Coenzyme Q10 treatment in infertile men with idiopathic asthenozoospermia: a placebo-controlled, double-blind randomized trial

OBJECTIVE: To evaluate the effectiveness of coenzyme Q(10) treatment in improving semen quality in men with idiopathic infertility. DESIGN: Placebo-controlled, double-blind randomized trial. SETTING: Andrology Unit, Department of Internal Medicine, Polytechnic University of Marche, Italy. PATIENT(S): Sixty infertile patients (27-39 years of age) with the following baseline sperm selection criteria: concentration >20 x 10(6)/mL, sperm forward motility 30%; 55 patients completed the study. INTERVENTION(S): Patients underwent double-blind therapy with coenzyme Q(10), 200 mg/day, or placebo; the study design was 1 month of run-in, 6 months of therapy or placebo, and 3 months of follow-up. MAIN OUTCOME MEASURE(S): Variations in semen parameters used for patient selection and variations of coenzyme Q(10) and ubiquinol concentrations in seminal plasma and spermatozoa. RESULT(S): Coenzyme Q(10) and ubiquinol increased significantly in both seminal plasma and sperm cells after treatment, as well as spermatozoa motility. A weak linear dependence among the relative variations, baseline and after treatment, of seminal plasma or intracellular coenzyme Q(10) and ubiquinol levels and kinetic parameters was found in the treated group. Patients with a lower baseline value of motility and levels of coenzyme Q(10) had a statistically significant higher probability to be responders to the treatment. CONCLUSION(S): The exogenous administration of coenzyme Q(10) increases the level of the same and ubiquinol in semen and is effective in improving sperm kinetic features in patients affected by idiopathic asthenozoospermia

The role of Coenzyme Q10 in statin-associated myopathy

Statins, or 3-hydroxyl-3-methylglutaryl coenzyme HMG-CoA reductase inhibitors,\ud are cholesterol-lowering drugs which are frequently used in the primary and secondary\ud prevention of coronary artery disease. Current research and recommendations support\ud and encourage more extensive use of these drugs.\ud However, statin usage is limited by many factors, including a high incidence of\ud statin-associated myalgia and myopathy. This review focuses on the use of Coenzyme Q\ud in statin-associated myopathy

Exogenous coenzyme Q10 modulates MMP-2 activity in MCF-7 cell line as a breast cancer cellular model

<p>Abstract</p> <p>Background/Aims</p> <p>Matrix Metalloproteinases 2 is a key molecule in cellular invasion and metastasis. Mitochondrial ROS has been established as a mediator of MMP activity. Coenzyme Q₁₀contributes to intracellular ROS regulation. Coenzyme Q₁₀beneficial effects on cancer are still in controversy but there are indications of Coenzyme Q₁₀complementing effect on tamoxifen receiving breast cancer patients.</p> <p>Methods</p> <p>In this study we aimed to investigate the correlation of the effects of co-incubation of coenzyme Q10 and N-acetyl-L-cysteine (NAC) on intracellular H2O2 content and Matrix Metalloproteinase 2 (MMP-2) activity in MCF-7 cell line.</p> <p>Results and Discussion</p> <p>Our experiment was designed to assess the effect in a time and dose related manner. Gelatin zymography and Flowcytometric measurement of H2O2 by 2'7',-dichlorofluorescin-diacetate probe were employed. The results showed that both coenzyme Q10 and N-acetyl-L-cysteine reduce MMP-2 activity along with the pro-oxidant capacity of the MCF-7 cell in a dose proportionate manner.</p> <p>Conclusions</p> <p>Collectively, the present study highlights the significance of Coenzyme Q₁₀effect on the cell invasion/metastasis effecter molecules.</p

Causes of low muscle coenzyme-Q levels beyond primary coenzyme-Q-deficiency

International audienceLetter to the Edito

Inhibition by coenzyme Q of ethanol- and carbon tetrachloride-stimulated lipid peroxidation in vivo and catalyzed by microsomal and mitochondrial systems

The ability of coenzyme Q to inhibit lipid peroxidation in intact animals as well as in mitochondrial, submitochondrial, and microsomal systems has been tested. Rats fed coenzyme Q prior to being treated with carbon tetrachloride or while being treated with ethanol excrete less thiobarbituric acid-reacting material in the urine than such rats not fed coenzyme Q. Liver homogenates, mitochondria, and microsomes isolated from rats treated with carbon tetrachloride and ethanol catalyze lipid peroxidation at rates which exceed those from animals also fed coenzyme Q. The rate of lipid peroxidation catalyzed by submitochondrial particles isolated from hearts of young, old, and endurance trained elderly rats was inversely proportional to the coenzyme Q content of the submitochondrial preparation in assays in which succinate was employed to reduce the endogenous coenzyme Q. Reduced, but not oxidized, coenzyme Q inhibited lipid peroxidation catalyzed by rat liver microsomal preparations. These results provide additional evidence in support of an antioxidant role for coenzyme Q.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27527/1/0000571.pd

Restoration of impaired cardiac function of patients with diverse muscular dystrophies by therapy with coenzyme Q10

The present invention relates to the use of Coenzyme Q in the treatment of slow muscle degeneration, commonly known to those of skill in the art so a dystrophy or atrophy, and the accompanying cardiac complications typically identified in such patients. Administration of Coenzyme Q, and particularly the analog Coenzyme Q.sub.10 (CoQ.sub.10) to humans increases the pumping of blood by the heart, and thereby increases tissue oxygeneration throughout the body. The net physiological effect halts the progression of muscle deterioration and improves cardiac function. An overall improvement in the quality of life for these human subjects is also observed, said patients reportedly experiencing less fatigue. A method for treating human patients with progressive muscular dystrophies or the neurogenic atrophies with Coenzyme Q.sub.10 (CoQ.sub.10) specifically disclosed. The method is similarly effective for the treatment of any form of muscle degeneration or cardiac muscular dysfunction independently.Board of Regents, University of Texas Syste

Biological validation of coenzyme Q redox state by HPLC-EC measurement: relationship between coenzyme Q redox state and coenzyme Q content in rat tissues

AbstractThe properties of coenzymes Q (CoQ9 and CoQ10) are closely linked to their redox state (CoQox/total CoQ)×100. In this work, CoQ redox state was biologically validated by high performance liquid chromatography-electrochemical measurement after modulation of mitochondrial electron flow of cultured cells by molecules increasing (rotenone, carbonyl cyanide chlorophenylhydrazone) or decreasing (antimycin) CoQ oxidation. The tissue specificity of CoQ redox state and content were investigated in control and hypoxic rats. In control rats, there was a strong negative linear regression between tissular CoQ redox state and CoQ content. Hypoxia increased CoQ9 redox state and decreased CoQ9 content in a negative linear relationship in the different tissues, except the heart and lung. This result demonstrates that, under conditions of mitochondrial impairment, CoQ redox control is tissue-specific

Human Coenzyme Q(10) Deficiency

Ubiquinone (coenzyme Q(10) or CoQ(10)) is a lipid-soluble component of virtually all cell membranes and has multiple metabolic functions. Deficiency of CoQ(10) (MIM 607426) has been associated with five different clinical presentations that suggest genetic heterogeneity, which may be related to the multiple steps in CoQ(10) biosynthesis. Patients with all forms of CoQ(10) deficiency have shown clinical improvements after initiating oral CoQ(10) supplementation. Thus, early diagnosis is of critical importance in the management of these patients. This year, the first molecular defect causing the infantile form of primary human CoQ(10) deficiency has been reported. The availability of genetic testing will allow for a better understanding of the pathogenesis of this disease and early initiation of therapy (even presymptomatically in siblings of patients) in this otherwise life-threatening infantile encephalomyopathy

Is supercomplex organization of the respiratory chain required for optimal electron transfer activity?

AbstractThe supra-molecular assembly of the main respiratory chain enzymatic complexes in the form of “supercomplexes” has been proved by structural and functional experimental evidence. This evidence strongly contrasts the previously accepted Random Diffusion Model stating that the complexes are functionally connected by lateral diffusion of small redox molecules (i.e. Coenzyme Q and cytochrome c).This review critically examines the available evidence and provides an analysis of the functional consequences of the intermolecular association of the respiratory complexes pointing out the role of Coenzyme Q and of cytochrome c as channeled or as freely diffusing intermediates in the electron transfer activity of their partner enzymes