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1 the synthesis of ubiquinone or coenzyme Q10 (CoQ10).
2 used for the determination of coenzyme Q10 (CoQ10).
3 SA-ST) was used to encapsulate coenzyme Q10 (CoQ10).
4 atin treatment reduces circulating levels of CoQ10.
5 s of O-2 generation than those obtained with CoQ10.
6 tion between SMPs reconstituted with CoQ9 or CoQ10.
7 and pork breakfast sausages, fortified with CoQ10.
8 plements, and substantial recent exposure to CoQ10.
9 in CoQ10 biosynthesis may be treatable with CoQ10.
10 e found to be more stable in the presence of CoQ10.
11 f age, which was significantly attenuated by CoQ10.
12 caspase-2 activation, which is regulated by CoQ10.
13 emulsions was compared to emulsions without CoQ10.
14 tandard feed pellets with or without dietary CoQ10 (1 mg/kg body weight per day) supplementation.
18 olled clinical trials of monopreparations of CoQ10 administered orally to cancer patients were includ
19 ated whether combining mild hypothermia with CoQ10 after out-of-hospital cardiac arrest provides addi
20 placebo, 1200 mg/d of CoQ10, or 2400 mg/d of CoQ10; all participants received 1200 IU/d of vitamin E.
24 systemic administration of the water-soluble CoQ10 analog reduced oxidative-induced cochlear damage,
26 ntly (62%) greater in the group treated with CoQ10 and MPTP than in the group treated with MPTP alone
27 antly higher (37%) in the group treated with CoQ10 and MPTP than in the group treated with MPTP alone
28 and biochemical reconstitution of FSP1 with CoQ10 and NADH suppresses triacylglycerol peroxidation i
29 affected subjects showed reduced amounts of CoQ10 and often displayed a decrease in CoQ10-dependent
31 sted by incorporating either reduced CoQ9 or CoQ10 and the lipophylic azoinitiator 2,2'-azobis(2,4-di
32 mg/d of CoQ10, and 86 received 2400 mg/d of CoQ10), and 65 participants (29 who received placebo, 19
33 ceived placebo, 19 who received 1200 mg/d of CoQ10, and 17 who received 2400 mg/d of CoQ10) withdrew
34 4 received placebo, 87 received 1200 mg/d of CoQ10, and 86 received 2400 mg/d of CoQ10), and 65 parti
35 roblasts from patients had reduced levels of CoQ10, and abnormal accumulation of the biosynthetic pre
37 nes or coenzyme Q (CoQ) homologues, CoQ9 and CoQ10, are related with the rate of O-2 generation was t
40 chromatography) resin and successfully bound CoQ10 at pH 5.0 with release of the CoQ10 at pH 9.0.
42 dings indicate a molecular pathway involving CoQ10 biosynthesis deficiency and mitochondrial dysfunct
44 ocytes, ADCK4 interacted with members of the CoQ10 biosynthesis pathway, including COQ6, which has be
46 fic respiratory chain complexes (I, III, and CoQ10 biosynthesis) increased ROS, whereas knockdown of
47 ects in three of the nine genes required for CoQ10 biosynthesis, all of which are associated with ear
54 entation can raise the circulating levels of CoQ10, but data on the effect of CoQ10 supplementation o
57 deletion of MDM12, we show that deletion of COQ10 by replacement with a HIS3 marker results in dimin
60 tigations are necessary to determine whether CoQ10 can improve the tolerability of cancer treatments.
61 strated that by blocking caspase-2 activity, CoQ10 can protect the cells from mitochondrial membrane
63 heart SMPs with different amounts of CoQ9 or CoQ10 caused an initial increase in the rates of O-2 gen
64 subsequent introduction of Triton X-100 and CoQ10 causes the MLs lysis and the cresyl violet oxidati
66 supplementation increased (P < 0.01) hepatic CoQ10 concentrations and ameliorated liver fibrosis (P <
68 y CoQ9 and cow heart SMPs, with high natural CoQ10 content, were chosen for depletion/reconstitution
69 ought that this interaction between sapB and CoQ10 could be a mechanism to avoid any possible CoQ10 t
70 in a cheese matrix, hence demonstrating that CoQ10 could be used in the development of functional che
71 whether oral administration of coenzyme Q10 (CoQ10) could attenuate 1-methyl-4-phenyl-1,2,3,6-tetrahy
73 s is recognized in the rare cases of primary CoQ10 deficiencies, a potential role for CoQ10 supplemen
77 ient evidence to prove the etiologic role of CoQ10 deficiency in statin-associated myopathy and that
79 prompted the hypothesis that statin-induced CoQ10 deficiency is involved in the pathogenesis of stat
80 have been previously associated with primary CoQ10 deficiency, a clinically heterogeneous multisystem
83 performed sequencing of known Coenzyme Q10 (CoQ10) deficiency genes in 22 patients with unexplained
85 in 1989, our understanding of coenzyme Q10 (CoQ10) deficiency is only now coming of age with the rec
87 ess, and unable to synthesize Q(6) The yeast coq10 deletion mutant is also respiratory-deficient and
93 ims were to choose between two high doses of CoQ10 for ALS, and to determine if it merits testing in
95 hypothesize that the therapeutic effects of CoQ10, frequently administered to patients with primary
102 demonstrate that recombinant sapB will bind CoQ10 in a pH-dependent manner similar to sapB binding w
105 us trials during the past 30 years examining CoQ10 in patients with HF have been limited by small num
106 aimed to determine the bio-accessibility of CoQ10 in processed meat products, beef patties and pork
111 sone (DX), melatonin (MEL) and coenzyme Q10 (CoQ10)) in a single formulation (DMQ-MSs) to create a no
112 s, we show that supraphysiological levels of CoQ10 induces an increase in the expression of SQOR in s
118 of statin therapy on intramuscular levels of CoQ10 is not clear, and data on intramuscular CoQ10 leve
123 strains expressing a functionally impaired (coq10-L96S) or truncated (coq10-R147*) Coq10 isoform usi
124 o examined the association between leukocyte CoQ10 levels and muscle markers, muscle performance, and
127 oQ10 is not clear, and data on intramuscular CoQ10 levels in symptomatic patients with statin-associa
129 guage articles relating statin treatment and CoQ10 levels via a PubMed search through August 2006.
132 uscle injury caused by reduced coenzyme Q10 (CoQ10) levels, which are postulated to produce mitochond
133 minergic axons in aged mice and suggest that CoQ10 may be useful in the treatment of Parkinson's dise
134 long-term administration of the antioxidant CoQ10 may represent a promising therapeutic strategy for
139 port the important role of the coenzyme Q10 (CoQ10) on the activity of caspase-2 upstream of mitochon
141 ly assigned to receive placebo, 1200 mg/d of CoQ10, or 2400 mg/d of CoQ10; all participants received
143 9 points (placebo), 7.5 points (1200 mg/d of CoQ10; P = .49 relative to placebo), and 8.0 points (240
152 efficient CoQ biosynthesis observed for the coq10-R147* mutant suggests these deleterious phenotypes
154 berberine groups (P<0.05) and the levels of CoQ10 remained within normal values in supplemented subj
155 and levels of coenzymes Q9 and Q10 (CoQ9 and CoQ10, respectively) as indicators of endogenous antioxi
157 ntaining homologs of CoQ, including CoQ9 and CoQ10, resulted in the essentially complete reduction of
160 like the coq10Delta mutant, indicating that Coq10's function is vital for respiration regardless of
161 ng a common component of cellular membranes, CoQ10's most prominent role is to facilitate the product
162 -I and Co-II shifts O*2- generation from the CoQ10 sites to more proximal sites, such as flavines, an
163 erate improvement of the fraction of reduced CoQ10, suggesting limited efficacy of NAC monotherapy.
164 urther proving that the metabolic effects of CoQ10 supplementation are mediated by the overexpression
165 in major adverse cardiovascular events with CoQ10 supplementation in a contemporary HF population.
169 ortant to evaluate the potential benefits of CoQ10 supplementation in the clinical outcome of the dis
171 lism and may explain some of the benefits of CoQ10 supplementation observed in mitochondrial diseases
172 g levels of CoQ10, but data on the effect of CoQ10 supplementation on myopathic symptoms are scarce a
178 ary CoQ10 deficiencies, a potential role for CoQ10 supplements in cardiovascular disease, particularl
182 s were fortified with a micellarized form of CoQ10 to enhance solubility to a concentration of 1mg/g
183 for oral supplementation with coenzyme Q10 (CoQ10) to improve the tolerability of cancer treatments.
186 ally completely absent after the 6-mo, daily CoQ10 treatment in db(-)/db(-) mice when started at 7 wk
195 verse effects of alcohol while coenzyme Q10 (CoQ10) was not very effective against alcohol insults.
196 enotypes resulting solely due to the loss of Coq10, we constructed strains expressing a functionally
197 Respiratory-chain enzyme activities and CoQ10 were decreased in severely affected patients but r
200 tosolic subunit of ERMES is coexpressed with COQ10, which encodes the putative CoQ chaperone Coq10, v