J Neurochem. 2007 Oct 31 [Epub ahead of print] Links
Therapeutic effects of Coenzyme Q(10) (CoQ(10)) and reduced CoQ(10) in
the 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine model of
Parkinsonism.Cleren C, Yang L, Lorenzo B, Calingasan NY, Schomer A,
Sireci A, Wille EJ, Beal MF.
Department of Neurology and Neuroscience, Weill Medical College of
Cornell University, New York-Presbyterian Hospital, New York, NY, USA.

Coenzyme Q(10) (CoQ(10)) is a promising agent for neuroprotection in
neurodegenerative diseases. We tested the effects of various doses of
two formulations of CoQ(10) in food, and found that administration in
the diet resulted in significant protection against loss of dopamine,
which was accompanied by a marked increase in plasma concentrations of
CoQ(10). We further investigated the neuroprotective effects of
CoQ(10), reduced CoQ(10) (ubiquinol), and CoQ(10) emulsions in the
(MPTP) model of Parkinson's disease (PD). We found neuroprotection
against MPTP induced loss of dopamine using both CoQ(10), and reduced
CoQ(10), which produced the largest increases in plasma
concentrations. Lastly, we administered CoQ(10) in the diet to test
its effects in a chronic MPTP model induced by administration of MPTP
by Alzet pump for one month. We found neuroprotective effects against
dopamine depletion, loss of tyrosine hydroxylase neurons and induction
of alpha-synuclein inclusions in the substantia nigra pars compacta.
The finding that CoQ(10) is effective in a chronic dosing model of
MPTP toxicity, is of particular interest, since this may be more
relevant to PD. These results provide further evidence that
administration of CoQ(10) is a promising therapeutic strategy for the
treatment of PD.


PMID: 17973981 [PubMed - as supplied by publisher]

...Mol Biotechnol. 2007 Sep;37(1):31-7. Links
Bioenergetic and antioxidant properties of coenzyme Q10: recent
developments.Littarru GP, Tiano L.
Institute of Biochemistry, Polytechnic University of the Marche, Via
Ranieri, Ancona 60131, Italy. g.litta...@univpm.it

For a number of years, coenzyme Q (CoQ10 in humans) was known for its
key role in mitochondrial bioenergetics; later studies demonstrated
its presence in other subcellular fractions and in plasma, and
extensively investigated its antioxidant role. These two functions
constitute the basis on which research supporting the clinical use of
CoQ10 is founded. Also at the inner mitochondrial membrane level,
coenzyme Q is recognized as an obligatory co-factor for the function
of uncoupling proteins and a modulator of the transition pore.
Furthermore, recent data reveal that CoQ10 affects expression of genes
involved in human cell signalling, metabolism, and transport and some
of the effects of exogenously administered CoQ10 may be due to this
property. Coenzyme Q is the only lipid soluble antioxidant synthesized
endogenously. In its reduced form, CoQH2, ubiquinol, inhibits protein
and DNA oxidation but it is the effect on lipid peroxidation that has
been most deeply studied. Ubiquinol inhibits the peroxidation of cell
membrane lipids and also that of lipoprotein lipids present in the
circulation. Dietary supplementation with CoQ10 results in increased
levels of ubiquinol-10 within circulating lipoproteins and increased
resistance of human low-density lipoproteins to the initiation of
lipid peroxidation. Moreover, CoQ10 has a direct anti-atherogenic
effect, which has been demonstrated in apolipoprotein E-deficient mice
fed with a high-fat diet. In this model, supplementation with CoQ10 at
pharmacological doses was capable of decreasing the absolute
concentration of lipid hydroperoxides in atherosclerotic lesions and
of minimizing the size of atherosclerotic lesions in the whole aorta.
Whether these protective effects are only due to the antioxidant
properties of coenzyme Q remains to be established; recent data point
out that CoQ10 could have a direct effect on endothelial function. In
patients with stable moderate CHF (congestive heart failure), oral CoQ10 supplementation was
shown to ameliorate cardiac contractility and endothelial dysfunction.
Recent data from our laboratory showed a strong correlation between
endothelium bound extra cellular SOD (ecSOD)(Super Oxide Dismutase is a powerful enzyme and cellular anti-oxidant that acts as a super-scavenger of dangerous free-radicals) and flow-dependent
endothelial-mediated dilation (FMD), a functional parameter commonly used as
a biomarker of vascular function. The study also highlighted that
supplementation with CoQ10 that significantly affects endothelium-
bound ecSOD activity. Furthermore, we showed a significant correlation
between increase in endothelial bound ecSOD activity and improvement
in FMD after CoQ10 supplementation. The effect was more pronounced in
patients with low basal values of ecSOD. Finally, we summarize the
findings, also from our laboratory, on the implications of CoQ10 in
seminal fluid integrity and sperm cell motility.


PMID: 17914161 [PubMed - indexed for MEDLINE]