Coenzyme Q is concentrated in Golgi apparatus membranes and mitochondria, but not in other membranes. Although it is difficult to prove the metabolic action of coenzyme Q administered exogenously in clinical cases, the effect of this substance can be evaluated by criteria based on clinical findings. In an attempt to evaluate the effect of coenzyme Q for the treatment of 67 patients(male 26 cases, female 41 cases) of congestive heart failure, we administered Coenzyme Q1030mg daily for 4 to 8 weeks. Most of them were valvular heart disease(74.6%) and hypertension (14.9%). Clinical effects were evaluated at least 4 weeks later by the criteria using a scoring method of severity of congestive heart failure which was devised by Ishiyama, etc. In summary, a definite effect was found in 13 cases(19%) and a mild effect was observed in 46 cases(69%). During treatment there were no significant side effects, and also no significant changes in heart rate and blood pressure.
Blood Pressure ; Estrogens, Conjugated (USP)* ; Female ; Golgi Apparatus ; Heart ; Heart Failure* ; Heart Rate ; Humans ; Hypertension ; Membranes ; Mitochondria ; Research Design ; Ubiquinone

BACKGROUND: In smokers, smoking causes many disease entities including cancers, chronic pulmonary diseases and cardiovascular diseases. Passive smoking is also accepted as a carcinogen and its adverse health effects are emphasized. We measured blood vitamin A, C, E (alpha-, beta- and gamma-tocopherol), coenzyme Q10 and urine cotinine concentrations in nonsmokers and smokers. METHODS: Twenty-one healthy nonsmokers and 24 healthy smokers were included in this study. Smoking status was assessed with a self-reported questionnaire. Plasma was analyzed for coenzyme Q10 and serum for vitamin A, C, E using HPLC (Agilent Technologies Inc., USA) and random urine for cotinine using LC/tandem mass spectrometry (Applied Biosystems Inc., Canada). RESULTS: Smokers had significantly lower serum concentrations of vitamin C than nonsmokers (P=0.0005). No significant differences in concentrations of serum vitamin A, E, and plasma coenzyme Q10 were observed. Smokers had highly elevated urine cotinine levels (1,454+/-903 ng/mL). In 16 (76.2%) of 21 nonsmokers, urine cotinine was detected (3.25+/-4.08 ng/mL). The correlations between urine cotinine and blood antioxidants levels were not found. Neither, the correlation between smoking status and blood antioxidants & urine cotinine was found. CONCLUSIONS: This study shows that smokers had significantly lower vitamin C levels among nonenzymatic antioxidants, namely, vitamin A, C, E and coenzyme Q10. High detection rate of urine cotinine in nonsmokers show the seriousness of passive smoking exposure, therefore more social efforts should be directed to reduce passive smoking exposure.
Adult ; Ascorbic Acid/*blood ; Chromatography, High Pressure Liquid ; Cotinine/*urine ; Female ; Humans ; Male ; *Smoking ; Tandem Mass Spectrometry ; Tobacco Smoke Pollution ; Tocopherols/*blood ; Ubiquinone/*blood ; Vitamin A/*blood

Forty guinea pigs were divided into four groups and fed 0.04% cholesterol based control diet, plus 0.05% simvastatin, and statin plus 0.1% CoQ10 or 10% Ardisia Japonica Blume (AJB) leave powder for 4 weeks. Plasma total cholesterol levels decreased significantly in all groups fed the statin-containing diet compared with that in guinea pigs fed the control diet (P < 0.01). Plasma and liver triglycerides decreased significantly in the statin plus CoQ10 group compared with those in the control (both P < 0.05). Maximum platelet aggregation was significantly higher in the statin plus CoQ10 group than that in the other groups (P < 0.05). Na-K ATPase activity increased in the statin group and decreased in the statin plus CoQ10 group (P < 0.01). Na-K co-transport and Na passive transport decreased significantly in the control group compared with those in the other groups (both P < 0.05). Intracellular Na was highest in the statin group and lowest in the statin plus CoQ10 group and was correlated with Na-K ATPase activity. Thiobarbituric acid reactive substance production in platelet-rich plasma and liver tended to decrease in the statin plus CoQ10 group compared with those in the other groups. Plasma glutamic-pyruvic transaminase and glutamic-oxaloacetic transaminase increased significantly in the statin group compared with those in the control (P < 0.05). These result suggest that antioxidant rich AJB did not have positive effects on cardiovascular disease parameters. The statin plus CoQ10 seemed to decrease cholesterol more efficiently than that of statin alone.
Adenosine Triphosphatases ; Alanine Transaminase ; Animals ; Ardisia ; Aspartate Aminotransferases ; Blood Platelets ; Cardiovascular Diseases ; Cholesterol ; Diet ; Erythrocytes ; Guinea ; Guinea Pigs ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Liver ; Plasma ; Platelet Aggregation ; Platelet-Rich Plasma ; Simvastatin ; Thiobarbiturates ; Triglycerides ; Ubiquinone