ubiquinone-q2 and Coronary-Disease

Ubiquinol-10 and ubiquinone-10 were measured in plasma of patients with several pathologies known to be associated with increased oxidative stress. Plasma ubiquinol-10, expressed as a percentage of total ubiquinol-10 + ubiquinone-10, was found to be significantly lower in hyperlipidaemic patients and in patients with liver diseases than in age-matched control subjects. In contrast, no decrease in ubiquinol-10 was detected in plasma of patients with coronary heart disease and Alzheimer's disease. Except for ubiquinol-10, no other lipophilic antioxidant was found to be decreased in patients with liver diseases. These data suggest that the level of ubiquinol-10 in human plasma may serve as a marker for liver dysfunction, reflecting its diminished reduction by the liver rather than increased consumption by oxidants.

Topics: Adult; Aged; Alzheimer Disease; Biomarkers; Cholesterol; Coronary Disease; Humans; Hyperlipidemias; Liver Diseases; Middle Aged; Models, Biological; Oxidative Stress; Reference Values; Reproducibility of Results; Triglycerides; Ubiquinone

Ubiquinol-10, the reduced form of ubiquinone-10 (coenzyme Q10), is a potent lipophilic antioxidant present in nearly all human tissues. The exceptional oxidative lability of ubiquinol-10 implies that it may represent a sensitive index of oxidative stress. The present study was undertaken to assess the hypothesis that the level of ubiquinol-10 in human plasma can discriminate between healthy subjects and patients who are expected to be subjected to an increased oxidative stress in vivo. Using a newly developed method, we measured plasma ubiquinol-10 in 38 hyperlipidaemic patients with and without further complications, such as coronary heart disease, hypertension, or liver disease, and in 30 healthy subjects. The oxidizability of plasma samples obtained from hyperlipidaemic patients was found to be increased in comparison with control subjects, suggesting that the patients were subjected to a higher oxidative stress in vivo than the controls. Plasma ubiquinol-10, expressed as a percentage of total ubiquinol-10 + ubiquinone-10 or normalized to plasma lipids, was lower in the patients than in controls (P = 0.001 and 0.008, respectively). The proportion of ubiquinol-10 decreased in the order young controls > aged controls > hyperlipidaemic patients without complications > hyperlipidaemic patients with complications (P = 0.003). A negative correlation was found between the proportion of ubiquinol-10 and plasma triglycerides. The hyperlipidaemic patients with hypertension had a lower proportion of ubiquinol-10 than subjects without. When the study population was divided into smokers and non-smokers, plasma ubiquinol-10 was found to be reduced amongst smokers, independently of whether it was expressed as a percentage of total ubiquinol-10 + ubiquinone-10 (P = 0.006) or normalized to plasma lipids (P = 0.009). These data suggest that the level of ubiquinol-10 in human plasma may represent a sensitive index of oxidative stress in vivo especially indicative of early oxidative damage. Measuring plasma ubiquinol-10 can be proposed as a practical approach to assess oxidative stress in humans.

Topics: Adult; Alcohol Drinking; Amidines; Antidotes; Body Mass Index; Coronary Disease; Female; Humans; Hyperlipidemias; Hypertension; Lipid Peroxidation; Lipoxygenase; Liver Diseases; Male; Middle Aged; Oxidation-Reduction; Oxidative Stress; Regression Analysis; Risk Factors; Smoking; Spectrophotometry; Triglycerides; Ubiquinone

The effect of pretreatment on the 3 hrs globally ischemic heart assessed from the myocardial enzymes, lysosomal enzymes and cyclic nucleotides in coronary sinus blood was studied in mongrel dogs. Combined administration of CoQ10, Aprotinin, Betamethasone and Nifedipine was done as pretreatment.. m-AST, NAG and beta-Glucuronidase were significantly lower in the pretreatment group. Significant positive correlations were obtained in order between beta-Glucuronidase and NAG (r = 0.6869), m-AST and beta-Glucuronidase (r = 0.6590), m-AST and NAG (r = 0.5381), m-AST and CK-MB (r = 0.49), respectively. Significant increase in cAMP/cGMP ratio was observed in the control group after reperfusion. Before aortic occlusion, significant negative correlations were obtained between cAMP and beta-Glucuronidase, NAG, m-AST, and after 5 min of reperfusion, significant negative correlations were obtained between cGMP and NAG, m-AST and significant positive correlations between cAMP/cGMP ratio and NAG, m-AST. These data suggested the effectiveness of pretreatment, the relation between lysosomal enzyme release and the ischemic myocardial injury, and the usefulness of m-AST to evaluate the degree of myocardial injury. Moreover, the increase of cAMP/cGMP ratio suggested the ischemic myocardial injury, and cGMP in the ischemic condition, and cAMP in the non-ischemic condition affected lysosomal enzyme release.

Topics: Animals; Aprotinin; Betamethasone; Coronary Disease; Creatine Kinase; Cyclic AMP; Cyclic GMP; Dogs; Heart Arrest, Induced; Isoenzymes; Lysosomes; Myocardium; Nifedipine; Perfusion; Ubiquinone