The Emerging Role of Coenzyme Q-10 in Aging, Neurodegeneration, Cardiovascular Disease, Cancer and Diabetes Mellitus

Dhanasekaran, Muralikrishnan; Ren, Jun

doi:10.2174/156720205774962656

Cited by 90 publications

(57 citation statements)

References 122 publications

(156 reference statements)

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“…However, several groups showed that membrane fluidity is an important factor for the efficiency of electron transport by quinone recycling as shown in mitochondrial electron transport system (43,44).…”

Section: Discussionmentioning

confidence: 99%

Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell

Lee

Kim

et al. 2009

Journal of Lipid Research

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Oxidized-1-palmitoyl-2-arachidonyl-sn -glycerol-3-phosphocholine (Ox-PAPC) has been demonstrated to accumulate in atherosclerotic lesions and regulates expression of more than 1,000 genes in human aortic endothelial cell (HAEC). Among the most highly induced is heme oxygenase-1 (HO-1), a cell-protective antioxidant enzyme, which is sensitively induced by oxidative stress. To identify the pathway by which Ox-PAPC induces HO-1, we focused on the plasma membrane electron transport (PMET) complex, which contains ecto-NADH oxidase 1 (eNOX1) and NADPH:quinone oxidoreductase 1 (NQO1) and affects cellular redox status by regulating levels of NAD(P)H. We demonstrated that Ox-PAPC and its active components stimulated electron transfer through the PMET complex in HAECs from inside to outside [as determined by extracellular 2-(4-iodophenyl)-3-(44-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium (WST-1) reduction] and from outside to inside of the cell (as determined by intracellular NBT reduction). Chemical inhibitors of PMET system and siRNAs to PMET components (NQO1 and eNOX1) significantly decreased HO-1 induction by Ox-PAPC. We present evidence that Ox-PAPC activation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in HAEC plays an important role in the induction of HO-1 and PMET inhibitors blocked Nrf2 activation by Ox-PAPC. We hypothesized that PMET activation by Ox-PAPC causes intracellular NAD(P)H depletion, which leads to the increased oxidative stress and HO-1 induction. Supporting this hypothesis, cotreatment of cells with exogenous NAD(P)H and Ox-PAPC significantly decreased oxidative stress and HO-1 induction by Ox-PAPC. Taken together, we demonstrated that the PMET system in HAEC plays an important role in the regulation of cellular redox status and HO-1 expression by Ox-PAPC.

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Section: Discussionmentioning

confidence: 99%

Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell

Lee

Kim

et al. 2009

Journal of Lipid Research

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“…Due to their role in reducing the damaging effects of the highly reactive free radicals, coenzyme Q-based antioxidants are seen as indispensible systems that protect the occurrence of many physiological processes in all living organisms. The potential of acting of various coenzyme Q antioxidants toward different targets (reactive oxygen species ROS) is described in several review works and books [20,[47][48][49][50][51][52][53]. Indeed, the antioxidant potential of all coenzyme Qs depends significantly on the nature of the substituents existing in their structural pattern [2,9,33].…”

Section: Antioxidant Properties Of Coenzyme Qsmentioning

confidence: 99%

Redox chemistry of coenzyme Q—a short overview of the voltammetric features

Gulaboski

Markovski

Zhu

2016

J Solid State Electrochem

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Quinones constitute a big family of organic redox active compounds that are overwhelmingly involved in important physiological processes. The most important members in the class of quinones are, indeed, the plastoquinones and the coenzyme Q (CoQ) derivatives. Voltammetry of coenzyme Q family members attracts significant attention since 50 years ago. In this work, we refer to some of the most important voltammetric features of coenzyme Qs studied in aprotic and in aqueous media. While the redox chemistry of coenzyme Q members in non-aqueous aprotic organic solvents can be described by two consecutive one-electron transfer steps, more complex situation exists in the voltammetry of coenzyme Qs performed in aqueous media. Although it has been claimed for a while that the voltammetric processes of coenzyme Qs in aqueous solutions proceed via formation of semiquinone radical intermediate species, it has been recently proven that this can be not completely true. Intensive voltammetric and spectroscopic studies of coenzyme Q systems in buffered and non-buffered aqueous media revealed that hydrogen bonding between electrochemically created CoQ species and the water molecules plays an important role in stabilizing electrochemically generated species of these systems. We also pay attention to the amazing redox chemistry of coenzyme Qs in strong alkaline media, while we refer to the chemical features of novel coenzyme Q derivatives obtained under such conditions. Hints are presented about the antioxidant capacity of some of the novel hydroxylated coenzyme Q systems. Also, the possibility of these systems to bind and transfer earth-alkaline cations across biomimetic membranes is shortly elaborated. In the end, we refer to some relevant theoretical works that describe closely the voltammetric behavior of various coenzyme Q systems. We believe that this short review will contribute towards better understanding of the amazing chemistry of coenzyme Q derivatives.

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“…3,4 Q10 has also been proposed to be helpful in prevention and treatment of neurodegenerative and mitochondrial related diseases.…”

mentioning

confidence: 99%

Coenzyme Q10, Glucose Homeostasis and the Probable Mediating Role of Adipokines

Hosseinzadeh‐Attar

Alipoor

Mehrdadi³

2016

Obes Res Open J

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Coenzyme Q10 is one of the most popular nutritional supplements, which has been discovered in 1955. It is also known as ubiquinone, Q10, CoQ and vitamin Q10. This coenzyme has two isoforms; the oxidized form, ubiquinone, is an electron carrier in mitochondrial respiratory chain and the reduced form, ubiquinol, acts as an antioxidant.1,2 Studies reported its beneficial effects in some diseases such as diabetes, heart failure, hypertension, and Parkinson disease. 3,4 Q10 has also been proposed to be helpful in prevention and treatment of neurodegenerative and mitochondrial related diseases.5 Q10 could potentially be effective on metabolic disorders including lipid profile, blood pressure, glycemic control and insulin resistance in different diseases. [6][7][8] Many diseases are accompanied with imapired glycemic control and insulin resistance.9 Phosphorylation of Insulin Receptor Substrates (IRS) is crucial for insulin signalling cascade, which in turn activates the mitogen-activated protein kinase (MAP-Kinase) with major mitogenic effects and phosphatidylinositol-3-Kinase (PI-3K) with prominent metabolic properties including appropriate cellular glucose distribution.10 Coenzyme Q10 might induce the tyrosine kinase and phosphatidylinositol 3 kinase (PI3k) activity in liver. These enzymes are involved in improving insulin cascade and increasing GLUT2 and tyrosine phosphorylation of IRS-1, which could in turn enhance glucose uptake and inhibit gluconeogenesis in liver. 11This antioxidant has been shown to reduce HbA1C levels in experimental and clinical studies and to improve long term glycemic control. 6,7,12,13 It could also increase insulin production and secretion probably by stimulating ATP generation in pancreatic beta cells.14 Other proposed mechanisms include regulation of insulin receptors, glucose transporters, lipid profile, redox system, and receptors of advanced glycated end products. 15 Obesity, the major growing health problem worldwide, is one the most important contributors of initiation and progression of insulin resistance. 16 The potential mechanisms include higher production of fatty acids, activation of Toll-like receptor 4 and the innate immune system, alterations in endocrine and inflammatory mediators and activation of nuclear factor-κB (NF-κB). 17Recently the metabolic functions of adipose derived peptides, adipokines, have been investigated progressively in different disorders. The changes in the secretion of adipokines in obesity could inhibit insulin signalling through increasing inflammatory adipocytokines and other mediators interfering the IRS phosphorylation and integrity. 17 The relationship between the major adipokines, leptin, adiponectin, resistin and visfatin with glucose homeostasis has previously been demonstrated. 18,19 Leptin could contribute to glucose homeostasis through direct and indirect actions on peripheral tissues. Direct leptin actions might inhibit insulin and glucagon secretion from pancreatic cells. Moreover, leptin could potentially affect insulin signaling in a...

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The Emerging Role of Coenzyme Q-10 in Aging, Neurodegeneration, Cardiovascular Disease, Cancer and Diabetes Mellitus

Cited by 90 publications

References 122 publications

Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell

Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell

Redox chemistry of coenzyme Q—a short overview of the voltammetric features

Coenzyme Q10, Glucose Homeostasis and the Probable Mediating Role of Adipokines

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