ascorbic-acid and Hyperthyroidism

In the course of hyperthyreosis reactive oxygen production increases and oxidative stress develops. The consequences of oxidative stress comprise disturbances in balance of pro- and antioxidative agents, including changes in concentration of antioxidative vitamins and microelements. Although the results of published studies concerning changes of concentrations of vitamins and microelements in hyperthyreosis are contradictory, most frequently a decrease of zinc and magnesium concentrations was observed.

Topics: Antioxidants; Ascorbic Acid; Calcium; Humans; Hyperthyroidism; Magnesium; Oxidative Stress; Trace Elements; Vitamin A; Vitamin E; Vitamins; Zinc

Thyroid hormones play a fundamental role in the regulation of metabolism of almost all mammalian tissue including the reproductive system. Hyperthyroidism in early life may cause delayed sexual maturation, although physical development is normal and skeletal growth may be accelerated. Hyperthyroidism after puberty influences reproductive functions and increases testosterone level. The aim of this work is to study the effect of induced hyperthyroidism by L-thyroxine sodium administration on the testis of rats and to evaluate the ameliorating role of different antioxidants as ascorbic acid and folic acid on the hyperthyroid state via the assessment of different biochemical markers, histopathological and immunochemical sections. DNA analysis of the D1 deiodinase was performed to determine genetic mutation due to hyperthyroidism. The results showed partially disrupted in the measured biochemical parameters and spermatogenesis in hyperthyroid rats. Post-administration of both folic and ascorbic acids together in hyperthyroid rats showed the best ameliorating effects on the thyroid hormones, testosterone, testicular GGT and ALP, and all oxidative stress markers. There is no genetic mutations that occurred in D1 deiodinase due to hyperthyroidism. These findings were indicated by the proliferating cell nuclear antigen (PCNA) studies of testes.

Topics: Animals; Antioxidants; Ascorbic Acid; Folic Acid; Hyperthyroidism; Male; Oxidative Stress; Rats; Rats, Sprague-Dawley; Spermatogenesis; Testicular Diseases; Testis; Testosterone; Thyroid Hormones; Thyroxine

The increasing consumption of fruits and vegetables has contributed to the improvement of populational health, due in part, to the abundance of antioxidants in these foods. Antioxidants reduce the level of oxidative damage to DNA caused by free radicals and ionizing radiation, including the radioisotope iodine-131 (131I). This isotope is used for the diagnosis and treatment of thyroid injuries, such as hyperthyroidism and cancer.. This study aimed to evaluate the radioprotective and cytotoxic activity of acute and subchronic treatments with Barbados Cherry (BC) (Malpighia glabra L.) fruit juice (5 mg), which is rich in potent antioxidants such as vitamin C, phenols, carotenoids, anthocyanins and yellow flavonoids and its activity against the mutagenic activity of the therapeutic dose of 25 μCi of radioiodine for hyperthyroidism. The test system used was the bone marrow cells of Wistar rats (Rattus norvegicus) that were treated in vivo by gavage.. BC showed radioprotective activity in acute treatments, which is most likely due to the joint action of its antioxidant components. In subchronic treatments, the continuous treatment presented an effective radioprotective activity, which was significantly different from treatment with the radiopharmaceutical only. Treatment with BC prior to (PRE) and simultaneous with (SIM) ionizing radiation decreased the number of induced chromosomal alterations, while post-treatment produced no protective effect. In addition, BC exhibited no cytotoxic activity.. These data serve as evidence that BC can be used as a preventive health measure to improve public health quality by countering the action of inevitable exposure to mutagens, such as 131I.

Topics: Animals; Antioxidants; Ascorbic Acid; Barbados; Bone Marrow Cells; Carotenoids; Chromosome Aberrations; Female; Fruit; Hyperthyroidism; Iodine; Iodine Radioisotopes; Male; Malpighiaceae; Oxidative Stress; Phytotherapy; Plant Extracts; Polyphenols; Radiation Injuries; Radiopharmaceuticals; Rats, Wistar

Excessive concentrations of free radicals in the developing brain may lead to neurons maldevelopment and neurons damage and death. Thyroid hormones (THs) states play an important role in affecting the modulation of oxidative stress and antioxidant defense system. Thus, the objective of this study was to clarify the effect of hypothyroidism and hyperthyroidism in rat dams on the neurons development of different brain regions of their offspring at several postnatal weeks in relation to changes in the oxidative stress and antioxidant defense system. The adult female rats were administered methimazole (MMI) in drinking water (0.02% w/v) from gestation day 1 to lactation day 21 to induce hypothyroidism and exogenous thyroxine (T4) in drinking water (0.002% w/v) beside intragastric incubation of 50--200 T4 μg/kg body weight (b. wt.) to induce hyperthyroidism. In normal female rats, the sera total thyroxine (TT4) and total triiodothyronine (TT3) levels were detectably increased at day 10 post-partum than those at day 10 of pregnancy. Free thyroxine (FT4), free triiodothyronine (FT3), thyrotropin (TSH) and growth hormone (GH) concentrations in normal offspring were elevated at first, second and third postnatal weeks in an age-dependent manner. In hypothyroid group, a marked depression was observed in sera of dam TT3 and TT4 as well as offspring FT3, FT4 and GH, while there was a significant increase in TSH level with the age progress. The reverse pattern to latter state was recorded in hyperthyroid group. Concomitantly, in control offspring, the rate of neuron development in both cerebellar and cerebral cortex was increased in its density and complexity with age progress. This development may depend, largely, on THs state. Both maternal hypothyroidism and hyperthyroidism caused severe growth retardation in neurons of these regions of their offspring from the first to third weeks. Additionally, in normal offspring, seven antioxidant enzymes, four non-enzymatic antioxidants and one oxidative stress marker (lipid peroxidation, LPO) followed a synchronized course of alterations in cerebrum, cerebellum and medulla oblongata. In both thyroid states, the oxidative damage has been demonstrated by the increased LPO and inhibition of enzymatic and non-enzymatic antioxidants in most examined ages and brain regions. These disturbances in the antioxidant defense system led to deterioration in the neuronal maturation and development. In conclusion, it can be suggested that the

Topics: Age Factors; alpha-Tocopherol; Analysis of Variance; Animals; Animals, Newborn; Antioxidants; Ascorbic Acid; Aspirin; Brain; Catalase; Catechol Oxidase; Disease Models, Animal; Drug Combinations; Female; Glutathione; Glutathione Peroxidase; Glutathione Reductase; Glutathione Transferase; Hyperthyroidism; Hypothyroidism; Lipid Peroxidation; Male; Neurons; Oxidative Stress; Peroxidase; Pregnancy; Pregnancy Complications; Radioimmunoassay; Rats; Silver Staining; Superoxide Dismutase; Thyrotropin; Thyroxine; Triiodothyronine

The role of thyroid hormones in the regulation of adrenal function during stress has been documented in mammals, but only limited reports are available in avian species. The present study was undertaken to analyze the effect of hyper- or hypothyroidism on the adrenal activity under control (hydrated) and osmotically stressed (water deprived, WD) conditions, with special emphasis on the expression of arginine vasotocin receptor VT2 (VT2R) in pituitary corticotrophs. Chickens were made hyper- or hypothyroidic by injecting thyroxine (T4) and 2-thiouracil (TU), respectively for 14 days. After 10 days of injections, one sub-group of both, T4- or TU-treated chickens were subjected to osmotic stress by water deprivation. Hyperthyroidism stimulated adrenal steroidogenic activity compared to euthyroid control birds, but no change was observed in the expression of VT2R. On the other hand, TU-induced hypothyroidism however showed no effect on adrenal gland, but a significant increase in the expression of VT2R was observed. Neither hyper- nor hypothyroidism altered pro-opiomelanocortin (POMC) mRNA levels. Following osmotic stress, no effect was observed either on the adrenal gland or on the VT2R expression in hyperthyroidic birds, but in hypothyroidic birds, osmotic stress stimulated adrenal steroidogenic activity and decreased VT2R expression in comparison to its respective controls (T4 or TU). Expression of POMC mRNA was again unaltered following osmotic stress. Although exact mechanism is not clear, the data indicate that high plasma T4 level stimulates adrenal activity and may also modulate function of the pituitary-adrenal axis during dehydration.

Topics: 3-Hydroxysteroid Dehydrogenases; Adrenal Glands; Animals; Ascorbic Acid; Chickens; Cholesterol; Dehydration; Gene Expression Regulation; Hyperthyroidism; Hypothalamo-Hypophyseal System; Hypothyroidism; Immunohistochemistry; In Situ Hybridization; Male; Pituitary Gland; Pituitary-Adrenal System; Pro-Opiomelanocortin; Receptors, Vasopressin; Thyroid Gland; Thyroxine; Triiodothyronine; Water-Electrolyte Balance

This study was conducted to test whether oxidative stress activates the intracellular protein kinase B (AKT1) signaling pathway, which culminates with cardiac hypertrophy in experimental hyperthyroidism. Male Wistar rats were divided into four groups: control, vitamin E, thyroxine (T(4)), and T(4)+vitamin E. Hyperthyroidism was induced by T(4) administration (12 mg/l in drinking water for 28 days). Vitamin E treatment was given during the same period via s.c. injections (20 mg/kg per day). Morphometric and hemodynamic parameters were evaluated at the end of the 4-week treatment period. Protein oxidation, redox state (reduced glutathione, GSH/glutathione dissulfide, GSSG), vitamin C, total radical-trapping antioxidant potential (TRAP), hydrogen peroxide (H2O2), and nitric oxide metabolites (NO(X)) were measured in heart homogenates. The p-AKT1/AKT1 ratio, p-glycogen-synthase kinase (GSK)3B/GSK3B ratio, FOS, and JUN myocardial protein expression were also quantified by western blot after 4 weeks. Increases in biochemical parameters, such as protein oxidation (41%), H2O2 (62%), and NO(X) (218%), and increase in the left ventricular end-diastolic pressure were observed in the T(4) group. T(4) treatment also caused a decrease in GSH/GSSG ratio (83%), vitamin C (34%), and TRAP (55%). These alterations were attenuated by vitamin E administration to the hyperthyroid rats. Expression of p-AKT1/AKT1, p-GSK3B/GSK3B, FOS, and JUN were elevated in the T(4) group (by 69, 37, 130, and 33% respectively), whereas vitamin E administration promoted a significant reduction in their expression. These results indicate that oxidative stress plays an important role in cardiac hypertrophy, and suggest redox activation of AKT1 and JUN/FOS signaling pathways with H2O2 acting as a possible intracellular mediator in this adaptive response to experimental hyperthyroidism.

Topics: Animals; Ascorbic Acid; Blotting, Western; Cardiomegaly; Disease Models, Animal; Glutathione; Hydrogen Peroxide; Hyperthyroidism; Male; Oxidation-Reduction; Rats; Rats, Wistar; Signal Transduction; Thyroxine

Increased oxidative stress with high free radical generation has been described previously in animal models of hyperthyroidism. The present study was designed to investigate the protective effects of caffeic acid phenylethyl ester (CAPE) on oxidative damage in rats with experimentally induced hyperthyroidism. The study was conducted on 32 male Sprague-Dawley rats. The experimental animals were divided into four groups (control, CAPE alone, hyperthyroidism, and hyperthyroidism + CAPE). Hyperthyroidism was induced by intraperitoneal administration of 0.3 mg/kg/day L-thyroxine for 4 weeks. CAPE (10 micro g/kg) was administered intraperitoneally for 4 weeks. At the end of the experimental period, blood samples and various organs (liver, heart and brain) of rats were taken for the determination of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), oxidized glutathione, vitamin C and superoxide dismutase (SOD) levels and concentrations of triiodothyronine (T3), thyroxine (T4) and thyroxine-stimulating hormone (TSH). Our results indicate that TBARS, oxidized glutathione, SOD levels and concentrations of T3 and T4 were higher in plasma and tissues of the hyperthyroid group compared to controls. Vitamin C, GSH and TSH levels were decreased significantly in the hyperthyroid group when compared to the control group. CAPE treatment decreased the elevated TBARS, SOD, T3 and T4 levels and increased the lowered GSH, vitamin C and TSH levels to control levels in rats with hyperthyroidism. In conclusion, our results indicate that CAPE is beneficial as a protective agent against oxidative stress induced by hyperthyroidism in rats. The protection is probably due to multiple mechanisms involving free radical scavenger properties, attenuating lipid peroxidation and increasing the antioxidant status.

Topics: Animals; Antioxidants; Ascorbic Acid; Brain; Caffeic Acids; Glutathione; Glutathione Disulfide; Hyperthyroidism; Liver; Male; Myocardium; Oxidative Stress; Phenylethyl Alcohol; Rats; Rats, Sprague-Dawley; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances; Thyrotropin; Thyroxine; Triiodothyronine

The effects of hyperthyroidism on oxidative DNA damage in liver tissue and modification by vitamin C supplementation were investigated in rats. Animals were rendered hyperthyroid by administration of L-thyroxine (0.4 mg/100 g food) for 25 d. In the plasma samples, T(3), T(4), and thyroid-stimulating hormone (TSH) were measured by radioimmunoassay and ascorbate spectrophotometrically. Oxidative damage to hepatic nuclear DNA was determined by measuring deoxy-guanosine (dG) and 8-oxodG by high-performance liquid chromatography with diode array detector electrochemical detection (HPLC-DAD-ECD). In hyperthyroidism, 8-oxodG/(10(5) dG) levels were significantly higher and plasma vitamin C levels lower than in control rats. The results of this experimental study show that oxidative damage to hepatic nuclear DNA increases in the hyperthyroid state and that vitamin C was not effective in preventing this damage.

Topics: Animals; Ascorbic Acid; Cell Nucleus; DNA Damage; Free Radical Scavengers; Hyperthyroidism; Liver; Male; Oxidative Stress; Rats; Rats, Wistar; Thyrotropin; Thyroxine; Triiodothyronine

Glycated hemoglobin (HbA1C) levels are enhanced by elevated glucose concentrations. Glycation of hemoglobin is also modulated by lipid peroxides, ascorbic acid and reduced glutathione (GSH). We determined the strength of the relationships among these variables in a group of hyperthyroid patients.. Twenty-two untreated hyperthyroid patients and 17 healthy controls were recruited for the study. Whole blood GSH, HbA1C, plasma lipid peroxides, ascorbic acid and fasting glucose were analyzed in both the groups. Direct and partial correlation analysis was performed to explore the possible relationships between these variables.. In hyperthyroid patients, HbA1C and lipid peroxides levels were found to be significantly increased than the controls. Ascorbic acid and GSH were decreased significantly in the test group when compared with the healthy control group. With partial correlation analysis, fasting glucose and lipid peroxides were found to have a significant positive correlation with HbA1C. Ascorbic acid and GSH showed no significant association with HbA1C levels.. These data suggest that HbA1C levels are closely associated with fasting glucose and lipid peroxides in hyperthyroid patients. Therefore, serum lipid peroxides level should be kept in mind while interpreting HbA1C as a long-term glycemic index in hyperthyroid cases.

Topics: Adolescent; Adult; Ascorbic Acid; Blood Glucose; Case-Control Studies; Female; Glutathione; Glycated Hemoglobin; Humans; Hyperthyroidism; Lipid Peroxidation; Lipid Peroxides; Male; Middle Aged

Increasing numbers of experimental and epidemiological studies suggest the involvement of free radicals in the pathogenesis of various disease entities. Similarly, oxidative processes have been implicated as playing roles in the genesis of hyperthyroidism-induced damage. In this study, we investigated the effects of vitamin E and vitamin C on plasma lipid peroxidation and the susceptibility of apolipoprotein B (apo B)-containing lipoproteins to oxidation in experimental hyperthyroidism. The study animals were initially divided into a control group (Group C) and a hyperthyroid group. The latter was further re-grouped later according to their vitamin supplementation status: Hyperthyroid group without vitamin supplementation (Group H), hyperthyroid group with vitamin E supplementation (Group H+E) and hyperthyroid group with vitamin C supplementation (Group H+C). Malondialdehyde (MDA) level was measured as an indicator of plasma lipid peroxidation. The apo B-containing lipoproteins were separated by precipitation and incubated with copper sulphate. The MDA levels of this non-HDL fraction were measured prior to and after 1, 2 and 3 hours of incubation. Plasma MDA levels showed no significant differences among groups. Whereas MDA levels measured in non-HDL fraction were significantly higher in Group H than Group C. Group H+E and Group H+C had significantly lower MDA levels than Group H in all these measurements. This finding strongly indicates an increased susceptibility of apo B-containing lipoproteins to oxidation in hyperthyroidism, and that vitamin E as well as vitamin C supplementation protect these lipoproteins from copper-induced oxidation.

Topics: Animals; Apolipoproteins B; Ascorbic Acid; Hyperthyroidism; Lipid Peroxidation; Male; Malondialdehyde; Oxidation-Reduction; Rats; Rats, Sprague-Dawley; Vitamin E

The present study was designed to evaluate the changes in the plasma lipid peroxidation and antioxidant system in 15 adult volunteer patients in hyperthyroid and euthyroid states. In these patients, plasma concentrations of lipid peroxides were decreased and, ascorbic acid and vitamin E levels were significantly increased in euthyroid status in comparison to hyperthyroid status. A significant increase in the plasma GPx activity (P < 0.01) and a decrease in GST (P < 0.001) was observed after euthyroidism was sustained with methimazole therapy. In conclusion, hyperthyroidism tends to enhance lipid peroxide content and an increase in GST and decreases in GPx, vitamin E and ascorbic acid levels accompany to this change in the plasma. The achievement of euthyroidism led an improvement in these parameters.

Topics: Adult; Antioxidants; Antithyroid Agents; Ascorbic Acid; Female; Glutathione Transferase; Humans; Hyperthyroidism; Lipid Peroxides; Male; Methimazole; Middle Aged; Vitamin E

In this study the impact of vitamin C supplementation on oxidative damage as assessed by thiobarbituric acid reactive substances and markers of antioxidant status: namely Cu/Zn superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione were investigated in 24 hyperthyroid patients under propylthiouracil therapy (3x100 mg/day) for five days and in 15 healthy controls. Ascorbic acid (1000 mg/day) was given as a supplement for 1 month to both the patients and controls during the study period. Heparinised blood samples were taken at the beginning and the end of one month ascorbic acid supplementation. Comparison of the hyperthyroid patients with the controls revealed higher lipid peroxidation (p<0.001), higher Cu/Zn superoxide dismutase activity (p<0.001), higher glutathione level (p<0.001) and lower glutathione reductase activity (p<0.001). Vitamin C supplementation to hyperthyroid patients caused significant increases in glutathione concentration (p<0.001) and glutathione peroxidase activity (p<0.001), whereas there were significant decreases in glutathione reductase (p<0.001) and Cu/Zn superoxide dismutase activities (p<0.01). Thiobarbituric acid reactive substances and thiobarbituric acid reactive substances/glutathione ratio were significantly decreased (p<0.01). Vitamin C supplementation to euthyroid controls caused significant increases in glutathione concentration (p<0.001) and glutathione peroxidase and Cu/Zn superoxide dismutase activities (p<0.001), whereas there was a significant decrease in glutathione reductase (p<0.001). The thiobarbituric acid reactive substances/glutathione ratio was significantly decreased (p<0.05). Our findings reveal the potentiation of antioxidant status and a relief in oxidative stress in both propylthiouracil treated hyperthyroid patients and controls in response to vitamin C supplementation.

Topics: Adult; Antithyroid Agents; Ascorbic Acid; Case-Control Studies; Female; Glutathione; Glutathione Disulfide; Glutathione Peroxidase; Humans; Hyperthyroidism; Male; Middle Aged; Oxidative Stress; Propylthiouracil; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances

Lack of uniform views concerning subcellular image and possible meaning of free radicals in the myocardial damage prompted us to study rat hearts submitted for chronic thyrotoxicosis. The studies were performed on 30 Wistar white rats. The material was obtained from anterior wall of the left ventricle of the heart. To confirm the role of free radicals one group of rats was given ascorbic acid, a well-known substance with anti-oxidation properties (free radical scavenger). In the control group we observed a typical structure of the myocardium. In the group with thyrotoxicosis a great degree of subcellular structural damage was noticed. These alterations correspond to nonspecific myocardial damage that can be meet in hypoxia, reperfusion or in toxic myocardial damage. However, in case of vitamin application generally known to have anti-oxidation properties, damages were significantly less intensive and occurred more rarely. It seems to indicate a significant role of free radicals in the generation of these alterations.

Topics: Animals; Ascorbic Acid; Cardiomyopathies; Female; Free Radicals; Hyperthyroidism; Male; Microscopy, Electron; Myocardium; Rats; Rats, Wistar; Thyroid Diseases; Thyroxine

Topics: Animals; Ascorbic Acid; Glutamates; Glutamic Acid; Hyperthyroidism; Hypothyroidism; Kinetics; Mitochondria, Heart; NAD(P)H Dehydrogenase (Quinone); Oxygen Consumption; Perchlorates; Phospholipids; Rats; Reference Values; Sodium Compounds; Succinates; Triiodothyronine

The capacity to respond to inflammatory stimuli was tested in hyperthyroid and hypothyroid rats when thyroid defects, induced by hormone administration or thyroparathyroidectomy, respectively, were fully established. Whereas hyperthyroid rats presented consistently depressed inflammatory responses, hypothyroid rats responded in a normal fashion. Decreased reactions to intracutaneously injected histamine and serotonin, inhibited swelling reaction to carrageenin, injected into one of the hind paws, and depressed primary and secondary reactions to adjuvant (heat-killed M. tuberculosis), only occurred in the hyperthyroid group. In addition, only in this group of animals enlargement of the adrenal glands, reduced content of adrenal ascorbic acid, and decreased number of circulating eosinophils, which characterize a circumstance of adrenal cortical hyperactivity, were observed. A spontaneous reversal of the acute inflammatory response of hyperthyroid animals to carrageenin occurred 3-4 days after interruption of hormone administration, and this was coincidental with the return to normal of the previously enlarged adrenal glands. Similarly, specific inhibition of adrenal cortical steroid biosynthesis in hyperthyroid rats with aminoglutethimide, restored the previously depressed response to carrageenin, without interference with the increased levels of seric thyroxin, thus suggesting that the inhibitory effects of thyroid hormones on inflammatory responses are likely to be indirect. It is concluded that an excess of circulating thyroid hormones, but not their deficiency, can impair the development of inflammatory reactions, and that this effect, at least partially, depends on an increased secretion of adrenal corticosteroids.

Topics: Adrenal Cortex Hormones; Adrenal Glands; Aminoglutethimide; Animals; Ascorbic Acid; Histamine; Hyperthyroidism; Hypothyroidism; Inflammation; Male; Organ Size; Rats; Rats, Inbred Strains; Serotonin

The rate of lipid peroxidation (LPO) in rat liver mitochondria induced by the Fe++ + ascorbate system was considerably reduced in 1--12-month-old rats, remained unchanged thereafter up to the 24th postnatal month and was decreased in hyperthyroid rats aged 1- and 3 months. The rate of NADPH-dependent LPO was also sharply decreased up to the 12th month of age, showing a further rise in 24-month-old animals, i. e. thus remained lower than in 1- and 3-month-old rats; under hyperthyroidism the LPO rate was increased in more highly 12-month-old animals. A reverse correlation between the level of reducibility of matrix pyridine nucleotides and the rate of enzymatic LPO in mitochondria was established. A physiological role of LPO is postulated.

Topics: Aging; Animals; Ascorbic Acid; Hyperthyroidism; Iron; Kinetics; Lipid Peroxides; Liver; Male; Mitochondria, Liver; Rats

Topics: Animals; Ascorbic Acid; Hyperthyroidism; Ketoglutarate Dehydrogenase Complex; Ketone Oxidoreductases; Male; Myocardium; Niacinamide; Pyruvate Dehydrogenase Complex; Rats; Stimulation, Chemical; Thiamine; Vitamins

Topics: Ascorbic Acid; Dehydroascorbic Acid; Humans; Hyperthyroidism; Thyroid Gland

The posterity of female albino rats given di-thyroxin (15 mkg/100 g) during gestation and lactation differ from off-springs of intact rats by less body weight and increased gas-exchange. Their thyroid galnds show evident signs of functional suppression, e. g. decreased relative weight, diminished height of thyrocytes, cytochemical shifts in the content and topography of RNP and the ascorbic acid. During the first 30 days of the postnatal life the parathyroid glands have greater weight than controls, are characterized by a number of morphological and cytochemical signs suggesting their increased functioning.

Topics: Animals; Ascorbic Acid; Female; Histocytochemistry; Hyperthyroidism; Maternal-Fetal Exchange; Organ Size; Polysaccharides; Pregnancy; Pregnancy Complications; Rats; Ribonucleoproteins; Thyroid Gland

Topics: Animals; Ascorbic Acid; Hyperthyroidism; Hypothermia, Induced; Hypothyroidism; Oxidoreductases; Phosphoric Monoester Hydrolases; Radiometry; Rats; Thyroid Gland; Thyroid Hormones

Topics: Adrenal Glands; Animals; Ascorbic Acid; Cerebral Cortex; Hyperthyroidism; Hypothermia, Induced; Hypothyroidism; Liver; Muscles; Myocardium; Rats

Topics: Animals; Ascorbic Acid; Electron Transport Complex IV; Hyperthyroidism; Hypothermia; Hypothermia, Induced; Hypothyroidism; Iodine Isotopes; Oxidoreductases; Phosphoric Monoester Hydrolases; Rats; Thyroid Gland

Topics: Ascorbic Acid; Aspirin; Asthma; Calcium; Citrates; Coronary Disease; Depression, Chemical; Diabetes Mellitus; Duodenal Ulcer; Dwarfism, Pituitary; Emphysema; Facial Paralysis; Gluconates; Histamine H1 Antagonists; Humans; Hypertension; Hyperthyroidism; Kidney Calculi; Liver Diseases, Parasitic; Magnesium; Oxalates; Phosphates; Pyridoxine; Schistosomiasis; Stimulation, Chemical; Terpenes; Tuberculosis, Pulmonary

Topics: Animal Feed; Animals; Ascorbic Acid; Dental Pulp; Dentinogenesis; Food Additives; Guinea Pigs; Hyperthyroidism; Thyroid Gland; Tissue Extracts

Topics: Alveolar Process; Animals; Ascorbic Acid; Food Additives; Guinea Pigs; Hyperthyroidism; Periodontium; Thyroid Hormones; Tooth

Topics: Animals; Ascorbic Acid; Brain; Hyperthyroidism; Mitochondria; Oxidative Phosphorylation; Rats

Topics: Animals; Ascorbic Acid; Glucuronates; Hyperthyroidism; Hypothyroidism; Iodine; Iodine Isotopes; Kidney Function Tests; Male; Methanol; Models, Biological; Propylthiouracil; Rats; Stimulation, Chemical; Thyroid Gland; Thyroxine; Uracil Nucleotides

Topics: Aged; Ascorbic Acid; Ascorbic Acid Deficiency; Female; Goiter; Humans; Hyperthyroidism; Hypothyroidism; Thyroid Function Tests; Tyrosine

Topics: Adrenal Cortex Hormones; Adrenal Glands; Adrenocorticotropic Hormone; Animals; Ascorbic Acid; Blood Chemical Analysis; Dinitrophenols; Electric Stimulation; Female; Hyperthyroidism; Hypophysectomy; Hypothalamo-Hypophyseal System; Hypothalamus; Organ Size; Ovary; Pituitary Gland; Pituitary-Adrenal Function Tests; Rats; Thyroxine; Triiodothyronine

Topics: Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Bile Acids and Salts; Carbon Isotopes; Collagen; Guinea Pigs; Hyperthyroidism; Hypothyroidism; Metabolism; Pharmacology; Proline; Research; Ribosomes; RNA; RNA, Messenger; Salts; Thyroxine

Topics: Animals; Ascorbic Acid; Estrous Cycle; Estrus; Female; Hyperthyroidism; Menstrual Cycle; Rats; Research

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Ascorbic Acid; Cholesterol; Corpus Luteum; Estrus; Female; Histocytochemistry; Hyperthyroidism; Hypophysectomy; In Vitro Techniques; Lipid Metabolism; Pregnancy; Rats; Succinate Dehydrogenase

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Ascorbic Acid; Corticosterone; Hyperthyroidism; Physiology; Rats; Research; Thyroid Gland

Topics: Animals; Ascorbic Acid; Collagen; Guinea Pigs; Hydroxyproline; Hyperthyroidism; Hypothyroidism; Metabolism; Pharmacology; Research; Ribosomes; RNA; RNA, Messenger; Scurvy; Thyroxine; Wound Healing

Topics: Animals; Ascorbic Acid; Hyperthyroidism; Liver Diseases; Microsomes; Microsomes, Liver; Rats; Thyrotoxicosis

Topics: 17-Hydroxycorticosteroids; Adrenal Cortex; Adrenal Cortex Hormones; Aldosterone; Animals; Ascorbic Acid; Humans; Hyperthyroidism; Lipid Metabolism; Lipids; Rats; Thyroxine; Vitamins

Topics: Ascorbic Acid; Carbohydrate Metabolism; Glutathione; Humans; Hyperthyroidism

Topics: Adrenal Cortex; Ascorbic Acid; Guinea Pigs; Hyperthyroidism; Scurvy; Thiouracil; Thyroxine; Vitamins

Topics: Ascorbic Acid; Humans; Hyperthyroidism; Vitamins

Topics: Ascorbic Acid; Citrus; Citrus sinensis; Fruit; Humans; Hyperthyroidism