1. Efficacy of coenzyme Q10 for improved tolerability of cancer treatments
Roffe L , Schmidt K , Ernst E .
School of Nursing and Midwifery, University of Southampton, Southampton, UK.
J Clin Oncol. 2004
PURPOSE: The aim of this systematic review was to summarize and evaluate the evidence available for oral supplementation with coenzyme Q10 (CoQ10) to improve the tolerability of cancer treatments. MATERIALS AND METHODS: Searches for all published and unpublished controlled trials were carried out on seven databases. Manufacturers of CoQ10 were identified and contacted. Controlled clinical trials of monopreparations of CoQ10 administered orally to cancer patients were included. No language restrictions were imposed. Data were extracted independently by two authors according to predefined criteria. RESULTS: Six studies were included in the review, including three randomized clinical trials and three nonrandomized clinical trials. Patients in five of six studies received anthracyclines. The results suggested that CoQ10 provides some protection against cardiotoxicity or liver toxicity during cancer treatment. However, because of inadequate reporting and analysis, as well as questionable validity of outcome measures, the results are not conclusive. CONCLUSION: Suggestions that CoQ10 might reduce the toxicity of cancer treatments have not been tested by rigorous trials. Further investigations are necessary to determine whether CoQ10 can improve the tolerability of cancer treatments.
2.Blood pressure lowering efficacy of coenzyme Q10 for primary hypertension
Ho MJ , Bellusci A , Wright JM .
Faculty of Medicine, University of Toronto, Toronto, ON, Canada.
Cochrane Database Syst Rev. 2009
BACKGROUND: Studies have shown that coenzyme Q10 deficiency is associated with cardiovascular disease. Hypertension is a commonly measured surrogate marker for non-fatal and fatal cardiovascular endpoints such as heart attacks and strokes. Clinical trials have suggested that coenzyme Q10 supplementation can effectively lower blood pressure (BP). OBJECTIVES: To determine the blood pressure lowering effect of coenzyme Q10 in primary hypertension. SEARCH STRATEGY: The Cochrane Central Register of Controlled Trials (2009 Issue 2), MEDLINE (1966 -May 2008), EMBASE (1982 - May 2008), and CINAHL (1970 - May 2008) as well as the reference lists of articles were searched for relevant clinical trials in any language. SELECTION CRITERIA: Double-blind, randomized, placebo-controlled parallel or crossover trials evaluating the BP lowering efficacy of coenzyme Q10 for a duration of at least 3 weeks in patients with primary hypertension. DATA COLLECTION AND ANALYSIS: The primary author independently assessed the risk of bias and extracted the data. The second author verified data extraction. MAIN RESULTS: Three clinical trials with a total of 96 participants were evaluated for the effects of coenzyme Q10 on blood pressure compared to placebo. Treatment with coenzyme Q10 in subjects with systolic BP (SBP) > 140 mmHg or diastolic BP (DBP) > 90 mmHg resulted in mean decreases in SBP of 11 mmHg (95% CI 8, 14) and DBP of 7 mmHg (95% CI 5, 8). AUTHORS' CONCLUSIONS: Due to the possible unreliability of some of the included studies, it is uncertain whether or not coenzyme Q10 reduces blood pressure in the long-term management of primary hypertension.
3. Coenzyme Q10 protects against oxidative stress-induced cell death and enhances the synthesis of basement membrane components in dermal and epidermal cells
Muta-Takada K , Terada T , Yamanishi H , Ashida Y , Inomata S , Nishiyama T , Amano S .
Shiseido Research Center, Yokohama, Japan
Biofactors. 2009
Coenzyme Q10 (CoQ10), which has both energizing and anti-oxidative effects, is also reported to have antiaging action, e.g., reducing the area of facial wrinkles. However, the mechanism of its anti-aging activity is not fully established. Here, we examined the effect of CoQ10 on human dermal and epidermal cells. CoQ10 promoted proliferation of fibroblasts but not keratinocytes. It also accelerated production of basement membrane components, i.e., laminin 332 and type IV and VII collagens, in keratinocytes and fibroblasts, respectively; however, it had no effect on type I collagen production in fibroblasts. CoQ10 also showed protective effects against cell death induced by several reactive oxygen species in keratinocytes, but only when its cellular absorption was enhanced by pretreatment of the cells with highly CoQ10-loaded serum. These results suggest that protection of epidermis against oxidative stress and enhancement of production of epidermal basement membrane components may be involved in the antiaging properties of CoQ10 in skin.
4. Aging skin is functionally anaerobic: importance of coenzyme Q10 for anti aging skin care
Prahl S , Kueper T , Biernoth T , Wöhrmann Y , Münster A , Fürstenau M , Schmidt M , Schulze C , Wittern KP , Wenck H , Muhr GM , Blatt T .
R&D, Beiersdorf AG, Hamburg, Germany.
Biofactors. 2008
The functional loss of mitochondria represents an inherent part in modern theories trying to explain the cutaneous aging process. The present study shows significant age-dependent differences in mitochondrial function of keratinocytes isolated from skin biopsies of young and old donors. Our data let us postulate that energy metabolism shifts to a predominantly non-mitochondrial pathway and is therefore functionally anaerobic with advancing age. CoQ10 positively influences the age-affected cellular metabolism and enables to combat signs of aging starting at the cellular level. As a consequence topical application of CoQ10 is beneficial for human skin as it rapidly improves mitochondrial function in skin in vivo.
5. Anti-inflammatory effects of CoQ10 and colorless carotenoids
Fuller B , Smith D , Howerton A , Kern D .
Department of Biochemistry and Molecular Biology, Univeristy of Oklahoma Health Science Center, Oklahoma City, OK 73104, USA
Cosmet Dermatol. 2006
BACKGROUND: CoQ10 (ubiquinone, coenzyme Q10) and carotenoids are popular antioxidants used in many skin care products to protect the skin from free radical damage. AIM: To evaluate the effects of CoQ10 and colorless carotenoids on the production of inflammatory mediators in human dermal fibroblasts treated with UV radiation (UVR) and to investigate the possible synergistic effects of these two antioxidants. METHODS: Normal human dermal fibroblast cell cultures were exposed to either 50 mJ of UVR or to IL-1 and then incubated with various concentrations of either CoQ10, the colorless carotenoids, phytoene and phytofluene, or to combinations of these antioxidants. After 24 h in culture, cells and spent medium were harvested and assayed by enzyme-linked immunosorbent assay for prostaglandin E2 (PGE-2), interleukin 6 (IL-6), and matrix metalloproteinase 1 (MMP-1). In addition, the ability of the carotenoids to protect CoQ10 from oxidation by the reactive oxygen species (ROS), hyperchlorite, was also determined. RESULTS: Human fibroblasts respond to UVR or to IL-1 by increasing the production of various inflammatory mediators including PGE-2, IL-1, and IL-6 and proteases such as collagenase (MMP-1). Treatment of fibroblasts with 10 microm of CoQ10 suppressed the UVR- or IL-1-induced increase in PGE-2, IL-6, and MMP-1. The combination of carotenoids and CoQ10 produced an enhanced inhibition of these three inflammatory mediators. Furthermore, the colorless carotenoids, phytoene and phytofluene, protected CoQ10 from degradation by the ROS, hypochlorite. CONCLUSION: CoQ10 is able to suppress the UVR- or IL-1-induced inflammatory response in dermal fibroblasts. Furthermore, this compound can block the UVR induction of the matrix-eroding enzyme, MMP-1. Finally, the combination of carotenoids plus CoQ10 results in enhanced suppression of inflammation. The results suggest that the combination of carotenoids and CoQ10 in topical skin care products may provide enhanced protection from inflammation and premature aging caused by sun exposure.
6. Beneficial effects of creatine, CoQ10, and lipoic acid in mitochondrial disorders
Rodriguez MC , MacDonald JR , Mahoney DJ , Parise G , Beal MF , Tarnopolsky MA .
Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada.
Muscle Nerve. 2007
Mitochondrial disorders share common cellular consequences: (1) decreased ATP production; (2) increased reliance on alternative anaerobic energy sources; and (3) increased production of reactive oxygen species. The purpose of the present study was to determine the effect of a combination therapy (creatine monohydrate, coenzyme Q(10), and lipoic acid to target the above-mentioned cellular consequences) on several outcome variables using a randomized, double-blind, placebo-controlled, crossover study design in patients with mitochondrial cytopathies. Three patients had mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), four had mitochondrial DNA deletions (three patients with chronic progressive external ophthalmoplegia and one with Kearns-Sayre syndrome), and nine had a variety of other mitochondrial diseases not falling into the two former groups. The combination therapy resulted in lower resting plasma lactate and urinary 8-isoprostanes, as well as attenuation of the decline in peak ankle dorsiflexion strength in all patient groups, whereas higher fat-free mass was observed only in the MELAS group. Together, these results suggest that combination therapies targeting multiple final common pathways of mitochondrial dysfunction favorably influence surrogate markers of cellular energy dysfunction. Future studies with larger sample sizes in relatively homogeneous groups will be required to determine whether such combination therapies influence function and quality of life.
7. Coenzyme Q10 and male infertility
Balercia G , Mancini A , Paggi F , Tiano L , Pontecorvi A , Boscaro M , Lenzi A , Littarru GP .
Endocrinology, Andrology Unit, Department of Clinical Medicine and Applied Biotechnologies, Polytechnic University of Marche, Umberto I Hospital, Ancona, Italy
J Endocrinol Invest. 2009
We had previously demonstrated that Coenzyme Q10 [(CoQ10) also commonly called ubiquinone] is present in well-measurable levels in human seminal fluid, where it probably exerts important metabolic and antioxidant functions; seminal CoQ10 concentrations show a direct correlation with seminal parameters (count and motility). Alterations of CoQ10 content were also shown in conditions associated with male infertility, such as asthenozoospermia and varicocele (VAR). The physiological role of this molecule was further clarified by inquiring into its variations in concentrations induced by different medical or surgical procedures used in male infertility treatment. We therefore evaluated CoQ10 concentration and distribution between seminal plasma and spermatozoa in VAR, before and after surgical treatment, and in infertile patients after recombinant human FSH therapy. The effect of CoQ10 on sperm motility and function had been addressed only through some in vitro experiments. In two distinct studies conducted by our group, 22 and 60 patients affected by idiopathic asthenozoospermia were enrolled, respectively. CoQ10 and its reduced form, ubiquinol, increased significantly both in seminal plasma and sperm cells after treatment, as well as spermatozoa motility. A weak linear dependence among the relative variations, at baseline and after treatment, of seminal plasma or intracellular CoQ10, ubiquinol levels and kinetic parameters was found in the treated group. Patients with lower baseline value of motility and CoQ10 levels had a statistically significant higher probability to be responders to the treatment. In conclusion, the exogenous administration of CoQ10 increases both ubiquinone and ubiquinol levels in semen and can be effective in improving sperm kinetic features in patients affected by idiopathic asthenozoospermia.
8. Oxidative stress, endothelial function and coenzyme Q10
Belardinelli R , Tiano L , Littarru GP .
Cardiologia Riabilitativa Lancisi, Azienda Ospedali Riuniti, Ancona, Italy.
Biofactors. 2008
Reactive oxygen species seem to play an important role in vascular homeostasis. In conditions of high oxidative stress, such as chronic heart failure and multiple coronary risk factors, the rate of inactivation of nitric oxide to peroxynitrite by superoxide anions may be reduced by CoQ10, which can also protect against nitrosative damage. CoQ10 may also influence vascular function indirectly via inhibition of oxidative damage to LDL. Patients with lower levels of extracellular superoxide dismutase (ecSOD) demonstrate greater improvements than patients with normal ec-SOD levels, suggesting that the higher the oxidative stress the greater the improvement in the endothelium-dependent relaxation after the administration of a compound with antioxidant properties like CoQ10. Future studies are needed to inquire whether these effects may translate into benefits in clinical practice.
9. The evolution of coenzyme Q
Crane FL .
Department of Biological Science, Purdue University, West Lafayette, IN, USA
Biofactors. 2008
In the 50 years since the identification of coenzyme Q as an electron carrier in mitochondria, it has been identified with diverse and unexpected functions in cells. Its discovery came as a result of a search for electron carriers in mitochondria following the identification of flavin and cytochromes by Warburg, Keilin, Chance and others. As a result of investigation of membrane lipids at D.E. Green's laboratory at University of Wisconsin coenzyme Q was identified as the electron carrier between primary flavoprotein dehydrogenases and the cytochromes. Then Peter Mitchell identified the role of transmembrane proton transfer as a basis for ATP synthesis. The general distribution of coenzyme Q in all cell membranes then led to the recognition of a role as a primary antioxidant. The protonophoric function was extended to acidification of Golgi and lysosomal vericles. A further role in proton release through the plasma membrane and its relation to cell proliferation has not been fully developed. A role in generation of H202 as a messenger for hormone and cytokine action is indicated as well as prevention of apoptosis by inhibition of ceramide release. Identification of the genes and proteins required for coenzyme Q synthesis has led to a basis for defining deficiency. For 50 years Karl Folkers has led the search for deficiency and therapeutic application. The development of large scale production, better formulation for uptake, and better methods for analysis have furthered this search. The story isn't over yet. Questions remain about effects on membrane structure, breakdown and control of cellular synthesis and uptake and the basis for therapeutic action.
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