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 Coenzyme Q10



Coenzyme Q10 in the central nervous system and its potential usefulness in the treatment of
neurodegenerative diseases.

Beal MF; Matthews RT
Mol Aspects Med, 1997, 18 Suppl:, S169-79

Coenzyme Q10 is an essential cofactor of the electron transport chain and is an antioxidant.
We examined the effects of oral feeding with coenzyme Q10 in young animals on brain
concentrations. Feeding with coenzyme Q10 at a dose of 200 mg/kg for 1-2 months in
young rats resulted in significant increases in liver concentrations, however, there was no
significant increase in brain concentrations of either reduced- or total coenzyme Q10 levels.
Nevertheless there was a reduction in malonate-induced increases in 2,5 dihydroxybenzoic
acid to salicylate, consistent with an antioxidant effect. In other studies we found that oral
administration of coenzyme Q10 significantly reduced increased concentrations of lactate in
the occipital cortex of Huntington's disease patients. These findings suggest that coenzyme
Q10 might be useful in treating neurodegenerative diseases.


Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts
neuroprotective effects.

Matthews RT; Yang L; Browne S; Baik M; Beal MF
Proc Natl Acad Sci U S A, 1998 Jul, 95:15, 8892-7

Coenzyme Q10 is an essential cofactor of the electron transport chain as well as a potent free
radical scavenger in lipid and mitochondrial membranes. Feeding with coenzyme Q10
increased cerebral cortex concentrations in 12- and 24-month-old rats. In 12-month-old rats
administration of coenzyme Q10 resulted in significant increases in cerebral cortex
mitochondrial concentrations of coenzyme Q10. Oral administration of coenzyme Q10
markedly attenuated striatal lesions produced by systemic administration of 3-nitropropionic
acid and significantly increased life span in a transgenic mouse model of familial
amyotrophic lateral sclerosis. These results show that oral administration of coenzyme Q10
increases both brain and brain mitochondrial concentrations. They provide further evidence
that coenzyme Q10 can exert neuroprotective effects that might be useful in the treatment of
neurodegenerative diseases.


Coenzyme Q10 in the diet--daily intake and relative bioavailability.

Weber C; Bysted A; H¦lmer G
Mol Aspects Med, 1997, 18 Suppl:, S251-4

The coenzyme Q10 content of the average Danish diet was estimated from consumption
data and from analysis of food items to be 3-5 mg coenzyme Q10 per day, primarily
derived (64% of the total) from meat and poultry. To investigate if coenzyme Q10 was
absorbed to any significant degree from a food item, a randomized cross-over study with
single doses of coenzyme Q10 (30 mg/person), administered either as a meal or as
capsules, was carried out in healthy subjects. The serum coenzyme Q10 concentration
increased significantly, and the maximum concentrations did not differ significantly for the
two forms of administration. The study indicates that coenzyme Q10 is present in food
items and absorbed to a significant degree. Thus, dietary coenzyme Q10 may contribute to
the plasma coenzyme Q10 concentration.


The coenzyme Q10 content of the average Danish diet.

Weber C; Bysted A; Hlmer G
Int J Vitam Nutr Res, 1997, 67:2, 123-9

The average dietary intake of coenzyme Q10 and coenzyme Q9 of the Danish population
was determined, based on food consumption data from a national dietary survey. Selected
food items in edible form were analyzed for the coenzyme Q content by HPCL with
UV-detection, and their contribution to the total intake calculated. The effect of cooking was
a 14-32% destruction of coenzyme Q10 by frying, and no detectable destruction by boiling.
The average coenzyme Q10 intake of the Danish population was estimated to 3-5 mg/day,
primarily derived from meat and poultry (64% of the daily intake), while cereals, fruit,
edible fats, and vegetables only make minor contributions. The intake of coenzyme Q10 is
approximately 1 mg/day, primarily derived from vegetable fats and cereals. The
alpha-tocopherol content of the selected food samples was analyzed by HPLC with
fluorescence detection, and the calculated average intake of alpha-tocopherol was
comparable to the estimate from the dietary survey (7-8 vs. 7.4 mg alpha-tocopherol/day,
respectively). The commercially available dietary supplements (capsules) provide 10-30 mg
CoQ10/day, thus the average diet. The optimal dietary intake of coenzyme Q10 is unknown.


Randomized, double-blind placebo-controlled trial of coenzyme Q10 in patients with acute
myocardial infarction.

Singh RB; Wander GS; Rastogi A; Shukla PK; Mittal A; Sharma JP; Mehrotra SK; Kapoor
R; Chopra RK
Cardiovasc Drugs Ther, 1998 Sep, 12:4, 347-53

The effects of oral treatment with coenzyme Q10 (120 mg/d) were compared for 28 days in
73 (intervention group A) and 71 (placebo group B) patients with acute myocardial
infarction (AMI). After treatment, angina pectoris (9.5 vs. 28.1), total arrhythmias (9.5% vs.
25.3%), and poor left ventricular function (8.2% vs. 22.5%) were significantly (P < 0.05)
reduced in the coenzyme Q group than placebo group. Total cardiac events, including
cardiac deaths and nonfatal infarction, were also significantly reduced in the coenzyme Q10
group compared with the placebo group (15.0% vs. 30.9%, P < 0.02). The extent of cardiac
disease, elevation in cardiac enzymes, and oxidative stress at entry to the study were
comparable between the two groups. Lipid peroxides, diene conjugates, and
malondialdehyde, which are indicators of oxidative stress, showed a greater reduction in the
treatment group than in the placebo group. The antioxidants vitamin A, E, and C and
beta-carotene, which were lower initially after AMI, increased more in the coenzyme Q10
group than in the placebo group. These findings suggest that coenzyme Q10 can provide
rapid protective effects in patients with AMI if administered within 3 days of the onset of
symptoms. More studies in a larger number of patients and long-term follow-up are needed
to confirm our results.


Antioxidant role of endogenous coenzyme Q against the ischemia and reperfusion-induced
lipid peroxidation in fetal rat brain.

Tsukahara Y; Wakatsuki A; Okatani Y
Acta Obstet Gynecol Scand, 1999 Sep, 78:8, 669-74

BACKGROUND: Ischemia and subsequent reperfusion induce lipid peroxidation in the
cerebrum of the fetal rat. The present study evaluated the antioxidant activity of endogenous
coenzyme Q in protecting against the lipid peroxidation induced in the fetal rat brain by
ischemia/reperfusion. METHODS: We used wistar rats at day 19 of pregnancy. Fetal
ischemia was induced by bilateral occlusion of the utero-ovarian artery for 20 minutes. For
reperfusion, the occlusion was released and the circulation was restored for 30 minutes.
Control rats underwent sham operation. We determined the levels of thiobarbituric
acid-reactive substances, the concentrations of coenzyme Q9, coenzyme Q10, and the
mitochondrial respiratory control index in fetal brains. RESULTS: Occlusion for 20
minutes significantly reduced the respiratory control index (p < 0.01), but did not alter the
levels of thiobarbituric acid-reactive substances, coenzyme Q9 or coenzyme Q10.
Subsequent reperfusion, however, significantly increased the level of thiobarbituric
acid-reactive substances (from 6.53+/-1.54 to 11.46+/-3.31 nM/mg of protein, p < 0.01)
and significantly decreased the level of coenzyme Q9 (from 291.73+/-108.94 to
162.44+/-56.83 pM/mg of protein, p < 0.05) and that of coenzyme Q10 (from
153.10+/-75.24 to 79.84+/-30.40 pM/mg of protein, p < 0.05). The respiratory control
index was still significantly lower following reperfusion than in controls (p < 0.01).
Significant negative correlations were observed between the level of thiobarbituric
acid-reactive substances and the concentrations of either coenzyme Q9 (r = -0.68, p < 0.001)
or coenzyme Q10 (r = -0.70, p < 0.001). CONCLUSION: Endogenous coenzyme Q may
protect the fetal rat brain against the lipid peroxidation induced by ischemia/reperfusion.


Coenzyme Q10 treatment in serious heart failure.

Munkholm H; Hansen HH; Rasmussen K
Biofactors, 1999, 9:2-4, 285-9

Several noninvasive studies have shown the effect on heart failure of treatment with
coenzyme Q10. In order to confirm this by invasive methods we studied 22 patients with
mean left ventricular (LV) ejection fraction 26%, mean LV internal diameter 71 mm and in
NYHA class 2-3. The patients received coenzyme Q10 100 mg twice daily or placebo for
12 weeks in a randomized double-blinded placebo controlled investigation. Before and after
the treatment period, a right heart catheterisation was done including a 3 minute exercise test.
The stroke index at rest and work improved significantly, the pulmonary artery pressure at
rest and work decreased (significantly at rest), and the pulmonary capillary wedge pressure
at rest and work decreased (significantly at 1 min work). These results suggest
improvement in LV performance. Patients with congestive heart failure may thus benefit
from adjunctive treatment with coenzyme Q10.


Effects of tamoxifen, melatonin, coenzyme Q10, and L-carnitine supplementation on
bacterial growth in the presence of mycotoxins.

Atroshi F; Rizzo A; Westermarck T; Ali vehmas T
Pharmacol Res, 1998 Oct, 38:4, 289-95

The involvement of toxic oxygen intermediates in the bacteriostatic effects of mycotoxins
(T-2 toxin, deoxynivalenol, ochratoxin A, aflatoxin B1, and fumonisin B1) was investigated
by producing bacterial growth curves using turbidimetry assays in the presence and absence
of oxygen radical-scavenging substances. The strains used in this study included
Escherichia coli (FT 101), Streptococcus agalactiae (FT 311, FT 313, FT 315),
Staphylococcus aureus (FT 192), Yersinia enterocolitica (FT 430), Salmonella infantis (FT
431), Erysipelothrix rhusiopathiae (FT 432), Lactobacillus plantarum (FT234) and
Lactobacillus casei (FT 232). Tamoxifen, melatonin, l-carnitine and coenzyme Q10 were
used as radical scavengers against oxygen toxicity to the strains studied. Tamoxifen was the
most effective in inhibiting bacterial growth when used at a high concentration, whereas
melatonin and l-carnitine were less effective. A combination of l-carnitine and coenzyme
Q10 provided better protection against oxygen toxicity caused by the mycotoxins growth
than they did individually. It was concluded that oxygen radicals are involved in the killing
of bacteria and that there is endogenous formation of toxic oxygen products by mycotoxins.
The objective of this study was to determine whether the antioxidants were able to
counteract the toxic effects of the mycotoxins. The data obtained indicate that bacterial
growth can be inhibited especially by T-2 toxin, aflatoxin B1 and ochratoxin A and that this
effect can be partially counteracted by antioxidants such as coenzyme Q10 plus l-carnitine.


Coenzyme Q10 levels correlate with the activities of complexes I and II/III in mitochondria
from parkinsonian and nonparkinsonian subjects.

Shults CW; Haas RH; Passov D; Beal MF
Neurology Service, Veterans Affairs Medical Center, San Diego, CA 92161, USA.

Ann Neurol, 1997 Aug, 42:2, 261-4

The activities of complex I and complex II/III in platelet mitochondria are reduced in
patients with early, untreated Parkinson's disease. Coenzyme Q10 is the electron acceptor
for complex I and complex II. We found that the level of coenzyme Q10 was significantly
lower in mitochondria from parkinsonian patients than in mitochondria from age- and
sex-matched control subjects and that the levels of coenzyme Q10 and the activities of
complex I and complex II/III were significantly correlated.


Impact of ubiquinone (coenzyme Q10) treatment on glycaemic control, insulin requirement
and well-being in patients with Type 1 diabetes mellitus.

Henriksen JE; Andersen CB; Hother Nielsen O; Vaag A; Mortensen SA; Beck Nielsen H
Diabet Med, 1999 Apr, 16:4, 312-8

AIM: To investigate the effect of ubiquinone (coenzyme Q10) on glycaemic control and
insulin requirement in patients with Type 1 diabetes mellitus (DM). METHODS: We
investigated 34 patients with Type 1 DM in a randomized, double-blind, placebo-controlled
study. Patients received either 100 mg Q10 or placebo daily for 3 months. The insulin doses
were adjusted according to patients' home measurements of blood glucose concentrations
and reported experience of hypoglycaemia. RESULTS: At randomization no differences
existed between the Q10 and the placebo groups in age, body mass index (BMI), HbA1c,
daily insulin dose or mean daily blood glucose concentration. Serum Q10 concentration
increased in the Q10 group (mean +/- SD: 0.9+/-0.2 vs. 2.0+/-1.0 microg/ml, P<0.005),
with no change in the placebo group (0.9+/-0.3 vs. 0.9+/-0.3 microg/ml, not significant
(NS)). Following intervention no differences existed between the Q10 and the placebo
groups regarding HbA1c (7.86+/-0.88 vs. 7.84+/-0.84%), mean daily blood glucose
concentrations (8.06+/-1.86 vs. 8.53+/-1.88 mM), mean insulin dose (52.1+/-13.2 vs.
52.6+/-21.4 U), hypoglycaemic episodes (2.0+/-1.8 vs. 2.5+/-2.1 episodes/week), or
cholesterol concentrations (4.81+/-0.91 vs. 4.78+/-1.07 mM). Furthermore, no differences
existed in the well-being of the patients reported from a visual analogue scale (physical:
0.67+/-0.21 vs. 0.71+/-0.18, psychological: 0.70+/-0.25 vs. 0.73+/-0.24). CONCLUSION:
Q10 treatment does not improve glycaemic control, nor does it reduce insulin requirement,
and it can therefore be taken by patients with Type 1 DM without any obvious risk of
hypoglycaemia. No major beneficial or unfavourable effects on the investigated parameters
could be demonstrated and no major changes in the sense of well-being occurred in the


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