dinoprost and Hyperthyroidism

dinoprost has been researched along with Hyperthyroidism* in 4 studies

Other Studies

4 other study(ies) available for dinoprost and Hyperthyroidism

ArticleYear
Evaluation of oxidative status with exhaled breath 8-isoprostane levels in patients with hyperthyroidism.
    Endocrine, metabolic & immune disorders drug targets, 2013, Volume: 13, Issue:4

    Studies conducted so far on the effect of hyperthyroidism on oxidative stress (OS) have employed blood and urine samples. Exhaled Breath Condensate (EBC) is a non-invasive technique used to take sample from lungs to determine many biological indications. The aim of the present study was determine the possibility of using 8- isoprostane levels in EBC as an indicator of OS in hyperthyroid patients.. The present study was performed on 42 patients with hyperthyroidism and 42 healthy control subjects. Hyperthyroid patients included patients with newly diagnosed Graves' disease, toxic multinodular goiter and toxic adenoma. Exhaled breath condensates were collected from patients in each group using a condensing device. 8- isoprostane levels as an indicator of OS in EBC were detected via immunoassay method.. Hyperthyroid patients and control groups had 8-isoprostane levels of 6.08±6.31 and 1.56±0.88 pg/ml, respectively. The difference between patient and control groups was statistically significant (p<0.001). Of the hyperthyroid patients, eleven had Graves', 21 multinodular goiter, and 10 toxic adenoma diagnosis. There were no significant differences among patients of different diagnoses for 8-isoprostane levels (p=0.541). No significant correlations were found between 8-isoprostane and free thyroxine (fT4) or thyroid stimulating hormone (TSH) levels.. In the present study, 8-isoprostane levels in EBC of hyperthyroid patients were found to be significantly higher than that in healthy control group. This study is important in that it is the first to evaluate the effects on respiratory system of elevated OS of hyperthyroidism in EBC.

    Topics: Adult; Breath Tests; Dinoprost; Exhalation; Female; Humans; Hyperthyroidism; Male; Middle Aged; Oxidative Stress

2013
Cardiac and renal antioxidant enzymes and effects of tempol in hyperthyroid rats.
    American journal of physiology. Endocrinology and metabolism, 2005, Volume: 289, Issue:5

    This study evaluated the activity of cardiac and renal antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and glutathione reductase (GR)] and whether chronic treatment with tempol, a cell membrane-permeable SOD mimetic, ameliorates the hypertension of hyperthyroidism. Two experiments were performed. In experiment I, the following four groups of male Wistar rats were used: control group and three groups that received thyroxine (T4) at 10, 50, or 75 microg x rat(-1) x day(-1). In experiment II, tempol was orally administered (18 mg x kg(-1) x day(-1)) to control and T4-treated (75 microg x rat(-1) x day(-1)) rats. All treatments were maintained for 6 wk. Body weight, tail systolic blood pressure (BP), and heart rate were measured one time a week, and direct BP and morphological, metabolic, plasma, and renal variables were measured at the end of the experiment. Enzymatic activities were measured in renal cortex and medulla and right and left ventricles. In renal cortex, SOD activity was decreased in the T4-75 group, and there was a dose-related increase in CAT activity and decrease in GPX and GR activities in T4-treated groups. Activity of all antioxidant enzymes was reduced in left ventricle in T4-50 and T4-75 groups and in right ventricle in the T4-75 group. Tempol reduced BP, plasma malondialdehyde, and total urinary excretion of F2 isoprostanes in hypertensive hyperthyroid rats but not in controls. Tempol did not improve cardiac hypertrophy, proteinuria, or creatinine clearance in hyperthyroid rats. In conclusion, the results obtained indicate that the activity of SOD, GPX, and GR in renal and cardiac tissues is decreased in hyperthyroidism and that antioxidant treatment with tempol ameliorates T4-induced hypertension.

    Topics: Animals; Antioxidants; Blood Pressure; Catalase; Cyclic N-Oxides; Dinoprost; Glutathione Peroxidase; Glutathione Reductase; Heart Rate; Hypertension; Hyperthyroidism; Kidney; Male; Malondialdehyde; Myocardium; Rats; Rats, Wistar; Spin Labels; Superoxide Dismutase; Thyroxine

2005
Radioiodine therapy induces dose-dependent in vivo oxidation injury: evidence by increased isoprostane 8-epi-PGF(2 alpha).
    Journal of nuclear medicine : official publication, Society of Nuclear Medicine, 2002, Volume: 43, Issue:9

    131I is the treatment of choice for differentiated thyroid cancer and hyperthyroidism. A relationship between low-density lipoprotein oxidation and radioiodine therapy-related side effects, consequently inducing increased formation of 8-epi-prostaglandin F(2 alpha) (PGF(2 alpha)) in situ, has recently been reported by several investigators. Isoprostanes, among them 8-epi-PGF(2 alpha), have been associated with increased oxidation injury due to various pathologic conditions in vivo. The aim of this study was to investigate the possible induction of oxidative stress as a consequence of (131)I therapy.. 8-epi-PGF(2 alpha) was examined in plasma, serum, and urine in 42 patients undergoing radioiodine treatment of hyperthyroidism or thyroid cancer. The 8-epi-PGF(2 alpha) levels were analyzed daily for 1 wk and thereafter at different points up to 12 wk after treatment.. The isoprostane levels showed an increase after application of radioiodine in all investigated compartments. The effect was significantly higher and longer lasting after higher-activity therapy (2,960 or 7,400 MBq) than after lower-activity therapy (185 or 740 MBq).. These findings document a significant, dose-dependent in vivo oxidation injury as a consequence of therapeutic radioiodine application to the salivary gland.

    Topics: Adult; Aged; Dinoprost; Dose-Response Relationship, Radiation; Female; Humans; Hyperthyroidism; Iodine Radioisotopes; Male; Middle Aged; Oxidative Stress; Thyroid Neoplasms

2002
Effects of hyperthyroidism on vascular contractile and relaxation responses.
    The American journal of physiology, 1998, Volume: 274, Issue:5

    Previous research has shown that skeletal muscle blood flow, at rest and during muscular contractions, is elevated in the hyperthyroid state. We hypothesized that reduced vascular contractile and enhanced endothelium-dependent relaxation responses contribute to these observations. To test these hypotheses, male rats were administered triiodothyronine (Hyper, n = 27; 300 micrograms/kg) for 6-12 wk. Compared with euthyroid control rats (Eut, n = 27), Hyper exhibited left ventricular hypertrophy (Eut, 2.01 +/- 0.04 mg/g body wt; Hyper, 2.70 +/- 0.06; P < 0.0005) and greater oxidative enzyme activity in several skeletal muscles (all P < 0.0005). Vascular rings, 2-3 mm in axial length, were prepared from abdominal aortas, and responses to vasoactive agents were determined in vitro. Compared with Eut, vascular rings with intact endothelium from Hyper exhibited reductions in contractile responses to norepinephrine (NE) across a range of NE concentrations (P < 0.05). Maximal tension developed in response to NE was reduced approximately 30% in hyperthyroidism (Eut, 3.8 +/- 0.2 g; Hyper, 2.6 +/- 0.4; P < 0.01). Contractile responses to NE were not different between Eut and Hyper in rings denuded of endothelium. Maximal vasorelaxation responses to acetylcholine (ACh), after precontraction with NE (10(-7) M), were enhanced in the hyperthyroid state (Eut, 65.1 +/- 4.8%; Hyper, 84.0 +/- 7.1; P < 0.05). Enhanced vasorelaxation to ACh was also observed when precontraction was induced by prostaglandin F2 alpha. These findings indicate that vascular contractile and relaxation responses are altered in male hyperthyroid rats.

    Topics: Acetylcholine; Animals; Aorta, Abdominal; Dinoprost; Endothelium, Vascular; Hyperthyroidism; In Vitro Techniques; Male; Norepinephrine; Rats; Rats, Sprague-Dawley; Triiodothyronine; Vasoconstriction; Vasoconstrictor Agents; Vasodilation; Vasodilator Agents

1998