Search

Abstract Purpose The Quality of Life in Adult Growth Hormone Deficiency Assessment (QoL-AGHDA) is a disease-specific quality of life measure specific to individuals who are growth hormone deficient. The present study describes the adaptation of the QoL-AGHDA for use in the following four Slavic languages; Czech, Polish, Serbian and Slovakian. Methods The study involved three stages in each language; translation, cognitive debriefing and validation. The validation stage assessed internal consistency (Cronbach's alpha), reproducibility (test-retest reliability using Spearman's rank correlations), convergent and divergent validity (Correlations with the NHP) and known group validity. Results The QoL-AGHDA was successfully translated into the target languages with minimal problems. Cognitive debriefing interviewees (n = 15-18) found the measures easy to complete and identified few problems with the content. Internal consistency (Czech Republic = 0.91, Poland = 0.91, Serbia = 0.91 and Slovakia = 0.89) and reproducibility (Czech Republic = 0.91, Poland = 0.91, Serbia = 0.88 and Slovakia = 0.93) were good in all adaptations. Convergent and divergent validity and known group validity data were not available for Slovakia. The QoL-AGHDA correlated as expected with the NHP scales most relevant to GHD. The QoL-AGHDA was able to distinguish between participants based on a range of variables. Conclusions The QoL-AGHDA was successfully adapted for use in the Czech Republic, Poland, Serbia and Slovakia. Further validation of the Slovakian version would be beneficial. The addition of these new lanaguage versions will prove valuable to multinational clinical trials and to clinical practice in the respective countries.

Background: Fc receptor-like (FCRL) genes play a role in the immune system by encoding proteins that function as receptors on the surface of immune cells. The clinical significance of FCRL gene expression in Graves' Disease (GD) and Graves' Orbitopathy (GO) remains unclear. We evaluated the expression of FCRL 2, 3, 4 mRNA in patients with GD and GO and its role in the development and activity of these diseases. Methods: Peripheral blood samples from patients with GD (n = 24) or GO (n = 49) hospitalized in the Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, were collected. Expressions of FCRL2, FCRL3 and FCRL4 were measured by real-time PCR. Results: FCRL3 expression was higher in patients with GD compared to GO (1.375 vs. 0.673, p = 0.004) and, specifically, active GO (1.375 vs. 0.639, p = 0.005). Regarding FCRL4, mRNA expression was higher in GD compared to Control (3.078 vs. 0.916, p = 0.003), GO (3.078 vs. 1.178, p < 0.001), active GO (3.078 vs. 1.186, p = 0.002) and inactive GO (3.078 vs. 1.171, p = 0.008). In turn, FCRL4 mRNA expression was higher in patients with hyperthyroidism (subclinical + overt) than in euthyroid patients (2.509 vs. 0.995, p = 0.001 when the whole group of individuals was considered; 2.509 vs. 1.073, p = 0.004 when GO + GD was considered). Conclusions: The increased FCRL mRNA expression in patients with GD is associated with hyperthyroidism (but not with positive TSHRAbs), and our study is the first one to confirm this relationship. [ABSTRACT FROM AUTHOR]

It has long been observed that thyroid diseases are more prevalent in women than in men. However, there are limited experimental data demonstrating mechanisms by which sex differences in thyroid diseases may occur and exact molecular mechanisms involved are still far from clear. The aim of the study was to evaluate if there are sex differences concerning oxidative damage to membrane lipids in thyroid homogenates in response to Fenton reaction substrates, i.e., Fe2+ and/or H2O2, and, additionally, in response to potentially protective agent, i.e., melatonin. Homogenates of male or female thyroids collected from adult swine (Sus scrofa domesticus) at slaughter were incubated in the presence of H2O2 and/or Fe2+ without or with addition of melatonin. Malondialdehyde + 4-hydroxyalkenals concentration (LPO index) was measured spectrophotometrically. Neither H2O2 nor Fe2+, when used separately, did affect the level of lipid peroxidation in both male and female porcine thyroid homogenates. When H2O2 (0.5 mM) was used together with different concentrations of Fe2+, the level of lipid peroxidation increased significantly in both male and female porcine thyroid homogenates, with clear Fe2+ concentration-dependent stimulatory effect, but without differences between sexes. No sex-specific differences was found concerning oxidative damage to membrane lipids in porcine thyroid in response to Fenton reaction substrates and/or to melatonin. The lack of expected differences may be due to potentially lower sensitivity of membrane lipids comparing to other biological macromolecules to pro-/antioxidative agents in the thyroid. However, further studies should be performed to explain the discussed issue. [ABSTRACT FROM AUTHOR]

Pro-Oxidative Effect of KIO 3 and Protective Effect of Melatonin in the Thyroid - Comparison to Other Tissues. Figure Graph: Figure 2 Lipid peroxidation, measured as MDA + 4-HDA level, in homogenates of porcine tissues (thyroid, ovary, spleen, liver, brain, small intestine, kidney), incubated without any substance (control; white bars), or with melatonin (5 mM) (grey bars), or with KIO3 (20; 15; 10; 7.5; 5.0 mM) (black bars), or with KIO3 (20; 15; 10; 7.5; 5.0 mM) + melatonin (5 mM) (striped bars). In the original article [[1]], there was a mistake in Figure 2 as published, namely the graph showing the levels of lipid peroxidation in the ovary was inserted twice and, at the same time, the graph showing the levels of lipid peroxidation in the spleen was not inserted at all. [Extracted from the article]

According to current recommendations, a TSH value of < 2.5 mIU/l should be maintained during preconception and pregnancy. The same recommendation, however, does not relate to all women of childbearing age. The aim of the study was to evaluate relationship between lipid peroxidation (LPO; index of oxidative damage to membrane lipids) and thyroid tests and other parameters, which may be affected by thyroid dysfunction, in euthyroid women of childbearing age. Ninety nine female inpatients with normal thyroid tests (TSH 0.27-4.2 mIU/l), aged 18-48 years, were prospectively enrolled. Blood concentrations of malondialdehyde + 4-hydroxyalkenals (LPO index) were measured spectrophotometrically. Thyroid tests (TSH, FT4, FT3), thyroid antibodies and other laboratory parameters [cholesterol, HDL cholesterol (HDLC), LDL cholesterol, HDLC/cholesterol ratio, triglycerides, glucose, CRP, iron] were measured with standard methods. Blood LPO level was higher in women with TSH = 2.5 mIU/l than in women with TSH < 2.5 mIU/l. Positive correlation was found between TSH concentration and LPO level (r = 0.210, p = 0.037). In the univariate regression analysis, blood LPO level did constitute the only independent factor associated with TSH = 2.5 mIU/l. Abnormal HDLC/cholesterol ratio occurred more frequently in subjects with TSH = 2.5 mIU/l. Additionally, LPO level correlated positively with triglyceride concentration (r = 0.340, p = 0.001), whereas it correlated negatively with HDLC concentration (r = -0.335, p = 0.001) and with HDL/cholesterol ratio (r = -0.331, p = 0.001). In conclusion, in women of childbearing age with normal thyroid tests, TSH = 2.5 mIU/l is associated with higher oxidative damage to membrane lipids and less favorable lipid profile, which supports our standpoint that TSH of less than 2.5 mIU/l should be maintained in all women of childbearing age. [ABSTRACT FROM AUTHOR]

Estrogens, with their principle representative 17β-estradiol, contribute to the redox state of cells showing both pro- and antioxidative properties. In the ovary, being the main source of estrogens, maintaining balance between the production and detoxification of ROS is crucial. Whereas ovary estrogen concentration is difficult to estimate, its circulating concentration in women may reach the nanomolar level. The aim of the study was to evaluate the effects of 17β-estradiol on oxidative damage to membrane lipids (lipid peroxidation, LPO) and to nuclear DNA in the porcine ovary under basal conditions and in the presence of Fenton reaction (Fe2++H2O2→Fe3++•OH + OH−) substrates. Ovary homogenates and DNA were incubated in the presence of 17β-estradiol (1 mM–1 pM), without/with FeSO4(30 μM) + H2O2(0.5 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. The concentration of 8-oxo-7,8-dihydro-2’-deoxyguanosine (8-oxodG) (DNA damage index) was measured by HPLC. We observed that 17β-estradiol did not alter the basal level of oxidative damage, but reduced Fe2++H2O2-induced oxidative damage to membrane lipids when ≥10 nM and to DNA at concentrations ≥1 nM. In the ovary at near physiological concentration, 17β-estradiol prevents experimentally induced oxidative damage. This suggests that under physiological conditions this hormone may contribute to protecting the ovary against oxidative damage. [ABSTRACT FROM PUBLISHER]

Background: Nitrobenzene is a carcinogen, which induces—among others—thyroid tumors. Melatonin is an effective antioxidant, whereas some antioxidative effects of propylthiouracil (PTU; an antithyroid medication used for the treatment of thyrotoxicosis) were also found. The aim of the study was to compare protective effects of melatonin and PTU against lipid peroxidation in homogenates of porcine thyroids, incubated in the presence of nitrobenzene. Methods: Homogenates of porcine thyroids were incubated for 30 min in the presence of nitrobenzene (0.001, 0.01, 0.1, 0.25, 0.5, 1.0, 2.5, 5.0, 7.5, and 10.0 mM). The level of lipid peroxidation products (malondialdehyde + 4-hydroxyalkenals) was measured spectrophotometrically. Nitrobenzene (7.5 and 10.0 mM) increased lipid peroxidation in the homogenates of porcine thyroids. Subsequently, homogenates of porcine thyroids were incubated for 30 min in the presence of nitrobenzene (7.5 mM) plus one of the antioxidants: melatonin (0.000001, 0.00001, 0.0001, 0.001, 0.01, 0.1, 0.25, 0.5, 1.0, 2.5, 5.0, and 7.5 mM) or PTU (0.01, 0.1, 0.25, 0.5, 1.0, 2.5, 5.0, and 7.5 mM). Results: Lipid peroxidation caused by nitrobenzene was effectively prevented by melatonin, with the lowest effective concentration of 0.0001 mM, being only two orders of magnitude higher than physiological blood concentration in humans. At the same time, PTU revealed protective effects only in the highest used concentration (7.5 mM), which is practically never reached during pharmacological treatment in patients with thyrotoxicosis. Conclusions: Melatonin can serve as an effective agent in protection against nitrobenzene-induced lipid peroxidation in porcine thyroid. [ABSTRACT FROM AUTHOR]

Background: Fenton reaction (Fe2++H2O2→Fe3++•OH+OH-) is of special significance in the thyroid gland, as both its substrates, i.e. H2O2 and Fe2+, are required for thyroid hormone synthesis. Also iodine, an essential element supplied by the diet, is indispensable for thyroid hormone synthesis. It is well known that iodine affects red-ox balance. One of the most frequently examined oxidative processes is lipid peroxidation (LPO), which results from oxidative damage to membrane lipids. Fenton reaction is used to experimentally induce lipid peroxidation. The aim of the study was to evaluate effects of iodine, used as potassium iodide (KI) or potassium iodate (KIO3), on lipid peroxidation in porcine thyroid homogenates under basal conditions and in the presence of Fenton reaction substrates. Methods: Porcine thyroid homogenates were incubated in the presence of either KI (0.00005 – 500 mM) or KIO3 (0.00005 – 200 mM), without or with addition of FeSO4 (30 μM) + H2O2 (0.5 mM). Concentration of malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) was measured spectrophotometrically, as an index of lipid peroxidation. Results: Potassium iodide, only when used in the highest concentrations (≥50 mM), increased lipid peroxidation in concentration-dependent manner. In the middle range of concentrations (5.0; 10; 25; 50 and 100 mM) KI reduced Fenton reaction-induced lipid peroxidation, with the strongest protective effect observed for the concentration of 25 mM. Potassium iodate increased lipid peroxidation in concentrations ≥2.5 mM. The damaging effect of KIO3 increased gradually from the concentration of 2.5 mM to 10 mM. The strongest damaging effect was observed at the KIO3 concentration of 10 mM, corresponding to physiological iodine concentration in the thyroid. Potassium iodate in concentrations of 5–200 mM enhanced Fenton reaction-induced lipid peroxidation with the strongest damaging effect found again for the concentration of 10 mM. Conclusions: Potassium iodide, used in doses generally recommended in iodide prophylaxis, may prevent oxidative damage to membrane lipids in this gland. Toxic effects of iodide overload may result from its prooxidative action. Potassium iodate does not possess any direct beneficial effects on oxidative damage to membrane lipids in the thyroid, which constitutes an additional argument against its utility in iodine prophylaxis. [ABSTRACT FROM AUTHOR]