA cycle intermediates were increased except for succinate which was decreased.
- A dramatic increase in lactate corresponds to a moderate decrease in VO2.

Metabolic crisis is a clinical condition primarily affecting patients with inherent mitochondrial dysfunction in situations of augmented energy demand. To model this, ten pigs received an infusion of rotenone, a mitochondrial complex I inhibitor, or vehicle. Clinical parameters, blood gases, continuous indirect calorimetry, in vivo muscle oxygen tension, ex vivo mitochondrial respiration and metabolomics were assessed. Rotenone induced a progressive increase in blood lactate which was paralleled by an increase in oxygen tension in venous blood and skeletal muscle. There was an initial decrease in whole body oxygen utilization, and there was a trend towards inhibited mitochondrial respiration in platelets. While levels of succinate were decreased, other intermediates of glycolysis and the TCA cycle were increased. This model may be suited for evaluating pharmaceutical interventions aimed at counteracting metabolic changes due to complex I dysfunction.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mitochondrion - Volume 31, November 2016, Pages 56-62
نویسندگان
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