ArticleJournal of bioenergetics and biomembranes2004
Redox state of endogenous coenzyme q modulates the inhibition of linoleic acid-induced uncoupling by guanosine triphosphate in isolated skeletal muscle mitochondria.
Article in Journal of bioenergetics and biomembranes, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 58 citations in OpenAlex.
- Understanding coenzyme Q.Physiological reviews · 2024Review
- Article
- Being right on Q: shaping eukaryotic evolution.The Biochemical journal · 2016Review
- Endurance training increases the efficiency of rat skeletal muscle mitochondria.Pflugers Archiv : European journal of physiology · 2016Article
- Novel therapeutic strategies for traumatic brain injury: acute antioxidant reinforcement.CNS drugs · 2014Review
- Functional characterization of an uncoupling protein in goldfish white skeletal muscle.Journal of bioenergetics and biomembranes · 2013Article
- Hydroxynonenal, a lipid peroxidation end product, stimulates uncoupling protein activity in Acanthamoeba castellanii mitochondria; the sensitivity of the inducible activity to purine nucleotides depends on the membranous ubiquinone redox state.Journal of bioenergetics and biomembranes · 2012Article
- Mitochondria in traumatic brain injury and mitochondrial-targeted multipotential therapeutic strategies.British journal of pharmacology · 2012Review
- Identification and characterization of uncoupling protein 4 in fat body and muscle mitochondria from the cockroach Gromphadorhina cocquereliana.Journal of bioenergetics and biomembranes · 2011Article
- Calorie restriction modifies ubiquinone and COQ transcript levels in mouse tissues.Free radical biology & medicine · 2011Article
- Metabolic manipulators: a well founded strategy to combat mitochondrial dysfunction.Journal of inherited metabolic disease · 2011Review
- Identification and characterization of uncoupling protein in heart and muscle mitochondria of canary birds.Journal of bioenergetics and biomembranes · 2010Article
- Fatty acid efficiency profile in uncoupling of Acanthamoeba castellanii mitochondria.Journal of bioenergetics and biomembranes · 2007Article
- Cycling efficiency in humans is related to low UCP3 content and to type I fibres but not to mitochondrial efficiency.The Journal of physiology · 2006Article
- Proton leak induced by reactive oxygen species produced during in vitro anoxia/reoxygenation in rat skeletal muscle mitochondria.Journal of bioenergetics and biomembranes · 2006Article
- In phosphorylating Acanthamoeba castellanii mitochondria the sensitivity of uncoupling protein activity to GTP depends on the redox state of quinone.Journal of bioenergetics and biomembranes · 2005Article
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The skeletal muscle mitochondria contain two isoforms of uncoupling protein, UCP2 and mainly UCP3, which had been shown to be activated by free fatty acids and inhibited by purine nucleotides in reconstituted systems. On the contrary in isolated mitochondria, the protonophoretic action of muscle UCPs had failed to be demonstrated in the absence of superoxide production. We showed here for the first time that muscle UCPs were activated in state 3 respiration by linoleic acid and dissipated energy from oxidative phosphorylation by decreasing the ADP/O ratio. The efficiency of UCPs in mitochondrial uncoupling increased when the state 3 respiratory rate decreased. The inhibition of the linoleic acid-induced uncoupling by a purine nucleotide (GTP), was not observed in state 4 respiration, in uninhibited state 3 respiration, as well as in state 3 respiration inhibited by complex III inhibitors. On the contrary, the progressive inhibition of state 3 respiration by n -butyl malonate, which inhibits the uptake of succinate, led to a full inhibitory effect of GTP. Therefore, as the inhibitory effect of GTP was observed only when the reduced state of coenzyme Q was decreased, we propose that the coenzyme Q redox state could be a metabolic sensor that modulates the purine nucleotide inhibition of FFA-activated UCPs in muscle mitochondria.
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