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Title
The effect of coenzyme Q10 on the exercise performance of cross-country
skiers.
Author
Ylikoski T; Piirainen J; Hanninen O; Penttinen J
Source
Mol Aspects Med, 1997, 18 Suppl:, S283-90
Abstract
Coenzyme Q10 supplementation (Bio-Qinon Pharma Nord, 90 mg/day)
was studied in a
double-blind cross-over study of 25 Finnish top-level cross-country
skiers. With CoQ10
supplementation, all measured indexes of physical performance
(AET, ANT and VO2Max)
improved significantly. During verum supplementation, 94% of
the athletes felt that the
preparation had been beneficial in improving their performance
and recovery time vs. only
33% in the placebo periods.
Title
Does exogenous coenzyme Q10 affect aerobic capacity in endurance
athletes?
Author
Weston SB; Zhou S; Weatherby RP; Robson SJ
Source
Int J Sport Nutr, 1997 Sep, 7:3, 197-206
Abstract
The effect of orally supplemented coenzyme Q10 (CoQ10) on plasma
CoQ10 concentration
and aerobic capacity in endurance athletes was evaluated. Eighteen
volunteer male road
cyclists and triathletes, 8 in a CoQ10 supplementation group
(QG) and 10 in a placebo
group (PG), successfully completed the experimental protocol.
Subjects were evaluated
during and following graded cycling exercise tests, which were
performed before and after
28 days of supplementation with 1 mg.kg-1.day-1 of CoQ10 or placebo.
The
presupplementation plasma CoQ10 concentration was significantly
increased from 0.91 +/-
0.13 microgram.ml-1 to 1.97 +/- 0.27 microgram.ml-1 in QG following
supplementation
(p < .05). However, the CoQ10 supplementation regime had no
consistently significant
effect on oxygen uptake, anaerobic and respiratory compensation
thresholds, blood lactate,
glucose and triglyceride kinetics, heart rate, and blood pressure
during and after graded
cycling to exhaustion.
Title
Coenzyme Q10 and colorectal neoplasms in aged patients.
Author
Palazzoni G; Pucello D; Littarru GP; Nardone L; Marin AW; Romagnoli
A
Source
Rays, 1997 Jan, 22:1 Suppl, 73-6
Abstract
Coenzyme Q10 (CoQ10), a quinone located in cellular membranes,
is a compound with
mitochondrial bioenergetic functions whose antioxidant activity
has recently been defined.
CoQ10 content in colorectal neoplasms is significantly higher
than in normal colorectal
mucosa. While older patients (aged over 70 years) have also a
significantly higher CoQ10
content, not observed in younger patients (aged under 70 years),
the normal mucosa,
instead; shows constant CoQ10 levels in both groups. For the
same local stage (T), an
increase in lymph node involvement (N) was observed in older
patients as compared to
younger ones, but not in distant metastases (M) with the same
5-year survival. These results
justify the same therapeutic approach for patients older or younger
than 70 years.
Title
Mitochondrial encephalomyopathy with coenzyme Q10 deficiency.
Author
Sobreira C; Hirano M; Shanske S; Keller RK; Haller RG; Davidson
E; Santorelli FM;
Miranda AF; Bonilla E; Mojon DS; Barreira AA; King MP; DiMauro
S
Source
Neurology, 1997 May, 48:5, 1238-43
Abstract
Coenzyme Q10 (CoQ10) transfers electrons from complexes I and
II of the mitochondrial
respiratory chain to complex III. There is one published report
of human CoQ10 deficiency
describing two sisters with encephalopathy, proximal weakness,
myoglobinuria, and lactic
acidosis. We report a patient who had delayed motor milestones,
proximal weakness,
premature exertional fatigue, and episodes of exercise-induced
pigmenturia. She also
developed partial-complex seizures. Serum creatine kinase was
approximately four times
the upper limit of normal and venous lactate was mildly elevated.
Skeletal muscle biopsy
revealed many ragged-red fibers, cytochrome c oxidase-deficient
fibers, and excess lipid. In
isolated muscle mitochondria, impaired oxygen consumption was
corrected by the addition
of decylubiquinone. During standardized exercise, ventilatory
and circulatory responses
were compatible with a defect of oxidation-phosphorylation, which
was confirmed by
near-infrared spectroscopy analysis. Biochemical analysis of
muscle extracts revealed
decreased activities of complexes I+II and I+III, while CoQ10
concentration was less than
25% of normal. With a brief course of CoQ10 (150 mg daily), the
patient reported
subjective improvement. The triad of CNS involvement, recurrent
myoglobinuria, and
ragged-red fibers should alert clinicians to the possibility
of CoQ10 deficiency.
Title
Energy metabolism defects in Huntington's disease and effects
of coenzyme Q10.
Author
Koroshetz WJ; Jenkins BG; Rosen BR; Beal MF
Source
Ann Neurol, 1997 Feb, 41:2, 160-5
Abstract
We investigated whether the Huntington's disease (HD) gene mutation
may produce either
primary or secondary effects on energy metabolism. 31P magnetic
resonance spectroscopy
demonstrated a significant decrease in the phosphocreatine to
inorganic phosphate ratio in
resting muscle of 8 patients as compared with 8 control subjects.
The cerebrospinal fluid
lactate-pyruvate ratio was significantly increased in 15 patients
as compared with 13 control
subjects. Lactate concentrations assessed using 1H magnetic resonance
spectroscopy are
increased in Huntington's disease cerebral cortex. Treatment
with coenzyme Q10, an
essential cofactor of the electron transport chain, resulted
in significant decreases in cortical
lactate concentrations in 18 patients, which reversed following
withdrawal of therapy. These
findings provide evidence for a generalized energy defect in
Huntington's disease, and
suggest a possible therapy.
Title
Can correction of sub-optimal coenzyme Q status improve beta-cell
function in type II
diabetics?
Author
McCarty MF
Address
NutriGuard Research, Encinitas, CA 92024, USA.
Source
Med Hypotheses, 1999 May, 52:5, 397-400
Abstract
A stimulus to mitochondrial respiratory activity is a crucial
component of the signal
transduction mechanism whereby increased plasma glucose evokes
insulin secretion by
beta-cells. Efficient function of the glycerol-3-phosphate shuttle
is important in this regard,
and the rate-limiting enzyme in this shuttle--the mitochondrial
glycerol-3-phosphate
dehydrogenase (G3PD)--is underexpressed in the beta cells of
human type II diabetics as
well of rodents that are models for this disorder. Suboptimal
tissue levels of coenzyme Q10
(CoQ) could be expected to further impair G3PD activity. Clinical
reports from Japan
suggest that supplemental CoQ may often improve beta-cell function
and glycemic control
in type II diabetics. Thus, it is proposed that correction of
suboptimal CoQ status, by aiding
the efficiency of G3PD and of respiratory chain function, will
improve the
glucose-stimulated insulin secretion of diabetic beta-cells.
Title
Recycling and redox cycling of phenolic antioxidants.
Author
Kagan VE; Tyurina YY
Source
Ann N Y Acad Sci, 1998 Nov 20, 854:, 425-34
Abstract
Effectiveness of phenolic antioxidants in protecting against
oxidative stress depends on their
reactivity towards reactive oxygen species and the reactivity
of the antioxidant phenoxyl
radicals towards critical biomolecules. Reduction of phenoxyl
radicals by intracellular
reductant (ascorbate, thiols) as well as by enzymes or intermediates
of electron transport
(e.g., in mitochondria and the endoplasmic reticulum) recycles
phenolic antioxidants, thus
enhancing antioxidant protection. Several cascades may be involved
in physiologically
relevant recycling of vitamin E from its phenoxyl radicals. The
two major ones are
dihydrolipoic acid-->(GSH)-->ascorbate, and enzymes of
electron transport-->coenzyme Q.
Importantly, phenoxyl radicals of vitamin E are not directly
reduced by intracellular thiols.
By contrast, a number of natural phenolic compounds that act
as very effective scavengers
of reactive oxygen species and organic radicals, may generate
reactive secondary radicals of
antioxidants. These secondary radicals react and modify critical
intracellular targets (lipids,
proteins, and DNA). As a result, the role of these phenolic compounds
as biological
antioxidants may be limited because of their ability to cause
cyto- and genotoxic effects.
Typical examples are some estrogens and phenolic drugs (e.g.,
the antitumor drug,
etoposide) that can protect lipids but oxidize GSH and protein
sulfhydryls. Moreover,
phenoxyl radicals produced in the course of radical scavenging
by some phenolic
compounds (e.g., phenol) are capable of oxidizing both proteins
and lipids. Hence, reactivity
of phenoxyl radicals should be considered as a critical factor
in the development of new
antioxidant protectants.
Title
Toward a new definition of essential nutrients: is it now time
for a third 'vitamin' paradigm?
Author
Challem JJ
Source
Med Hypotheses, 1999 May, 52:5, 417-22
Abstract
The concepts of vitamin 'deficiency' diseases and the recommended
dietary allowances
(RDAs) have not kept pace with the growing understanding of the
cellular and molecular
functions of vitamins and other micronutrients. As a consequence,
many researchers and
clinicians rely on outdated signs and symptoms in assessing nutritional
deficiencies. A new
paradigm, presented here, proposes that: (1) deficiencies can
be identified on biochemical
and molecular levels long before they become clinically visible;
(2) the definition of essential
micronutrients be broadened to include some carotenoids and flavonoids,
as well as various
human metabolites, such as coenzyme Q10, carnitine, and alpha-lipoic
acid, which are also
dietary constituents; (4) individual nutritional requirements
are partly fixed by genetics but
also dynamically influenced by variations in the body's biochemical
milieu and external
stresses; and (5) the distinction between nutritional and pharmacological
doses of vitamins
is meaningless, since high doses of micronutrients may be required
to achieve normal
metabolic processes in some people.
Title
High serum coenzyme Q10, positively correlated with age, selenium
and cholesterol, in
Inuit of Greenland. A pilot study.
Author
Pedersen HS; Mortensen SA; Rohde M; Deguchi Y; Mulvad G; Bjerregaard
P; Hansen JC
Source
Biofactors, 1999, 9:2-4, 319-23
Abstract
Greenlanders (Eskimos) have low prevalence of ischaemic heart
disease, partly explained
by a lower extent of atherosclerosis and a low n-6/n-3 ratio
of polyunsaturated fatty acids.
As atherosclerosis is also a result of oxidative stress, the
total antioxidative readiness could
have a substantial impact. From a health survey we chose the
subpopulation from the most
remote area, where the traditional Greenlandic diet with high
intake of sea mammals and
fish predominates. The mean (SD) of S-CoQ10 in males was 1.495
(0.529) nmol/ml and
1.421 (0.629) nmol/ml in females, significantly higher (p <
0.001) compared to a Danish
population. In a linear multiple regression model the S-CoQ10
level is significantly
positively associated with age and S-selenium in males, and S-total
cholesterol in females.
The high level of CoQ10 in Greenlanders probably reflects diet,
since no bioaccumulation
takes place, and it could probably be a substantial part of the
antioxidative defense.
Title
Antiglutamate therapies in Huntington's disease.
Author
Kieburtz K
Source
J Neural Transm Suppl, 1999, 55:, 97-102
Abstract
Huntington's disease is an autosomal dominant neurodegenerative
disorder caused by an
unstable trinucleotide CAG repeat. The mechanism by which the
genetic defect leads to
neuronal injury and death is unknown, but is thought to include
glutamate-mediated
excitotoxicity and abnormalities of mitochondrial energy production.
Both of these
mechanisms may lead to a final common pathway of increased production
of free radical
species. Prior clinical trials in patients with Huntington's
disease that have addressed these
hypotheses have been limited by size. A current, NIH-funded trial
of remacemide
hydrochloride and Coenzyme Q10 in 340 patients with Huntington's
disease is described.
This is the largest and longest multi-center trial in Huntington's
disease to address the
glutamate- and mitochondrial-mediated hypotheses of neurodegeneration. |
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