General Info
CoQ10_Facts_or_Fabrications/Lies
Absorption
Coenzyme Q10: Absorption, tissue uptake, metabolism and pharmacokinetics, 2006
Commercial Products
Nutri-Nano CoQ10 Solgar
bio-quinone-q10-gold-100-mg, pharmanord
CoQ reduces P53
P53 Coenzyme Q
Statins induce P53 and its nuclear translocation
P53 mevalonate
Supplementation of coenzyme Q10 and alpha-tocopherol lowers glycated hemoglobin level and lipid peroxidation in pancreas of diabetic rats. 2008
Coenzima Q10 allevia sintomi miopatici nei pazienti trattati con statine
Il trattamento con coenzima Q10 allevia i sintomi di miopatia nei pazienti trattati con statine. Tale trattamento diminuisce sia la biosintesi del colesterolo che quella del coenzima Q10, ed il risultante deficit di tale coenzima può contribuire allo sviluppo di miopatie e sintomi muscolari descritti nei pazienti trattati con statine. L'integrazione del coenzima in questione diminuisce il dolore muscolare del 40 percento e migliora l'interferenza del dolore con le attività quotidiane del 38 percento. Ciò suggerisce che il coenzima Q10 può essere di beneficio nei pazienti sotto statine migliorando i sintomi miopatici ed il benessere e la funzionalità individuale nelle attività quotidiane. (Am J Cardiol 2007; 99: 1409-12)
Chin J Physiol. 2007 Oct 31;50(5):217-24.Links
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Erratum in:
Chin J Physiol. 2007 Dec 31;50(6):330.
Effects of coenzyme Q10 on the heart ultrastructure and nitric oxide synthase during hyperthyroidism.
Oztay F, Ergin B, Ustunova S, Balci H, Kapucu A, Caner M, Demirci C.
Department of Biology, Faculty of Science, Istanbul University, Vezneciler. fusunoztay@yahoo.com
Coenzyme Q10 is an important component of mitochondrial electron transport chain and antioxidant. Hyperthyroidism manifests hyperdynamic circulation with increased cardiac output, increased heart rate and decreased peripheral resistance. The heart is also under the oxidative stress in the hyperthyroidism. The aim of this study was to examine both how the coenzyme Q10 can affect heart ultrastructure in the hyperthyroidism and how the relationship between nitric oxide synthase (NOS) and heart damage and coenzyme Q10. Swiss Black C57 mice received 5 mg/kg L-thyroxine. Coenzyme Q10 (1.5 mg/kg) and L-thyroxine together was given to second group mice. Coenzyme Q10 and serum physiologic were applied to another two groups, respectively. All treatments were performed daily for 15 days by gavage. Free triiodothyronine and thyroxine were increased in two groups given L-thyroxine; thyroid-stimulating hormone level did not change. Hyperthyroid heart showed an increased endothelial NOS (eNOS) and inducible NOS (iNOS) immunoreactivity in the tissue. Coenzyme Q10 administration decreased these NOS immunoreactivities in the hyperthyroid animals. Cardiomyocytes of the hyperthyroid animals was characterized by abnormal shape and invaginated nuclei, and degenerative giant mitochondria. Desmosome plaques reduced in density. In hyperthyroid mice given coenzyme Q10, the structural disorganization and mitochondrial damage regressed. However, hearts of healthy mice given coenzyme Q10 displayed normal ultrastructure, except for increased mitochondria and some of them were partially damaged. Coenzyme Q10 increased the glycogen in the cardiomyocytes. In conclusion, coenzyme Q10 administration can prevent the ultrastructural disorganization and decrease the iNOS and eNOS increment in the hyperthyroid heart.
CoQ Tissues distribution according to drug preparation
CoQ, Riboflavin, Niacin
In association with Tamoxifen
Papers Niacin Coenzyme Q
Vitamin D3 hydroxylation
The influence of Coenzyme Q10 on total serum calcium concentration in two patients with Kearns-Sayre Syndrome and hypoparathyroidism. 1996
Two patients with Kearns-Sayre Syndrome and hypoparathyroidism were treated with alfacalcidol (1a-OH D3) and total serum calcium concentration remained within normal range for a long period. After two months of combined therapy with Coenzyme Q10 (CoQ10), hypercalcemia was noticed and as a result, 1a-OHD3 was gradually discontinued. Normal total serum calcium concentration was obtained with CoQ10 monotherapy while the replacement of CoQ10 with placebo led to hypocalcemia. The mechanism of action of CoQ10 is difficult to explain. Since the parathormone level remained unchanged during CoQ10 or placebo therapy, we speculate that the capacity of producing an active form of vitamin D in mitochondria of proximal tubules was restored by CoQ10 therapy.
Coenzyme Q10 and adriamycin toxicity in mice. 1980
Res Commun Chem Pathol Pharmacol (1980) Show Abstract »
At higher i.v. adriamycin dose levels, CoQ10 pretreatment significantly enhanced acute toxicity.
[Chronic cardiotoxicity of anthracycline derivatives and possible prevention by coenzyme Q10]. 1984
Gan No Rinsho (1984) Show Abstract »
We studied the cardiotoxicity caused by ADR in New Zealand white rabbits and its protection by the medication of CoQ10.
A water soluble CoQ10 formulation improves intracellular distribution and promotes mitochondrial respiration in cultured cells. 2012
- BACKGROUND:
Mitochondria are both the cellular powerhouse and the major source of reactive oxygen species. Coenzyme Q(10) plays a key role in mitochondrial energy production and is recognized as a powerful antioxidant. For these reasons it can be argued that higher mitochondrial ubiquinone levels may enhance the energy state and protect from oxidative stress. Despite the large number of clinical studies on the effect of CoQ supplementation, there are very few experimental data about the mitochondrial ubiquinone content and the cellular bioenergetic state after supplementation. Controversial clinical and in vitro results are mainly due to the high hydrophobicity of this compound, which reduces its bioavailability.
PRINCIPAL FINDINGS:
We measured the cellular and mitochondrial ubiquinone content in two cell lines (T67 and H9c2) after supplementation with a hydrophilic CoQ formulation (Qter®) and native CoQ. Our results show that the water soluble formulation is more efficient in increasing ubiquinone levels. We have evaluated the bioenergetics effect of ubiquinone treatment, demonstrating that intracellular CoQ content after Qter supplementation positively correlates with an improved mitochondrial functionality (increased oxygen consumption rate, transmembrane potential, ATP synthesis) and resistance to oxidative stress.
CONCLUSIONS:
The improved cellular energy metabolism related to increased CoQ content represents a strong rationale for the clinical use of coenzyme Q(10) and highlights the biological effects of Qter®, that make it the eligible CoQ formulation for the ubiquinone supplementation.
T67 cells were treated for 24 hours with 100 nM Qter or 10 µM native CoQ10, then ubiquinone was immediately extracted, from an equal number of cells, with isopropyl alcohol (for further details see Materials and methods) and the UV spectra were recorded between 320 and 240 nm. The ubiquinone extracted from 100 nM Qter treated sample appears to be completely reduced with a maximum absorption peak at 290 nm, while the ubiquinone extracted from 10 µM native CoQ10 treated sample has a maximum absorption peak shifted towards 275 nm, indicating the presence of the ubiquinone oxidized form. Spectra are representative of three different experiments.
UV Spectra of conjugated dienes.
Membrane lipids were extracted from T67 cells treated for 24 hours with Qter (100 nM and 10 µM) and CoQ10 (10 µM) after 30 minutes exposure to 100 µM TBH. Each spectrum was obtained as a difference spectra between TBH treated and TBH untreated samples. Spectra are normalized on total protein content and are representative of three different sets of experiments.
Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer's disease. 2011
- Increased oxidative stress is implicated in the pathogenesis of Alzheimer's disease (AD). A large body of evidence suggests that mitochondrial dysfunction and increased reactive oxygen species occur prior to amyloid-β (Aβ) deposition. Coenzyme Q10 (CoQ10), a component of the mitochondrial electron transport chain, is well characterized as a neuroprotective antioxidant in animal models and human trials of Huntington's disease and Parkinson's disease, and reduces plaque burden in AβPP/PS1 mice. We now show that CoQ10 reduces oxidative stress and amyloid pathology and improves behavioral performance in the Tg19959 mouse model of AD. CoQ10 treatment decreased brain levels of protein carbonyls, a marker of oxidative stress. CoQ10 treatment resulted in decreased plaque area and number in hippocampus and in overlying cortex immunostained with an Aβ42-specific antibody. Brain Aβ42 levels were also decreased by CoQ10 supplementation. Levels of amyloid-β protein precursor (AβPP) β-carboxyterminal fragments were decreased. Importantly, CoQ10-treated mice showed improved cognitive performance during Morris water maze testing. Our results show decreased pathology and improved behavior in transgenic AD mice treated with the naturally occurring antioxidant compound CoQ10. CoQ10 is well tolerated in humans and may be promising for therapeutic trials in AD.
AMPK and CoQ
AMPK and CoQ Quetzal
