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Koji Kido, Hiroyuki Ito, Yudai Yamamoto, Koshi Makita, Tokujiro Uchida
PURPOSE: Propofol infusion syndrome (PRIS) is a lethal condition caused by propofol overdose. Previous studies suggest that pathophysiological mechanisms underlying PRIS involve mitochondrial dysfunction; however, these mechanisms have not been fully elucidated. This study aimed to establish an experimental model of propofol-induced cytotoxicity using cultured human induced pluripotent stem cell (iPSC)-derived cardiomyocytes to determine the mechanisms behind propofol-induced mitochondrial dysfunction, and to evaluate the protective effects of coenzyme Q10 (CoQ10)...
February 2018: Journal of Anesthesia
David Ross, David Siegel
NQO1 is one of the two major quinone reductases in mammalian systems. It is highly inducible and plays multiple roles in cellular adaptation to stress. A prevalent polymorphic form of NQO1 results in an absence of NQO1 protein and activity so it is important to elucidate the specific cellular functions of NQO1. Established roles of NQO1 include its ability to prevent certain quinones from one electron redox cycling but its role in quinone detoxification is dependent on the redox stability of the hydroquinone generated by two-electron reduction...
2017: Frontiers in Physiology
Yongqiang Zhu, Lidan Ye, Zhaofeng Chen, Weijiang Hu, Yanghui Shi, Jianbo Chen, Chenfei Wang, Yong Li, Weifeng Li, Hongwei Yu
The physiological role of Coenzyme Q10 (CoQ10) as an electron carrier suggests its association with redox potential. Overexpression of glyceraldehyde-3-phosphate dehydrogenase type I (gapA-1) in Rhodobacter sphaeroides elevated the NADH/NAD(+) ratio and meanwhile enhanced the CoQ10 content by 58%, but at the sacrifice of biomass. On the other hand, Vitreoscilla hemoglobin was heterologously expressed to enhance the oxygen uptake ability of the cells, leading to 127% improvement of biomass. Subsequent coexpression of gapA-1 and vgb resulted in a CoQ10 titer of 83...
June 2017: Enzyme and Microbial Technology
Moon Hee Jeong, Jin Hwan Kim, Kang-Sik Seo, Tae Hwan Kwak, Woo Jin Park
Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is a mitochondrial disease caused by mutations in the mitochondrial genome. This study investigated the efficacy of β-lapachone (β-lap), a natural quinone compound, in rescuing mitochondrial dysfunction in MELAS cybrid cells. β-Lap significantly restored energy production and mitochondrial membrane potential as well as normalized the elevated ROS level in MELAS cybrid cells. Additionally, β-lap reduced lactic acidosis and restored glucose uptake in the MELAS cybrid cells...
November 21, 2014: Biochemical and Biophysical Research Communications
Jesús Castro-Marrero, Mario D Cordero, María José Segundo, Naia Sáez-Francàs, Natalia Calvo, Lourdes Román-Malo, Luisa Aliste, Tomás Fernández de Sevilla, José Alegre
Chronic fatigue syndrome (CFS) is a chronic and extremely debilitating illness characterized by prolonged fatigue and multiple symptoms with unknown cause, diagnostic test, or universally effective treatment. Inflammation, oxidative stress, mitochondrial dysfunction, and CoQ10 deficiency have been well documented in CFS. We conducted an 8-week, randomized, double-blind placebo-controlled trial to evaluate the benefits of oral CoQ10 (200 mg/day) plus NADH (20 mg/day) supplementation on fatigue and biochemical parameters in 73 Spanish CFS patients...
March 10, 2015: Antioxidants & Redox Signaling
Garth L Nicolson
Loss of function in mitochondria, the key organelle responsible for cellular energy production, can result in the excess fatigue and other symptoms that are common complaints in almost every chronic disease. At the molecular level, a reduction in mitochondrial function occurs as a result of the following changes: (1) a loss of maintenance of the electrical and chemical transmembrane potential of the inner mitochondrial membrane, (2) alterations in the function of the electron transport chain, or (3) a reduction in the transport of critical metabolites into mitochondria...
2014: Alternative Therapies in Health and Medicine
G López-Lluch, M Rios, M A Lane, P Navas, R de Cabo
Caloric restriction (CR) is known as the only non-genetic method proven to slow the rate of aging and extend lifespan in animals. Free radicals production emerges from normal metabolic activity and generates the accumulation of oxidized macromolecules, one of the main characteristics of aging. Due to its central role in cell bioenergetics, a great interest has been paid to CR-induced modifications in mitochondria, where CR has been suggested to decrease reactive oxygen species production. The plasma membrane contains a trans-membrane redox system (PMRS) that provides electrons to recycle lipophilic antioxidants, such as α-tocopherol and coenzyme Q (CoQ), and to modulate cytosolic redox homeostasis...
June 2005: Age (2005-)
Fernando Gomes, Erich B Tahara, Cleverson Busso, Alicia J Kowaltowski, Mario H Barros
Saccharomyces cerevisiae has three distinct inner mitochondrial membrane NADH dehydrogenases mediating the transfer of electrons from NADH to CoQ (coenzyme Q): Nde1p, Nde2p and Ndi1p. The active site of Ndi1p faces the matrix side, whereas the enzymatic activities of Nde1p and Nde2p are restricted to the intermembrane space side, where they are responsible for cytosolic NADH oxidation. In the present study we genetically manipulated yeast strains in order to alter the redox state of CoQ and NADH dehydrogenases to evaluate the consequences on mtDNA (mitochondrial DNA) maintenance...
February 1, 2013: Biochemical Journal
Nina Mikirova, Joseph Casciari, Ronald Hunninghake
CONTEXT: Chronic fatigue syndrome (CFS) is a debilitating fatigue illness that has unknown etiology and lacks an objective diagnostic marker. OBJECTIVE: To examine the metabolic component of CFS to determine if practitioners can use serum NAD(P)H concentration measurements to monitor metabolism and fatigue status in patients with CFS. DESIGN: The research team conducted a case-control study, comparing a group of patients who were diagnosed with CFS with a control group of healthy subjects...
January 2012: Alternative Therapies in Health and Medicine
Roman H Haefeli, Michael Erb, Anja C Gemperli, Dimitri Robay, Isabelle Courdier Fruh, Corinne Anklin, Robert Dallmann, Nuri Gueven
Short-chain quinones are described as potent antioxidants and in the case of idebenone have already been under clinical investigation for the treatment of neuromuscular disorders. Due to their analogy to coenzyme Q10 (CoQ10), a long-chain quinone, they are widely regarded as a substitute for CoQ10. However, apart from their antioxidant function, this provides no clear rationale for their use in disorders with normal CoQ10 levels. Using recombinant NAD(P)H:quinone oxidoreductase (NQO) enzymes, we observed that contrary to CoQ10 short-chain quinones such as idebenone are good substrates for both NQO1 and NQO2...
2011: PloS One
Francesca Bruge, Samantha Virgili, Tiziana Cacciamani, Federica Principi, Luca Tiano, Gian Paolo Littarru
Two-electron reduction of quinones catalyzed by NAD(P)H:quinone oxidoreductase (NQO1) protects cells against oxidative stress and toxic quinones. In fact, low level of NQO1 activity is often associated with increased risk of developing different types of tumours and with toxic effects linked to environmental quinones. In a previous report we analyzed the relationship between the oxidative stress induced by UV radiation and CoQ10 content in Burkitt's lymphoma cell lines compared to HL-60. The basal content of CoQ10 in Raji cells was slightly higher compared to HL-60...
2008: BioFactors
Mario H Barros, Alisha Johnson, Peter Gin, Beth N Marbois, Catherine F Clarke, Alexander Tzagoloff
Deletion of the Saccharomyces cerevisiae gene YOL008W, here referred to as COQ10, elicits a respiratory defect as a result of the inability of the mutant to oxidize NADH and succinate. Both activities are restored by exogenous coenzyme Q2. Respiration is also partially rescued by COQ2, COQ7, or COQ8/ABC1, when these genes are present in high copy. Unlike other coq mutants, all of which lack Q6, the coq10 mutant has near normal amounts of Q6 in mitochondria. Coq10p is widely distributed in bacteria and eukaryotes and is homologous to proteins of the "aromatic-rich protein family" Pfam03654 and to members of the START domain superfamily that have a hydrophobic tunnel implicated in binding lipophilic molecules such as cholesterol and polyketides...
December 30, 2005: Journal of Biological Chemistry
Rosario I Bello, Consuelo Gómez-Díaz, María I Burón, Francisco J Alcaín, Plácido Navas, José M Villalba
Coenzyme Q10 supplementation increases life-span of rats fed on a diet enriched with polyunsaturated fatty acids (Quiles, J.L., Ochoa, J.J., Huertas, J.R., Mataix, J., 2004b. Coenzyme Q supplementation protects from age-related DNA double-strand breaks and increased lifespan in rats fed on a PUFA-rich diet. Exp. Gerontol. 39, 189-194). Our study was set as a first attempt to establish a mechanistic link between life span extension and CoQ10 supplementation. When rats were fed on a PUFAn-6 plus CoQ10 diet, levels of CoQ10 were increased in plasma membrane at every time point compared to control rats fed on a PUFAn-6-alone diet...
August 2005: Experimental Gerontology
Milena Merlo Pich, Alida Castagnoli, Annalisa Biondi, Andrea Bernacchia, Pier Luigi Tazzari, Marilena D'Aurelio, Giovanna Parenti Castelli, Gabriella Formiggini, Roberto Conte, Carla Bovina, Giorgio Lenaz
The conditions under which Coenzyme Q (CoQ) may protect platelet mitochondrial function of transfusional buffy coats from aging and from induced oxidative stress were investigated. The Pasteur effect, i.e. the enhancement of lactate production after inhibition of mitochondrial respiratory chain, was exploited as a marker of mitochondrial function as it allows to calculate the ratio of mitochondrial ATP to glycolytic ATP. Reduced CoQ10 improves platelet mitochondrial function of transfusional buffy coats and protects the cells from induced oxidative stress...
April 2002: Free Radical Research
A Arroyo, V E Kagan, V A Tyurin, J R Burgess, R de Cabo, P Navas, J M Villalba
High affinity for NADH, and low affinity for NADPH, for reduction of endogenous coenzyme Q10 (CoQ10) by pig liver plasma membrane is reported in the present work. CoQ reduction in plasma membrane is carried out, in addition to other mechanisms, by plasma membrane coenzyme Q reductase (PMQR). We show that PMQR-catalyzed reduction of CoQ0 by both NADH and NADPH is accompanied by generation of CoQ0 semiquinone radicals in a superoxide-dependent reaction. In the presence of a water-soluble vitamin E homologue, Trolox, this reduction leads to quenching of the Trolox phenoxyl radicals...
2000: Antioxidants & Redox Signaling
A Gvozdjáková, J Kucharská, S Mizera, Z Braunová, Z Schreinerová, E Schrameková, I Pechán, J Fabián
UNLABELLED: Sixty endomyocardial biopsies (EMB) and whole blood or plasma samples from 34 patients after heart transplantation (HTx-pts) were studied. Acute rejection of the transplanted heart was histologically graded as: 0 (without), 0-1 (incipient), 1 (mild), 2 (moderate). The level of coenzyme Q10 (CoQ10) in 28 EMB was estimated by HPLC. Mitochondrial respiratory chain function and energy production were measured in 60 EMB. This study is the first report showing a correlation between: (a) histological signs of rejection in the human transplanted heart and (b) CoQ10 level of EMB, CoQ10 blood level, and mitochondrial bioenergetic processes: inhibition in FAD-part, but not in NAD-part of respiratory chain...
1999: BioFactors
C W Shults, M F Beal, D Fontaine, K Nakano, R H Haas
We report a pilot study of three oral doses of coenzyme Q10 (CoQ10) (200 mg administered two, three, or four times per day for 1 month) in 15 subjects with Parkinson's disease. Oral CoQ10 caused a substantial increase in the plasma CoQ10 level. It was well tolerated, but at the highest dose (200 mg four times per day) mild, transient changes in the urine were noted. CoQ10 did not change the mean score on the motor portion of the Unified Parkinson's Disease Rating Scale. There was a trend toward an increase in complex I activity in the subjects...
March 1998: Neurology
R E Beyer, J Segura-Aguilar, S di Bernardo, M Cavazzoni, R Fato, D Fiorentini, M C Galli, M Setti, L Landi, G Lenaz
The experiments reported here were undertaken to test the hypothesis that the antioxidative, reduced form of hydrophobic phase coenzyme Q (CoQ) may be generated and maintained by the two-electron quinone reductase, DT-diaphorase [NAD(P)H:(quinone-acceptor) oxidoreductase, EC] by catalyzing formation of the hydroquinone form of CoQ. This enzyme was isolated and purified from rat liver cytosol and its reduction of several CoQ homologs incorporated into large unilamellar vesicles (LUVETs) was demonstrated...
1997: Molecular Aspects of Medicine
C Gómez-Díaz, J M Villalba, R Pérez-Vicente, F L Crane, P Navas
Long-term treatment with ethidium bromide of HL-60 cells induced a mitochondria-deficient rho degree cell line, where mitochondrial DNA can not be identified by PCR and cytochrome c oxidase activity was 80% decreased. These cells showed a progressive increase of ascorbate stabilization which was 52% higher in the established rho degree HL-60 cells. Both CoQ10 and NADH-ascorbate free radical reductase of the plasma membrane were increased in rho(0)HL-60 cells compared to parental cells, while NADH-cytochrome c reductase was unchanged...
May 8, 1997: Biochemical and Biophysical Research Communications
R E Beyer, J Segura-Aguilar, S Di Bernardo, M Cavazzoni, R Fato, D Fiorentini, M C Galli, M Setti, L Landi, G Lenaz
The experiments reported here were designed to test the hypothesis that the two-electron quinone reductase DT-diaphorase [NAD(P)H:(quinone-acceptor) oxidoreductase, EC] functions to maintain membrane-bound coenzyme Q (CoQ) in its reduced antioxidant state, thereby providing protection from free radical damage. DT-diaphorase was isolated and purified from rat liver cytosol, and its ability to reduce several CoQ homologs incorporated into large unilamellar vesicles was demonstrated. Addition of NADH and DT-diaphorase to either large unilamellar or multilamellar vesicles containing homologs of CoQ, including CoQ9 and CoQ10, resulted in the essentially complete reduction of the CoQ...
March 19, 1996: Proceedings of the National Academy of Sciences of the United States of America
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