Metabolism and function of coenzyme Q

Turunen, Mikael J.; Olsson, Jerker M.; Dallner, Gustav

doi:10.1016/j.bbamem.2003.11.012

Cited by 925 publications

(808 citation statements)

References 300 publications

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“…The fact that similar hydroxylated forms are precursors of CoQ1 and CoQ10 during their biosynthesis adds to the physiological significance of our findings. 6 These new hydroxyl derivatives of CoQ1 and CoQ10 have distinct chemical properties. They can complex and transfer Ca 2þ across artificial biomembranes, have more negative reduction potentials than the native CoQs, and show a relatively pH insensitive redox chemistry.…”

Section: ' Discussionmentioning

confidence: 99%

“…CoQs can act as scavengers of free radicals, regenerators of R-tocopherol and ascorbic acid, and regulators of the mitochondrial permeability transition pore (PTP) and the mitochondrial uncoupling proteins (UCP). 5,6 Under certain conditions, in contrast to their antioxidant function, a variety of quinones in their reduced (quinol) form can also contribute to the generation of reactive oxygen species (ROS). 8À10 Numerous electrochemical studies of CoQ10 have been performed to characterize its redox properties.…”

Section: ' Introductionmentioning

confidence: 99%

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Calcium Binding and Transport by Coenzyme Q

et al. 2011

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Coenzyme Q10 (CoQ10) is one of the essential components of the mitochondrial electron-transport chain (ETC) with the primary function to transfer electrons along and protons across the inner mitochondrial membrane (IMM). The concomitant proton gradient across the IMM is essential for the process of oxidative phosphorylation and consequently ATP production. Cytochrome P450 (CYP450) monoxygenase enzymes are known to induce structural changes in a variety of compounds and are expressed in the IMM. However, it is unknown if CYP450 interacts with CoQ10 and how such an interaction would affect mitochondrial function. Using voltammetry, UV–vis spectrometry, electron paramagnetic resonance (EPR), nuclear magnetic resonance (NMR), fluorescence microscopy and high performance liquid chromatography–mass spectrometry (HPLC–MS), we show that both CoQ10 and its analogue CoQ1, when exposed to CYP450 or alkaline media, undergo structural changes through a complex reaction pathway and form quinone structures with distinct properties. Hereby, one or both methoxy groups at positions 2 and 3 on the quinone ring are replaced by hydroxyl groups in a time-dependent manner. In comparison with the native forms, the electrochemically reduced forms of the new hydroxylated CoQs have higher antioxidative potential and are also now able to bind and transport Ca2+ across artificial biomimetic membranes. Our results open new perspectives on the physiological importance of CoQ10 and its analogues, not only as electron and proton transporters, but also as potential regulators of mitochondrial Ca2+ and redox homeostasis.

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Section: ' Discussionmentioning

confidence: 99%

Section: ' Introductionmentioning

confidence: 99%

Calcium Binding and Transport by Coenzyme Q

et al. 2011

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“…CoQ10 is an important cofactor of the electron transport chain in mitochondrial respiration, being involved in energy homeostasis [17,19,48,49]. Furthermore it is also a cofactor of mitochondrial uncoupling proteins, which activation leads to a reduction of mitochondrial-free radical generation [50,51].…”

Section: Page 16 Of 42mentioning

confidence: 99%

Coenzyme Q10 supplementation lowers hepatic oxidative stress and inflammation associated with diet-induced obesity in mice

Sohet

Neyrinck

Pachikian

et al. 2009

Biochemical Pharmacology

150

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Please cite this article as: Sohet FM, Neyrinck AM, Pachikian BD, de Backer FC, Bindels LB, Niklowitz P, Menke T, Cani PD, Delzenne NM, Coenzyme Q10 supplementation lowers hepatic oxidative stress and inflammation associated with diet-induced obesity in mice, Biochemical Pharmacology (2008Pharmacology ( ), doi:10.1016Pharmacology ( /j.bcp.2009 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Aims:The aim of the study is to investigate the effect of the antioxidant coenzyme Q10 (CoQ10) on hepatic metabolic and inflammatory disorders associated with diet-induced obesity and glucose intolerance.Methods: C57bl6/j mice were fed for 8 weeks, either a control diet (CT) or a high fat diet plus 21% fructose in the drinking water (HFF). CoQ10 supplementation was performed in this later condition (HFFQ).Results HFF mice exhibit increased energy consumption, fat mass development, fasting glycemia and insulinemia and impaired glucose tolerance. HFF treatment promoted the expression of genes involved in reactive oxygen species production (NADPH oxidase), inflammation (CRP, STAMP-2) and metabolism (CPT1) in the liver. CoQ10 supplementation decreased the global hepatic mRNA expression of inflammatory and metabolic stresses markers without changing obesity and tissue lipid peroxides compared to HFF mice. HFF diets paradoxically decreased TBARS (reflecting lipid peroxides) levels in liver, muscle and adipose tissue versus CT group, an effect related to vitamin E content of the diet. Conclusion:In conclusion, HFF model promotes glucose intolerance and obesity by a mechanism independent on the level of tissue peroxides. CoQ10 tends to decrease hepatic stress gene expression, independently of any modulation of lipid peroxidation, which is classically considered as its most relevant effect.

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“…CoQ 10 undergoes oxidation and/or reduction in other cell membranes, such as Golgi vesicles, lysosomes, or plasma membrane, where it modulates vesicles acidification, subcellular redox state and is responsible for the generation of superoxide anion and hydrogen peroxide, which constitute a major regulatory signaling system essential for normal cell function and metabolism (Crane, 2001;Gille and Nohl, 2000). In most membranes CoQ 10 exists in the reduced form of quinol and acts as a powerful antioxidant protecting cells from ROS-induced damage either by direct reaction with ROS or by regenerating α-tocopherol and ascorbate (Crane, 2001;Turunen et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Nanomicellar formulation of coenzyme Q10 (Ubisol-Q10) effectively blocks ongoing neurodegeneration in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model: potential use as an adjuvant treatment in Parkinson's disease

Sikorska

Lanthier

Miller

et al. 2014

Neurobiology of Aging

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Although the support for the use of antioxidants, such as coenzyme Q 10 (CoQ 10 ), to treat Parkinson's disease (PD) comes from the extensive scientific evidence, the results of conducted thus far clinical trials are inconclusive. It is assumed that the efficacy of CoQ 10 is hindered by insolubility, poor bioavailability, and lack of brain penetration. We have developed a nanomicellar formulation of CoQ 10 (Ubisol-Q 10 ) with improved properties, including the brain penetration, and tested its effectiveness in mouse MPTP (1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine) model with the objectives to assess its potential use as an adjuvant therapy for PD. We used a subchronic MPTP model (5-daily MPTP injections), characterized by 50% loss of dopamine neurons over a period of 28 days. Ubisol-Q 10 was delivered in drinking water. Prophylactic application of Ubisol-Q 10 , started 2 weeks before the MPTP exposure, significantly offset the neurotoxicity (approximately 50% neurons died in MPTP group vs. 17% in MPTP+ Ubisol-Q 10 group by day 28). Therapeutic application of Ubisol-Q 10 , given after the last MPTP injection, was equally effective. At the time of intervention on day 5 nearly 25% of dopamine neurons were already lost, but the treatment saved the remaining 25% of cells, which otherwise would have died by day 28. This was confirmed by cell counts, analyses of striatal dopamine levels, and improved animals' motor skill on a beam walk test. Similar levels of neuroprotection were obtained with 3 different Ubisol-Q 10 concentrations tested, that is, 30 mg, 6 mg, or 3 mg CoQ 10 /kg body weight/day, showing clearly that high doses of CoQ 10 were not required to deliver these effects. Furthermore, the Ubisol-Q 10 treatments brought about a robust astrocytic activation in the brain parenchyma, indicating that astroglia played an active role in this neuroprotection. Thus, we have shown for the first time that Ubisol-Q 10 was capable of halting the neurodegeneration already in progress;

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Metabolism and function of coenzyme Q

Cited by 925 publications

References 300 publications

Calcium Binding and Transport by Coenzyme Q

Calcium Binding and Transport by Coenzyme Q

Coenzyme Q10 supplementation lowers hepatic oxidative stress and inflammation associated with diet-induced obesity in mice

Nanomicellar formulation of coenzyme Q10 (Ubisol-Q10) effectively blocks ongoing neurodegeneration in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model: potential use as an adjuvant treatment in Parkinson's disease

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