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)

The acute effects of carbon monoxide (CO) on cardiac metabolism at the mitochondrial level were investigated. Rats were exposed to 4% CO for 4 minutes in a closed chamber. Immediately after exposure, hearts were removed and frozen with a precooled clamp. Blood from the thoracic cavity was sampled for analysis. Gas analysis of arterial blood taken from the abdominal aorta demonstrated severe hypoxia with oxygen partial pressure less than 20 mmHg, metabolic acidosis and reduced pH value. There were no significant changes in the plasma level of glucose and non esterified fatty acids (NEFA). In the myocardium, ATP levels decreased significantly, and concomitantly, a significant increase in the plasma uric acid level was observed. Although no significant change was observed in short chain acyl carnitine, free carnitine levels decreased to one fourth of the control value. Long chain acylcarnitine increased 11-fold. Coenzyme Q9 (CoQ9) level decreased significantly, but there was no significant change in Coenzyme Q10 (CoQ10).
Mol Cell Biochem 1990 Jun 25
PMID:The metabolic effect of carbon monoxide on the heart. 236 54

A 40% reduction of the diameter of the ascending aorta maintained for 60 days induced the formation of a compensate cardiac hypertrophy in rabbits without changing the value of the azide insensitive Ca2+-ATPase activity in comparison to control hearts. The cardiac mitochondria isolated from constricted animals assayed in presence of glutamate and succinate did not show a change in the R.C.I. and ADP/O values in comparison to the controls, whilst the QO2 value enhanced or decreased respectively when determined with glutamate or succinate. The intramuscular injections of CoQ10 (12 mg/kg body weight/48 h) enhanced the mitochondrial CoQ10 concentrations both in the control and in the constricted animals and further increased the QO2 value determined in both groups of animals when glutamate was used as the substrate. The production of O2.- radicals by the level of the complexes I and III of the respiratory chain, did not change in the constricted animals, nor in the animals administered with CoQ10 in comparison to the control. CoQ10 augmented the rate of oxygen consumption by the submitochondrial particles only in the constricted animals. Moreover, the treatment with the coenzyme or the constriction of the aorta, did not modify the cardiac superoxide dismutase activity, but increased the glutathione peroxidase activity only in the banded animals. In addition, in the CoQ10 treated animals there was a reduction of NADH-diaphorase activity both in the control and constricted animals, while the malondialdehyde, generated during the thiobarbituric acid test, and the cardiac content of lipofuscin were decreased.
J Mol Cell Cardiol 1987 Jan
PMID:The effect of treatment with coenzyme Q10 on the mitochondrial function and superoxide radical formation in cardiac muscle hypertrophied by mild aortic stenosis. 303 17

Coenzyme Q10 (CoQ10) was studied in papillary muscle from 18 patients (52-67 years, 2 females) subjected to open heart surgery due to mitral valve disease. In addition the enzyme activities of lactate dehydrogenase (LD) with its five isozymes, citrate synthase (CS) and mitochondrial CK (CK-MIT) were determined. Myocardial function was assessed by means of left ventricle (LV) angiography. CoQ10 averaged 0.39 (range 0.26-0.59) micrograms x mg-1 dw. On an individual basis CoQ10 was related to CS activity although not as closely as CK-MIT (r = 0.45, p less than 0.05 versus r = 0.86, p less than 0.001). The ratio (CoQ10) x (CS activity)-1 was calculated to represent mitochondrial quality. The level of LD3 fraction increase was used to mark for the degree of metabolic stress in the heart. LD3 fraction was negatively related to the quality index (r = -0.71, p less than 0.001). Thus, those with a low CoQ10 per unit of CS activity had also a high LD3 isozyme fraction. In a subset of 12 patients with isolated mitral regurgitation due to myxomatous valve degeneration, CoQ10 and the ratio CoQ10 over CS decreased with the degree of LV function impairment (r = -0.58, p less than 0.05 and r = -0.68, p less than 0.05, respectively). The quality index takes into account not only enzyme activity but also the potential for control of free oxygen radicals.
Mol Cell Biochem 1988 Nov
PMID:Coenzyme Q10 and key enzyme activities in papillary muscle related to left ventricle function in mitral valve disease. 323 Dec 16

The mechanism of mitochondrial damage during reperfusion injury of ischemic myocardium was studied using mongrel dogs in vivo and isolated mitochondria in vitro. Seventy-seven adult dogs were divided into three groups: the control group (n = 38), the Coenzyme Q10 (CoQ10)-5 mg group (n = 24), and the CoQ10-15 mg group (n = 15). In the control group, the left anterior descending coronary artery (LAD) of the dog was occluded for 15 min followed by 5 min of reperfusion after 40 min of premedication with physiological saline. In both CoQ10 groups, 5 mg/kg or 15 mg/kg of CoQ10 was infused intravenously for 20 min and then physiological saline was administered for 20 min before 15 min occlusion of the LAD. Subsequently, reperfusion was allowed for 5 min. Each group was further divided into two subgroups depending on the presence (arrhythmia group) or the absence (non-arrhythmia group) of ventricular arrhythmias. Immediately after 15 min occlusion, myocardial samples were taken from the normal and reperfused areas to measure CoQ10 content of myocardium. Heart mitochondria were prepared after 5 min of reperfusion from both areas. Arrhythmias appeared in 12 of 38 dogs in the control group (32%), two of 24 dogs in the CoQ10-5 mg group (8%) and none of 15 dogs in the CoQ10-15 mg group (0%). Premedication with CoQ10 increased tissue CoQ10 content in a dose-dependent manner. In the CoQ10-5 mg group, the increase in CoQ10 content of dogs with reperfusion arrhythmias was relatively less than that of dogs without reperfusion arrhythmias. In each group, mitochondrial function was decreased in the arrhythmia group compared to that of the non-arrhythmia group. The increase in free fatty acid (FFA) content and the decrease in phospholipid content were also observed in mitochondria from the reperfused area of each arrhythmia group. The increase in FFA and mitochondrial dysfunction were induced by the incubation of mitochondria in vitro with phospholipase (PLase) A2 or PLase C, and protected by the addition of CoQ10. These results suggest that PLase plays an important role in the development of mitochondrial damage associated with reperfusion.
J Mol Cell Cardiol 1985 Sep
PMID:The effect of Coenzyme Q10 on reperfusion injury in canine myocardium. 404 48

With electrophysiological methods, mechanisms of the restorative action of coenzyme Q10 (CoQ10) in 2,4-dinitrophenol-depressed electrical and mechanical activities of isolated guinea-pig hearts were studied. Isoproterenol (3 X 10(-8) M)-induced action potential and contraction of the heart in 27 mM KCl Tyrode solution were abolished by 6 X 10(-6) M 2,4-dinitrophenol, while the additional application of CoQ10 (50 micrograms/ml) restored both these activities of the heart. This restorative action of CoQ10 was dose related (2 to 50 micrograms/ml) and was inhibited by 10 micrograms/ml 15-hydroperoxyarachidonic acid (15-HPAA) or pretreatment of the animals with indomethacin (5 mg/kg i.v.). When exogenously applied, 200 ng/ml prostacyclin also restored the 2,4-dinitrophenol-depressed electrical and contractile activities of the heart, but this restorative action of prostacyclin was affected neither by 15-HPAA nor by indomethacin pretreatment. These results suggest the possible participation of prostacyclin in the restorative action of CoQ10 in 2,4-dinitrophenol-depressed electrical and mechanical activities of the heart.
J Mol Cell Cardiol 1983 Sep
PMID:The restorative action of coenzyme Q10 in 2,4-dinitrophenol-depressed electrical and contractile activities of guinea-pig heart. 635 90

Histochemical alterations of acute and chronic doxorubicin (DOX) cardiotoxicity in the mouse were assessed by the localization of succinate dehydrogenase (SDH), coenzyme Q10 (CoQ), cytochrome oxidase (COX), creatine phosphokinase (CPK), lactate dehydrogenase (LDH), reduced glutathione (GSH), and intracellular calcium. Isolated myocytes intensely stained for calcium were found at 72 and 120 h under the acute protocol; altered staining patterns of SDH, CoQ, and COX, were evident at 120 h. Chronically, two patterns of intracellular calcium staining were evident: (1) intensely stained myocytes as found in the acute protocol; and (2) multiple discrete intracellular deposits suggestive of mitochondrial localization. Altered staining patterns of SDH, CoQ, COX, CPK, and LDH under the chronic protocol were only seen after abnormal staining was evident in trichrome stained sections. The presence of characteristic vacuolated myocardial cells in both acute and chronic protocols was confirmed by one micron epon-embedded toluidine blue stained sections and electron microscopy. These histochemical findings suggest that DOX alters the functional integrity of mitochondrial respiratory chain enzymes in the myocardial cell.
J Mol Cell Cardiol 1983 Aug
PMID:Histochemical alterations of acute and chronic doxorubicin cardiotoxicity. 667 10

Ubiquinone-10 and rhodoquinone-10 were detected in stages of the life-cycle of a pseudophyllidean cestode, Spirometra mansonoides, by chromatographic, UV spectrophotometric, proton nuclear magnetic resonance spectrometric and electron impact mass spectrometric methods. Ubiquinone-10 was identified in 1-day-old eggs and coracidia, and rhodoquinone-10 in coracidia, plerocercoids and adult tapeworms. Tentative identification were also made of ubiquinone-10 in procercoids and rhodoquinone-10 in 10-day-old eggs. The roles of benzoquinones in helminth aerobic and anaerobic metabolism are discussed in relation to their distribution in stages of the S. mansonoides life-cycle.
Mol Biochem Parasitol 1980 Sep
PMID:Benzoquinones in stages of the life-cycle of the cestode Spirometra mansonoides. 744 18

This experiment was designed to evaluate whether or not liposomal encapsulated-doxorubicin and combination therapy of free doxorubicin with coenzyme Q10, an antioxidant, mitigate the delayed adverse effects on cardiac muscle mitochondria. Rats aged 7 weeks were divided into the following four groups; rats were injected with doxorubicin or liposomal encapsulated-doxorubicin, total dose 15 mg/kg. The doxorubicin group consisted of two subgroups depending on diet, i.e., standard diet or 0.2% coenzyme Q10 diet. Mitochondria from cardiac muscles were prepared from rats aged 13 and 35 weeks. No significant decrease in the activity of complex I of the mitochondrial electron transport chain was observed in rats aged 13 weeks among the groups, however, significant decreases in the activity in rats aged 35 weeks were observed in the doxorubicin and liposomal doxorubicin groups compared with the corresponding control rats. In contrast, no significant change in complex I activity was observed in rats fed with coenzyme Q10 diet irrespective of doxorubicin treatment. From these results, not liposomal encapsulation of doxorubicin but combination therapy with antioxidant might be expected to reduce the delayed adverse effects of doxorubicin on heart mitochondria.
Biochem Mol Biol Int 1995 Aug
PMID:Approaches that mitigate doxorubicin-induced delayed adverse effects on mitochondrial function in rat hearts; liposome-encapsulated doxorubicin or combination therapy with antioxidant. 758 Sep 95

The plasma membrane of eukaryotic cells contains an NADH oxidase which can transfer electrons across the membrane. This oxidase is controlled by hormones, growth factors and other ligands which bind to receptors in the plasma membrane. Oncogenes also affect activity of the oxidase. Natural serum components such as diferric transferrin and ceruloplasmin which stimulate proliferation also stimulate membrane oxidase activity. Additional growth factors can be required to complement the proliferative effect. Electron transport across the plasma membrane can be measured by the reduction of impermeable electron acceptors, such as ferricyanide, which also stimulate cell growth. The oxidants activate growth-related signals such as cytosolic alkalinization and calcium mobilization. Antiproliferative agents such as adriamycin and retinoic acid inhibit the plasma membrane electron transport. Flavin, Coenzyme Q and an iron chelate on the cell surface are apparent electron carriers for the transmembrane electron transport. Coenzyme Q10 stimulates cell growth, and Coenzyme Q analogs such as capsaicin and chloroquine reversibly inhibit both growth and transmembrane electron transport. Addition of iron salts to the depleted cells restores activity and growth. The ligand-activated oxidase in the plasma membrane introduces a new basis for control of signal transduction in cells. The redox state of the quinone in the oxidase is proposed to control tyrosine kinase either by generation of H2O2 or redox-induced conformational change.
Mol Aspects Med 1994
PMID:Coenzyme Q10, plasma membrane oxidase and growth control. 775 19

The effect of long-term (18 months) selenium deficiency on the levels of liver coenzyme Q was studied in the rat. Levels of coenzyme Q9 and coenzyme Q10 in the liver of selenium-deficient rats were 40 and 67% of the levels in selenium-adequate animals, respectively. The results are similar to the findings using a shorter feeding period.
Mol Aspects Med 1994
PMID:Selenium deficiency and decreased coenzyme Q levels. 775 21


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