ubiquinone and Hyperthyroidism

In previous works we demonstrated an inverse correlation between plasma Coenzyme Q10 (CoQ10) and thyroid hormones; in fact, CoQ10 levels in hyperthyroid patients were found among the lowest detected in human diseases. On the contrary, CoQ10 is elevated in hypothyroid subjects, also in subclinical conditions, suggesting the usefulness of this index in assessing metabolic status in thyroid disorders. A Low-T3 syndrome is a condition observed in several chronic diseases: it is considered an adaptation mechanism, where there is a reduction in pro-hormone T4 conversion. Low T3-Syndrome is not usually considered to be corrected with replacement therapy. We review the role of thyroid hormones in regulation of antioxidant systems, also presenting data on total antioxidant capacity and Coenzyme Q10. Published studies suggest that oxidative stress could be involved in the clinical course of different heart diseases; our data could support the rationale of replacement therapy in low-T3 conditions.

Topics: Antioxidants; Cardiovascular Diseases; Humans; Hyperthyroidism; Lung Diseases; Oxidative Stress; Reactive Oxygen Species; Thyroid Hormones; Ubiquinone

Digitonin solubilizes mitochondrial membrane, breaks the integrity of the respiratory chain and releases two mobile redox-active components: coenzyme Q (CoQ) and cytochrome c (cyt c). In the present study we report the inhibition of glycerol-3-phosphate- and succinate-dependent oxygen consumption rates by digitonin treatment. Our results show that the inhibition of oxygen consumption rates is recovered by the addition of exogenous synthetic analog of CoQ idebenone (hydroxydecyl-ubiquinone; IDB) and cyt c. Glycerol-3-phosphate oxidation rate is recovered to 148 % of control values, whereas succinate-dependent oxidation rate only to 68 %. We find a similar effect on the activities of glycerol-3-phosphate and succinate cytochrome c oxidoreductase. Our results also indicate that succinate-dependent oxidation is less sensitive to digitonin treatment and less activated by IDB in comparison with glycerol-3-phosphate-dependent oxidation. These findings might indicate the different mechanism of the electron transfer from two flavoprotein-dependent dehydrogenases (glycerol-3-phosphate dehydrogenase and succinate dehydrogenase) localized on the outer and inner face of the inner mitochondrial membrane, respectively.

Topics: Animals; Cytochromes c; Digitonin; Disease Models, Animal; Dose-Response Relationship, Drug; Glycerolphosphate Dehydrogenase; Glycerophosphates; Hyperthyroidism; Kinetics; Male; Mitochondria, Liver; Mitochondrial Membranes; Oxidation-Reduction; Oxygen Consumption; Rats; Rats, Wistar; Recovery of Function; Succinate Cytochrome c Oxidoreductase; Succinic Acid; Ubiquinone

Coenzyme Q10 is an important component of mitochondrial electron transport chain and antioxidant. Hyperthyroidism manifests hyperdynamic circulation with increased cardiac output, increased heart rate and decreased peripheral resistance. The heart is also under the oxidative stress in the hyperthyroidism. The aim of this study was to examine both how the coenzyme Q10 can affect heart ultrastructure in the hyperthyroidism and how the relationship between nitric oxide synthase (NOS) and heart damage and coenzyme Q10. Swiss Black C57 mice received 5 mg/kg L-thyroxine. Coenzyme Q10 (1.5 mg/kg) and L-thyroxine together was given to second group mice. Coenzyme Q10 and serum physiologic were applied to another two groups, respectively. All treatments were performed daily for 15 days by gavage. Free triiodothyronine and thyroxine were increased in two groups given L-thyroxine; thyroid-stimulating hormone level did not change. Hyperthyroid heart showed an increased endothelial NOS (eNOS) and inducible NOS (iNOS) immunoreactivity in the tissue. Coenzyme Q10 administration decreased these NOS immunoreactivities in the hyperthyroid animals. Cardiomyocytes of the hyperthyroid animals was characterized by abnormal shape and invaginated nuclei, and degenerative giant mitochondria. Desmosome plaques reduced in density. In hyperthyroid mice given coenzyme Q10, the structural disorganization and mitochondrial damage regressed. However, hearts of healthy mice given coenzyme Q10 displayed normal ultrastructure, except for increased mitochondria and some of them were partially damaged. Coenzyme Q10 increased the glycogen in the cardiomyocytes. In conclusion, coenzyme Q10 administration can prevent the ultrastructural disorganization and decrease the iNOS and eNOS increment in the hyperthyroid heart.

Topics: Animals; Heart; Hyperthyroidism; Immunohistochemistry; Male; Mice; Microscopy, Electron; Myocardium; Nitric Oxide Synthase Type II; Nitric Oxide Synthase Type III; Ubiquinone

In vitro, uncoupling protein 3 (UCP3)-mediated uncoupling requires cofactors [e.g., superoxides, coenzyme Q (CoQ) and fatty acids (FA)] or their derivatives, but it is not yet clear whether or how such activators interact with each other under given physiological or pathophysiological conditions. Since triiodothyronine (T3) stimulates lipid metabolism, UCP3 expression and mitochondrial uncoupling, we examined its effects on some biochemical pathways that may underlie UCP3-mediated uncoupling. T3-treated rats (Hyper) showed increased mitochondrial lipid-oxidation rates, increased expression and activity of enzymes involved in lipid handling and increased mitochondrial superoxide production and CoQ levels. Despite the higher mitochondrial superoxide production in Hyper, euthyroid and hyperthyroid mitochondria showed no differences in proton-conductance when FA were chelated by bovine serum albumin. However, mitochondria from Hyper showed a palmitoyl-carnitine-induced and GDP-inhibited increased proton-conductance in the presence of carboxyatractylate. We suggest that T3 stimulates the UCP3 activity in vivo by affecting the complex network of biochemical pathways underlying the UCP3 activation.

Topics: Animals; Carnitine O-Palmitoyltransferase; Carrier Proteins; Fatty Acids; Hyperthyroidism; Intracellular Membranes; Ion Channels; Membrane Potentials; Mitochondria, Muscle; Mitochondrial Proteins; Muscle, Skeletal; Oxidation-Reduction; Oxygen Consumption; Palmitoyl-CoA Hydrolase; Palmitoylcarnitine; Rats; RNA, Messenger; Superoxides; Triiodothyronine; Ubiquinone; Uncoupling Protein 3

In hyperthyroidism, increased oxygen consumption and free radical production in the stimulated respiratory chain leads to oxidative stress. Apart from its antioxidative function, coenzyme Q10 (CoQ10) is involved in electron transport in the respiratory chain. The aim of this study was to determine whether there is a correlation between an increased respiratory chain activity and the state of CoQ10 in children with hyperthyroidism.. The CoQ10 plasma concentration was measured by high-performance liquid chromatography in 12 children with hyperthyroidism before and after treatment.. In the hyperthyroid state, the plasma level of CoQ10 was significantly decreased in comparison with the level in the euthyroid state. The correction of the hyperthyroid state resulted in a normalization of the CoQ10 level.. Plasma CoQ10 deficiency appears to be related to the stimulated respiratory chain activity in children with hyperthyroidism.

Topics: Adolescent; Case-Control Studies; Child; Child, Preschool; Chromatography, High Pressure Liquid; Coenzymes; Electron Transport; Female; Humans; Hyperthyroidism; Infant; Infant, Newborn; Male; Osmolar Concentration; Oxidative Stress; Ubiquinone

Previous studies have shown that T3 treatment and cold exposure induce similar biochemical changes predisposing rat liver to oxidative stress. This suggests that the liver oxidative damage observed in experimental and functional hyperthyroidism is mediated by thyroid hormone. To support this hypothesis we investigated whether middle-term cold exposure (2 and 10 days), like T3 treatment, also increases H2O2 release by liver mitochondria. We found that the rate of H2O2 release increased only during State 4 respiration, but faster flow of reactive oxygen species (ROS) from mitochondria to the cytosolic compartment was ensured by the concomitant increase in tissue mitochondrial proteins. Cold exposure also increased the capacity of mitochondria to remove H2O2. This indicates that cold causes accelerated H2O2 production, which might depend on enhanced autoxidizable carrier content and should lead to increased mitochondrial damage. Accordingly, mitochondrial levels of hydroperoxides and protein-bound carbonyls were higher after cold exposure. Levels of low-molecular weight antioxidants were not related to the extent of oxidative damage, but susceptibility to both in vitro oxidative challenge and Ca2+-induced swelling increased in mitochondria from cold exposed rats. The cold-induced changes in several parameters, including susceptibility to swelling, were time dependent, because they were apparent or greater after 10 days cold exposure. The cold-induced increase in swelling may be a feedback mechanism to limit tissue oxidative stress, purifying the mitochondrial population from ROS-overproducing mitochondria, and the time course for such change is consistent with the gradual development of cold adaptation.

Topics: Animals; Antioxidants; Cold Temperature; Electron Transport Complex IV; Hydrogen Peroxide; Hyperthyroidism; Lipid Peroxidation; Male; Mitochondria, Liver; Mitochondrial Swelling; Oxidative Stress; Oxygen Consumption; Rats; Rats, Wistar; Thyroid Gland; Time Factors; Ubiquinone; Uncoupling Agents; Vitamin E

The purpose of this study was to investigate the effects of thyroid state on rates and sites of H(2)O(2) production in rat muscle mitochondria. With Complex I- and Complex II-linked substrates, hypothyroidism decreased and hyperthyroidism increased the rates of O(2) consumption during State 4 and State 3 respiration and the rates of H(2)O(2) release during State 4 respiration. During State 3, the rates of H(2)O(2) release were not affected by thyroid state. However, the mitochondrial capacity to remove H(2)O(2) increased in the transition from hypothyroid to hyperthyroid state, thus suggesting that an increase in H(2)O(2) production rate also occurred in such a transition during State 3 respiration. The observation that mitochondrial coenzyme Q levels and cytochrome oxidase activities are higher in the hyperthyroid and lower in the hypothyroid groups suggests that the modifications of H(2)O(2) production are due to a modulation by thyroid hormone of the mitochondrial content of autoxidizable electron carriers. This idea is supported by measurements of H(2)O(2) release in the presence of respiratory inhibitors. In fact, such measurements indicate that the thyroid state-linked changes in H(2)O(2) production occur at both generator sites of the respiratory chain.

Topics: Animals; Electron Transport Complex I; Electron Transport Complex IV; Hydrogen Peroxide; Hyperthyroidism; Hypothyroidism; Male; Mitochondria, Muscle; Muscle, Skeletal; NADH, NADPH Oxidoreductases; Oxygen Consumption; Rats; Rats, Wistar; Thyroid Gland; Ubiquinone

This work was designed to determine possible effects of altered thyroid states on rates and sites of H 2 O 2 production by rat heart mitochondria. Rates of O 2 consumption and H 2 O 2 release, capacities to remove the peroxide, lipid peroxidation, cytochrome oxidase activities and ubiquinone levels were determined in heart mitochondria from euthyroid, hypothyroid, and hyperthyroid rats. Hypothyroidism decreased, whereas hyperthyroidism increased the rates of O 2 consumption and H 2 O 2 release during both state 4 and state 3 respiration with Complex I- or Complex II-linked substrates. The percentage of O 2 released as H 2 O 2 was not significantly affected by thyroid state. However, the mitochondrial capacity to remove H 2 O 2 increased in the transition from hypothyroid to hyperthyroid state, which indicates that H 2 O 2 production did not modify in proportion to the rate of O 2 consumption. The thyroid-state-linked changes in H 2 O 2 production were well correlated with the levels of hydroperoxides. Rates of H 2 O 2 release in the presence of respiratory inhibitors indicated that changes in the H 2 O 2 production occurred at both sites at which H 2 O 2 was generated in euthyroid state. This result and the observation that ubiquinol levels and cytochrome oxidase activities increase in the transition from hypothyroid to hyperthyroid state suggest that the modifications of H 2 O 2 production are due to a modulation by thyroid hormone of mitochondrial content of autoxidisable electron carriers.

Topics: Animals; Electron Transport; Electron Transport Complex I; Electron Transport Complex II; Hydrogen Peroxide; Hyperthyroidism; Hypothyroidism; Kinetics; Lipid Peroxidation; Male; Mitochondria, Heart; Oxygen Consumption; Rats; Rats, Wistar; Thyroid Gland; Ubiquinone

The effects of the thyroid state on oxidative damage, antioxidant capacity, susceptibility to in vitro oxidative stress and Ca(2+)-induced permeabilization of mitochondria from rat tissues (liver, heart, and gastrocnemious muscle) were examined. Hypothyroidism was induced by administering methimazole in drinking water for 15 d. Hyperthyroidism was elicited by a 10 d treatment of hypothyroid rats with triiodothyronine (10 micro g/100 g body weight). Mitochondrial levels of hydroperoxides and protein-bound carbonyls significantly decreased in hypothyroid tissues and were reported above euthroid values in hypothyroid rats after T(3) treatment. Mitochondrial vitamin E levels were not affected by changes of animal thyroid state. Mitochondrial Coenzyme Q9 levels decreased in liver and heart from hypothyroid rats and increased in all hyperthyroid tissues, while Coenzyme Q10 levels decreased in hypothyroid liver and increased in all hyperthyroid tissues. The antioxidant capacity of mitochondria was not significantly different in hypothyroid and euthyroid tissues, whereas it decreased in the hyperthyroid ones. Susceptibility to in vitro oxidative challenge decreased in mitochondria from hypothyroid tissues and increased in mitochondria from hyperthyroid tissues, while susceptibility to Ca(2+)-induced swelling decreased only in hypothyroid liver mitochondria and increased in mitochondria from all hyperthyroid tissues. The tissue-dependence of the mitochondrial susceptibility to stressful conditions in altered thyroid states can be explained by different thyroid hormone-induced changes in mitochondrial ROS production and relative amounts of mitochondrial hemoproteins and antioxidants. We suggest that susceptibilities to oxidants and Ca(2+)-induced swelling may have important implications for the thyroid hormone regulation of the turnover of proteins and whole mitochondria, respectively.

Topics: Animals; Antioxidants; Calcium; Hyperthyroidism; Hypothyroidism; In Vitro Techniques; Lipid Peroxidation; Male; Methimazole; Mitochondria, Heart; Mitochondria, Liver; Mitochondria, Muscle; Mitochondrial Swelling; Oxidative Stress; Rats; Rats, Wistar; Triiodothyronine; Ubiquinone; Vitamin E

We investigated the effect of hyperthyroidism on the functional response of mitochondria to ischemia-reperfusion and its relationship with changes in mitochondrial susceptibility to stress conditions.. Hyperthyroidism was elicited by ten daily intraperitoneal injections of T3 (10 microg/100 g body weight). Mitochondria were isolated at 3000xg (M3) from homogenates of hearts perfused by the Langendorff technique after either 25 min reperfusion following 20 min ischemia or 45 min perfusion (controls). Rates of O2 consumption and H2O2 release with complex II-linked substrate, capacity to remove H2O2, extent of oxidative damage, levels of liposoluble antioxidants, such as ubiquinols and vitamin E, and susceptibility to Ca2+ -induced swelling were determined.. During reperfusion, hyperthyroid hearts displayed a significant tachycardia together with a low functional recovery. In comparison to the respective controls, mitochondria from both euthyroid and hyperthyroid hearts subjected to ischemia-reperfusion protocol exhibited decreases in the rate of O2 consumption, capacity to remove H2O2, and concentration of antioxidants, and increases in the rate of H2O2 release, concentration of hydroperoxides and protein-bound carbonyls, and susceptibility to Ca2+ -induced swelling. Such changes were higher in mitochondria from hyperthyroid hearts. The increase in the protein percent content and cytochrome oxidase activity of a mitochondrial fraction isolated at 8000xg (M8) from hyperthyroid hearts after reperfusion, suggests that the decline of mitochondrial respiration of M3 fraction could be due to the degradation of the oldest, mature mitochondria endowed of high oxidative capacity, but low antioxidant capacity, which would be lost by heavy mitochondrial fraction and recovered in the light fraction.. The higher susceptibility to ischemia-reperfusion of the heart from hyperthyroid animals is associated with a significant increase in mitochondrial dysfunction.

Topics: Animals; Antioxidants; Calcium; Coenzymes; Disease Susceptibility; Heart Rate; Hydrogen Peroxide; Hyperthyroidism; Male; Membrane Potentials; Mitochondria, Heart; Myocardial Reperfusion Injury; Oxygen Consumption; Rats; Rats, Wistar; Triiodothyronine; Ubiquinone; Vitamin E

Coenzyme Q10 (CoQ10) plays an essential physiologic role in oxidative phosphorylation and its plasma and tissue concentration has been evaluated in various pathologic conditions, both endocrine and non endocrine; among the latter particularly in cardiac failure. Plasma CoQ10 determination has been reported in the literature an a useful diagnostic tool in differential diagnosis of thyroid diseases. In the present study we have evaluated CoQ10 circulating levels both in hypo- and hyperthyroidism. For this purpose plasma CoQ10, fT3-fT4 and TSH concentrations have been determined (HPLC, RIA and IRMA respectively) in a group of hypothyroid patients, hyperthyroid and control subjects. No patient was harbouring cardiovascular, metabolic or systemic disease. CoQ10 has resulted 0.97 +/- 0.46 mcg/ml in the hypothyroid group, 0.51 +/- 0.35 in hyperthyroid and 0.73 +/- 0.16 in control group, with a significative difference between first and second group only; more, the prevalence of high levels has appeared greater in hypo- towards hyperthyroid patients and that of low levels in the latter greater than in the former. Finally an inverse relation of CoQ10 with fT3 and tT3, but not with fT4 and tT4, has been shown. In conclusion, plasma CoQ10 levels have not given in this study a sharp distinction between euthyroidism on a side and hypo- and hyperthyroidism on the other, but necessity of longitudinal studies after therapy is outlined, both to know time of normalization of plasma concentrations and to verify the opportunity of exogenous administration of CoQ10 in hyperthyroid patients with risk factors for heart failure.

Topics: Adult; Coenzymes; Female; Humans; Hyperthyroidism; Hypothyroidism; Male; Middle Aged; Ubiquinone

Blood levels of CoQ10 were found to be lower in patients affected by hyperthyroidism and in athletes during a severe training period. In patients who had received a kidney transplant decreasing CoQ10 levels were found, during the first 30 min after transplant, in the blood leaving the newly transplanted organ. No decrease was detectable in patients who had received the kidney from a sibling. It may reasonably be hypothesized that the ischaemia/reperfusion damage is responsible for a certain degree of impoverishment of CoQ10, leading to a CoQ10 uptake from perfusing blood. A comparable trend was also evident in liver transplants. Low CoQ10 plasma levels may therefore reflect increased metabolic needs from various tissues, on the basis of increased overall metabolic rate and/or peroxidative damage.

Topics: Coenzymes; Humans; Hyperthyroidism; Kidney Transplantation; Liver Transplantation; Physical Exertion; Ubiquinone

In previous works we have demonstrated that Coenzyme Q10 (CoQ10) levels have a significant inverse correlation with thyroid hormone concentration in patients with spontaneous hyper- or hypothyroidism. In order to verify whether this correlation is maintained in patients on long-term amiodarone therapy, in whom thyroid metabolism is altered by the iodine contained in the drug, we have studied 30 patients with thyroid dysfunction induced by chronic amiodarone treatment. We have distinguished four groups of patients: group A (n = 8): patients with true hyperthyroidism induced by drug administration; group B (n = 11): patients with mild hyperthyroid symptoms, but isolated thyroxine increase or dissociation between different indexes of thyroid function; group C (n = 5): patients with normal thyroid hormone levels, but increased TSH levels; group D (n = 6): patients who appeared really clinically euthyroid, with normal thyroid hormone levels and normal TSH response to TRH. In group A patients, plasma CoQ10 levels averaged 0.49 +/- 0.03 micrograms/ml, significantly lower than those in normal subjects and similar to those observed in spontaneous hyperthyroid patients. In group B patients, CoQ10 levels were in the normal range (0.88 +/- 0.10 microgram/ml). In group C patients, CoQ10 levels were lower than those in normal subjects and similar to those of group A patients (0.49 +/- 0.04 microgram/ml); they differed, in regards to CoQ10 values, in comparison with spontaneous primary hypothyroid patients, who had very high levels of plasma CoQ10. Finally, in group D patients, CoQ10 levels were in the normal range (0.77 +/- 0.04 microgram/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Amiodarone; Female; Goiter; Humans; Hyperthyroidism; Hypothyroidism; Male; Middle Aged; Thyroid Gland; Thyrotropin; Thyroxine; Ubiquinone

Adriamycin was used in situ, in isolated liver mitochondria of hyperthyroid rats to study the role of cardiolipin in the functioning of FAD-linked L-glycerol-3-phosphate dehydrogenase. The apparent kinetic parameters of the reaction catalyzed by the enzyme were affected by adriamycin. The effect of adriamycin was dependent on the electron acceptor, suggesting the existence of distinct binding sites for hydrophobic and hydrophilic acceptors. Assuming a correlation between the two plateaus observed upon binding of adriamycin to the mitochondria and the penetration of the drug into the two leaflets of the inner membrane [Cheneval et al. (1985) J. Biol. Chem. 260, 13003-13007], we can deduce that cardiolipin in both leaflets influences predominantly the electron acceptor binding site(s).

Topics: Animals; Binding Sites; Cardiolipins; Doxorubicin; Glycerolphosphate Dehydrogenase; Glycerophosphates; Hyperthyroidism; Kinetics; Male; Methylphenazonium Methosulfate; Mitochondria, Liver; Oxidation-Reduction; Rats; Ubiquinone; Vitamin K

Ubiquinone was extracted from liver mitochondria isolated from euthyroid and hyperthyroid rats. The redox state of ubiquinone was determined during States III and IV respiration with succinate or glutamate-malate substrates. Ubiquinone was more reduced during State III or IV in the hyperthyroid mitochondria with either substrate. Furthermore, the concentration of ubiquinone increased in the hyperthyroid rats.

Topics: Animals; Glutamates; Glutamic Acid; Hyperthyroidism; Malates; Male; Mitochondria, Liver; Oxidation-Reduction; Oxygen Consumption; Rats; Rats, Inbred Strains; Succinates; Succinic Acid; Thyroxine; Ubiquinone

By using the pre-ejection period (PEP), the left ventricular ejection time (LVET) and LVET/PEP ratio, cardiac function was investigated in 35 patients with Graves' disease (mild and severe), 13 patients with primary hypothyroidism and 35 normal subjects. The effect of treatment with antithyroid drugs, T4 or Co-Q10 was also evaluated. Before treatment, PEP was significantly shorter and the LVET/PEP ratio was greater in mild thyrotoxic patients than in the control subjects. PEP and LVET/PEP ratio returned to control levels after the euthyroid state was maintained with antithyroid drugs. In severe thyrotoxic patients, PEP and LVET/PEP ratio did not show any significant change compared with the control subjects, although LVET was significantly shorter. In hypothyroid patients, marked prolongation of PEP, shortening of LVET and decrease in LVET/PEP ratio were shown and returned to control levels after the euthyroid state was maintained with T4. PEP correlated curvilinearly with serum T3 and T4 concentrations. However, LVET/PEP ratio increased linearly from hypothyroid to mild thyrotoxic patients and decreased gradually in severe thyrotoxic patients. The inverse correlations between serum Co-Q10 and T3 and T4 concentrations were shown in patients suffering from hypothyroidism to mild thyrotoxicosis. After the administration of 120 mg Co-Q10 for 7 days in mild untreated thyrotoxic patients, a significant shortening of PEP and an increase in LVET/PEP ratio and stroke volume were shown. These data indicate that cardiac function in terms of PEP and LVET/PEP ratio is markedly influenced by serum thyroid hormone concentrations and Co-Q10 modulates it.

Topics: Adolescent; Adult; Aged; Cardiac Output; Coenzymes; Electrocardiography; Female; Heart; Humans; Hyperthyroidism; Male; Middle Aged; Myocardial Contraction; Stroke Volume; Systole; Ubiquinone

To investigate the relationship between serum levels of Coenzyme Q10 and cardiac performance in thyroid disorders, we studied the cardiac performance and assessed serum levels of thyroid hormones and Coenzyme Q10 in 20 patients with hyperthyroidism, 5 patients with hypothyroidism and 10 normal subjects. A significant inverse correlation between thyroid hormones and Coenzyme Q10 levels was found by performing partial correlation analysis. Because low serum levels of Coenzyme Q10 were found in thyrotoxic patients and congestive heart failure may occur as a result of severe hyperthyroidism, 120 mg of Coenzyme Q10 was administered daily for one week to 12 hyperthyroid patients and the change in cardiac performance was assessed. Further augmentation of cardiac performance was found in hyperthyroid hearts, which were already augmented, after the administration of Coenzyme Q10. It appears, therefore, that the Coenzyme Q10 dose actually has a therapeutic value for congestive heart failure induced by severe thyrotoxicosis.

Topics: Adolescent; Adult; Aged; Cardiac Output; Coenzymes; Female; Heart; Humans; Hyperthyroidism; Middle Aged; Systole; Thyroid Diseases; Thyroid Hormones; Ubiquinone

The correlation between serum CoQ10 levels and serum thyroid hormones in thyroid disorders was investigated in the present studies. Serum CoQ10 was measured by high speed liquid chromatography utilizing ultraviolet detector. In normal controls, serum CoQ10 level of the male was higher than that of the female. Serum CoQ10 level in hyperthyroidism was significantly lower than that of euthyroid subjects. But in hypothyroidism, serum CoQ10 level did not show any significant difference from that of euthyroid subjects. Significant inverse correlations were demonstrated between log CoQ10 and log T3, log T4, log free T4, or log rT3. These data suggested abnormalities in the mitochondrial electron transport system in thyroid disorders.

Topics: Adolescent; Adult; Aged; Child; Coenzymes; Female; Humans; Hyperthyroidism; Hypothyroidism; Male; Middle Aged; Thyroid Diseases; Thyroid Hormones; Thyroidectomy; Ubiquinone

Topics: Analysis of Variance; Animals; Body Weight; Hyperthyroidism; Male; Manometry; Methionine; Mitochondria, Liver; Oxygen Consumption; Phosphorus; Rats; Thyroid Hormones; Ubiquinone; Ultracentrifugation

1. Under conditions of thyrotoxicosis induced by feeding rats with iodinated casein, ubiquinone concentration was found to increase in the liver by increased synthesis and by partly decreased catabolism leading to its accumulation. The increased ubiquinone was found primarily in the mitochondrial and supernatant fractions. 2. Supplementing the diet with thyroxine, at less than toxic doses, also increased the synthesis and the concentration of ubiquinone in the liver. 3. In the condition of hypothyroidism obtained by feeding rats with thiouracil the concentration and the synthesis of ubiquinone in the liver showed a small decrease. 4. Synthesis of ubiquinone in liver slices was partially inhibited by addition of thyroxine in vitro. Therefore the activation effect on ubiquinone synthesis of excess of thyroxine in the intact animals appears to be by an indirect mechanism.

Topics: Animals; Depression, Chemical; Diet; Hyperthyroidism; Hypothyroidism; In Vitro Techniques; Liver; Mitochondria, Liver; Rats; Stimulation, Chemical; Thyroid Diseases; Thyroxine; Ubiquinone

Topics: Animals; Coenzymes; Cytoplasm; Hyperthyroidism; Quinones; Rats; Thyrotoxicosis; Ubiquinone