The function of coenzyme Q in mitochondria

Lenaz, Giorgio; Fato, Romana; Castelluccio, Cinzia; Genova, Maria Luisa; Bovina, Carla; Estornell, Ernesto; Valls, Victoria; Pallotti, Francesco; Castelli, Giovanna Parenti

doi:10.1007/bf00226843

Cited by 58 publications

(32 citation statements)

References 14 publications

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“…Instead, it seems more likely that the mutations in clk-1 and the resulting effects on life span and development in C. elegans may relate to changes in the amount of Q. In this event, the abundance of Q may influence the extent to which oxidants are generated by mitochondrial respiration (68,69). Many in vitro studies implicate ubisemiquinone (Q . )…”

Section: Coq7p/cat5p: Localization and Specificity In Q Biosynthesismentioning

confidence: 99%

Yeast Clk-1 Homologue (Coq7/Cat5) Is a Mitochondrial Protein in Coenzyme Q Synthesis

Jonassen¹,

Proft²,

Rández-Gil³

et al. 1998

Journal of Biological Chemistry

125

106

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Mutations in the clk-1 gene result in slower development and increased life span in Caenorhabditis elegans. The Saccharomyces cerevisiae homologue COQ7/CAT5 is essential for several metabolic pathways including ubiquinone biosynthesis, respiration, and gluconeogenic gene activation. We show here that Coq7p/Cat5p is a mitochondrial inner membrane protein directly involved in ubiquinone biosynthesis, and that the defect in gluconeogenic gene activation in coq7/cat5 null mutants is a general consequence of a defect in respiration. These results obtained in the yeast model suggest that the effects on development and life span in C. elegans clk-1 mutants may relate to changes in the amount of ubiquinone, an essential electron transport component and a lipid soluble antioxidant.

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Section: Coq7p/cat5p: Localization and Specificity In Q Biosynthesismentioning

confidence: 99%

Yeast Clk-1 Homologue (Coq7/Cat5) Is a Mitochondrial Protein in Coenzyme Q Synthesis

Jonassen¹,

Proft²,

Rández-Gil³

et al. 1998

Journal of Biological Chemistry

125

106

View full text Add to dashboard Cite

show abstract

“…C oenzyme Q10 (CoQ10) is a well-known essential electron transporter in complexes I (NADH-ubiquinone oxidoreductase, EC 1.6.5.3), II (succinate-ubiquinone oxidoreductase, EC 1.3.5.1), and III (ubiquinone-cytochrome c oxidoreductase, EC 1.10.2.2) of the mitochondrial respiratory chain (RC) (24,26). Ubiquinone-10 (oxidized form of CoQ10) is enzymatically reduced to ubiquinol-10 (the reduced form of CoQ10, 2,3-dimethoxy-5-methyl-6-decaprenyl-1,4-benzoquinol) (32,67), which acts as a fat-soluble antioxidant that effectively protects lipid membranes and lipoproteins from oxidative damage and has beneficial effects in preventing DNA damage (53).…”

Section: Introductionmentioning

confidence: 99%

Ubiquinol-10 Supplementation Activates Mitochondria Functions to Decelerate Senescence in Senescence-Accelerated Mice

Tian

Sawashita

Kubo

et al. 2014

Antioxidants & Redox Signaling

104

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Aim: The present study was conducted to define the relationship between the anti-aging effect of ubiquinol-10 supplementation and mitochondrial activation in senescence-accelerated mouse prone 1 (SAMP1) mice. Results: Here, we report that dietary supplementation with ubiquinol-10 prevents age-related decreases in the expression of sirtuin gene family members, which results in the activation of peroxisome proliferator-activated receptor c coactivator 1a (PGC-1a), a major factor that controls mitochondrial biogenesis and respiration, as well as superoxide dismutase 2 (SOD2) and isocitrate dehydrogenase 2 (IDH2), which are major mitochondrial antioxidant enzymes. Ubiquinol-10 supplementation can also increase mitochondrial complex I activity and decrease levels of oxidative stress markers, including protein carbonyls, apurinic/apyrimidinic sites, malondialdehydes, and increase the reduced glutathione/oxidized glutathione ratio. Furthermore, ubiquinol-10 may activate Sirt1 and PGC-1a by increasing cyclic adenosine monophosphate (cAMP) levels that, in turn, activate cAMP response element-binding protein (CREB) and AMP-activated protein kinase (AMPK). Innovation and Conclusion: These results show that ubiquinol-10 may enhance mitochondrial activity by increasing levels of SIRT1, PGC-1a, and SIRT3 that slow the rate of age-related hearing loss and protect against the progression of aging and symptoms of age-related diseases.

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“…Ubiquinone Q 10 (coenzyme Q 10 (CoQ 10 ) 3 ) is a well known electron transporter in complexes I (NADH-ubiquinone oxidoreductase), II (succinate-ubiquinone oxidoreductase), and III (ubiquinone-cytochrome c oxidoreductase) of the mitochondrial respiratory chain (21,22). CoQ 10 serves as a critical regulator of mitochondrial apoptosis, functioning as a ubiquitous free radical scavenger or control of the mitochondrial transition pore opening (21,(23)(24)(25)(26)(27)(28).…”

mentioning

confidence: 99%

“…CoQ 10 serves as a critical regulator of mitochondrial apoptosis, functioning as a ubiquitous free radical scavenger or control of the mitochondrial transition pore opening (21,(23)(24)(25)(26)(27)(28). CoQ 10 reduces the number of apoptotic keratocytes produced in response to excimer laser irradiation to a much greater extent than do other free radical scavengers, such as ascorbic acid and vitamin E (27).…”

mentioning

confidence: 99%

Coenzyme Q10 Rescues Ethanol-induced Corneal Fibroblast Apoptosis through the Inhibition of Caspase-2 Activation

Chen

Liou

Chen

et al. 2013

Journal of Biological Chemistry

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The function of coenzyme Q in mitochondria

Cited by 58 publications

References 14 publications

Yeast Clk-1 Homologue (Coq7/Cat5) Is a Mitochondrial Protein in Coenzyme Q Synthesis

Yeast Clk-1 Homologue (Coq7/Cat5) Is a Mitochondrial Protein in Coenzyme Q Synthesis

Ubiquinol-10 Supplementation Activates Mitochondria Functions to Decelerate Senescence in Senescence-Accelerated Mice

Coenzyme Q10 Rescues Ethanol-induced Corneal Fibroblast Apoptosis through the Inhibition of Caspase-2 Activation

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