Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Improved cardiovascular morbidity and mortality have been observed in several clinical studies of dietary supplementation with coenzyme Q10 (CoQ10, ubiquinone). Several mechanisms have been proposed to explain the effects of CoQ10. One attractive theory links ubiquinone with the inhibition of platelets. The effect of CoQ10 intake on platelet surface antigens, and certain hemostatic parameters was examined in 15 humans and 10 swine. Study participants received 100 mg of CoQ10 twice daily in addition to their usual diet for 20 days resulting in a three-fold increase of total serum CoQ10 level. We observed a decline in plasma fibronectin (-20.2%), thromboxane B2 (-20.6%), prostacyclin (-23.2%), and endothelin-1 (-17.9%) level. Significant inhibition of vitronectin receptor expression was observed consistently throughout ubiquinone treatment. Inhibition of the platelet vitronectin receptor is a direct evidence of a link between dietary CoQ10 intake, platelets, and hemostasis. These findings may contribute to the observed clinical benefits by a diminished incidence of thrombotic complications in such patients.
Mol Aspects Med 1997
PMID:Could coenzyme Q10 affect hemostasis by inhibiting platelet vitronectin (CD51/CD61) receptor? 926 21

It has been hypothesized that CoQ10 (CoQ) pretreatment protects myocardium from ischemia reperfusion (I/R) injury by its ability to increase aerobic energy production as well as its activity as an antioxidant. Isolated hearts from rats pretreated with either CoQ 20 mg/kg i.m. and 10 mg/kg i.p. or vehicle 24 and 2 h prior to the experiment, were subjected to 15 min of equilibration (EQ), 25 min of ischemia, and 40 min of reperfusion (RP). Developed pressure, +/-dp/dt, myocardial oxygen consumption, and myocardial aerobic efficiency (DP/MVO2) were measured. 31P NMR spectroscopy was used to determine ATP and PCr concentrations. Lucigenin-enhanced chemiluminescence of the coronary sinus effluent was utilized to determine oxidative stress through the protocol. CoQ pretreatment improved myocardial function after ischemia reperfusion. CoQ pretreatment improved tolerance to myocardial ischemia reperfusion injury by its ability to increase aerobic energy production, and by preserving myocardial aerobic efficiency during reperfusion. Furthermore, the oxidative burst during RP was diminished with CoQ. Similarly it was hypothesized that CoQ protected coronary vascular reactivity after I/R via an antioxidant mechanism. Utilizing a newly developed lyposomal CoQ preparation given i.v. 15 min prior to ischemia, ischemia reperfusion was carried out on Langendorff apparatus as previously described. Just prior to ischemia and after RP, hearts were challenged with bradykinin (BK) and sodium nitroprusside (SNP) and change in coronary flow was measured. CoQ pretreatment protected endothelial-dependent and endothelial-independent vasodilation after I/R. We conclude that CoQ pretreatment protects coronary vascular reactivity after I/R via OH radical scavenger action.
Mol Aspects Med 1997
PMID:The mechanisms of coenzyme Q10 as therapy for myocardial ischemia reperfusion injury. 926 22

The individual and combined effects of ethanol and lovastatin on rats and their prevention by supplemental coenzyme Q10 (CoQ10) was studied. The ethanol and lovastatin findings are reported elsewhere. This paper focuses on the food restriction which occurred in rats fed 35% of energy as ethanol and those control rats pair-fed to the 35% of energy as ethanol group. Six groups of rats received 35% of energy as ethanol (with or without lovastatin and/or CoQ10 treatment). One group served as a 0% ethanol ad libitum control and one 0% ethanol control group was pair-fed to the 35% ethanol group. Rats receiving 35% of energy as ethanol and their pair-fed controls consumed 83% of the energy/day consumed by the ad libitum controls. This was consistent regardless of lovastatin or CoQ10 treatment. Weight gains were 84% of control. The energy reduction was consistently associated with a substantial (48%+) increase in liver CoQ9 concentrations. Reports by others of associations between food restriction and increased longevity in rodents has focused on a decrease in oxidant damage in tissues of food restricted animals. The increase in CoQ levels in the food restricted animals would result in an increase in antioxidant protection and might explain the observed increases in longevity.
Mol Aspects Med 1997
PMID:The effect of ethanol and/or food restriction on coenzyme Q in liver in rats. 926 23

In sperm cells, the majority of coenzyme Q10 (CoQ10) an energy promoting agent and antioxidant, is concentrated in the mitochondria of the midpiece, so that the energy for movement and all other energy-dependent processes in the sperm cell also depend on the availability of CoQ10. The reduced form of CoQ10-ubiquinol also acts as an antioxidant, preventing lipid peroxidation in sperm membranes. The objective of the study was to evaluate the effect of CoQ10 on sperm motility in vitro, after incubation with 38 samples of asthenospermic and normal motility sperm, and to evaluate the effect of CoQ10 administration in vivo in 17 patients with low fertilization rates after in vitro fertilization with intracytoplasmic sperm injection (ICSI) for male factor infertility. All 38 sperm samples from patients registered in our infertility clinic had normal concentrations and morphology. Of these, 16 patients had normal motility (mean 47.5%) and 22 patients were asthenospermic (mean motility 19.1%). Sperm samples were divided into four equal parts and incubated for 24 h in: HAM's medium alone, in HAM's medium with 1% DMSO and HAM's with 5 microM or 50 microM CoQ10. While no significant change in motility after incubation was observed in the samples with initial normal motility, a significant increase in motility was observed in the 50 microM CoQ10 subgroup of sperm from asthenospermic men, with a motility rate of 35.7 +/- 19.5%, as compared to 19.1 +/- 9.3% in the controls (P < 0.05). The 17 patients with low fertilization rates after ICSI were treated with oral CoQ10, 60 mg/day, for a mean of 103 days before the next ICSI treatment. No significant change was noted in most sperm parameters, but a significant improvement was noted in fertilization rates, from a mean of 10.3 +/- 10.5% in their previous cycles, to 26.3 +/- 22.8% after CoQ10 (P < 0.05). In conclusion, the administration of CoQ10 may result in improvement in sperm functions in selective patients. Further investigation into the mechanisms related to these effects is needed.
Mol Aspects Med 1997
PMID:The effect of coenzyme Q10 on sperm motility and function. 926 24

Defective sperm function in infertile men has been associated with increased lipid peroxidation and impaired function of antioxidant defenses in spermatozoa. Evidence strongly suggests that CoQ10, a lipid-soluble component of the respiratory chain acts, in its reduced form (ubiquinol), as a potent antioxidant in various biological systems, such as lipoproteins and membranes. In this study we assayed CoQ10 content in both the reduced and oxidized form (ubiquinol/ubiquinone), and hydroperoxide levels in seminal plasma and seminal fluid from 32 subjects with a history of infertility. Our results showed a significant correlation between ubiquinol content and sperm count (r = 0.62; P < 0.05) in seminal plasma. An inverse correlation between ubiquinol content and hydroperoxide levels both in seminal plasma and in seminal fluid (r = -0.56; P = 0.01) was found. Using multiple regression analysis we also found a strong correlation among sperm count, motility and ubiquinol-10 content (P < 0.01) in seminal fluid. An inverse correlation between ubiquinol/ubiquinone ratio and percentage of abnormal morphology was also observed in total fluid. These results suggest that ubiquinol-10 inhibits hydroperoxide formation in seminal fluid and in seminal plasma. Since peroxidation in sperm cells is an important factor affecting male infertility, ubiquinol could assume a diagnostic and/or a therapeutic role in these patients.
Mol Aspects Med 1997
PMID:The protective role of ubiquinol-10 against formation of lipid hydroperoxides in human seminal fluid. 926 25

The aim of this investigation was to elucidate a possible correlation between lipid peroxidation, antioxidant concentrations and erythrocyte membrane fluidity in plasma from newborns. Ten healthy newborns were recruited. Venous blood samples were collected at birth, and thereafter at 3 and 72 h postnatal age. The following parameters were assessed: hydroperoxides, Coenzyme Q10 and alpha-tocopherol both in plasma and in erythrocyte membranes, and fluorescence polarization (as a tool for assessing membrane fluidity). Hydroperoxides were shown to be high in erythrocyte membranes at birth and significantly decreased at 3 and 72 h after birth. In the erythrocyte membranes, coenzyme Q10 content showed an opposite behaviour with respect to the plasma compartment. Membrane fluidity appeared unchanged even in the presence of the above mentioned modifications.
Mol Aspects Med 1997
PMID:Lipid peroxidation and antioxidants in newborns. 926 26

The development of the atherosclerosis is mediated by the accumulation of oxidized lipids in the arterial wall. There is a relationship between average intake of dietary fat, its quality, and incidence of atherosclerosis. The goal of this work was to study the effect of different dietary fats on the coenzyme Q10 and hydroperoxide content of liver mitochondria in rabbits affected by an induced atherosclerosis. The results show that the induction of experimental atherosclerosis leads to a significant increase in hydroperoxides of rabbit liver membrane mitochondria and to a significant drop in the content of CoQ10. Furthermore, treatment of atherosclerotic rabbits with different diets resulted in an increase of membrane hydroperoxides in the group fed sunflower oil whereas the increase was significantly lower for animals fed virgin olive oil and fish oil stabilized with vitamin E (1 g/kg). CoQ10 levels only recovered partially in all groups; however, values in the sunflower oil were significantly lower as compared to corresponding values of the other groups. The use of either virgin olive oil or vitamin E stabilized fish oil in the dietary treatment of atherosclerosis appears to be a valid alternative for maintaining adequate levels of CoQ10 and hydroperoxides in liver mitochondria.
Mol Aspects Med 1997
PMID:Rabbit liver mitochondria coenzyme Q10 and hydroperoxide levels: an experimental model of atherosclerosis. 926 27

It has been widely indicated that several pathological conditions depend upon concomitant risk factors rather than a unique one and that also the putative protective factors do not act alone. For these reasons it could be useful to consider subjects that present sufficiently homogeneous lifestyles (i.e. nutrition and physical activity). We carried out an investigation in a free-living community in order to clarify the possible correlations and differences among plasma metabolic and antioxidant markers in non-agonistic athletes. When subjects were divided in two main groups according to age (35-44 and 45-54 years) without considering the activity they performed, Duncan's analysis of variance revealed that they showed similar characteristics and only triglyceride levels were different. A clear negative correlation was found between vitamin E and VO2max in both age groups, a negative correlation was also found between CoQ10 and VO2max in the younger subjects and finally CoQ10 and vitamin E were also positively correlated in this first group. It appears, therefore, that people with a higher aerobic capacity have lower circulating levels of antioxidants.
Mol Aspects Med 1997
PMID:Metabolic and antioxidant markers in the plasma of sportsmen from a Mediterranean town performing non-agonistic activity. 926 29

The coenzyme Q10 content of the average Danish diet was estimated from consumption data and from analysis of food items to be 3-5 mg coenzyme Q10 per day, primarily derived (64% of the total) from meat and poultry. To investigate if coenzyme Q10 was absorbed to any significant degree from a food item, a randomized cross-over study with single doses of coenzyme Q10 (30 mg/person), administered either as a meal or as capsules, was carried out in healthy subjects. The serum coenzyme Q10 concentration increased significantly, and the maximum concentrations did not differ significantly for the two forms of administration. The study indicates that coenzyme Q10 is present in food items and absorbed to a significant degree. Thus, dietary coenzyme Q10 may contribute to the plasma coenzyme Q10 concentration.
Mol Aspects Med 1997
PMID:Coenzyme Q10 in the diet--daily intake and relative bioavailability. 926 31

Active oxygen species are reported to cause organ damage. This study was therefore designed to determine whether oxidative stress contributed to the initiation or progression of hepatic DNA damage produced by T-2 toxin. The aim of the study was also to investigate the behaviour of the antioxidants coenzyme Q10 (CoQ10), and alpha-tocopherol (vitamin E) against DNA damage in the livers of mice fed T-2 toxin. Treatment of fasted mice with a single dose of T-2 toxin (1.8 or 2.8 mg/kg body weight) by oral gavage led to 76% hepatic DNA fragmentation. T-2 toxin also decreased hepatic glutathione (GSH) levels markedly. Pretreatment with CoQ10 (6 mg/kg) together with alpha tocopherol (6 mg/kg) decreased DNA damage. The CoQ10 and vitamin E showed some protection against toxic cell death and glutathione depletion caused by T-2 toxin. Oxidative damage caused by T-2 toxin may be one of the underlying mechanisms for T-2 toxin-induced cell injury and DNA damage, which eventually lead to tumourigenesis.
Mol Aspects Med 1997
PMID:T-2 toxin-induced DNA damage in mouse livers: the effect of pretreatment with coenzyme Q10 and alpha-tocopherol. 926 32


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