AIMTo know the effect of cysteamine (CS) on the plasma levels of somatostatin (SS) and some metabolic hormones in adult geese.

METHODSFourteen adult crossbred geese (Chuan white x Tai lake) fitted with chronic wing vein cannulas were used in this study to evaluate the effect of CS on SS, TSH, T3 and T4 levels. The experiment was consisted of control and treated phase. The diet was added CS at dosage of 100 mg/kg bw on the first day of the treated phase. The blood samples were collected from the cannulas and analyzed by radioimmunoassay.

RESULTSThe plasma SS concentration was (1.87 +/- 0.10) microg/L in control phase. Whereas SS concentrations on day 1, 3, 5, 7 of treated phase were decreased markedly (P < 0.05 or P < 0.01). Thereafter it was rose on the seventh day, however it was still lower than that of control. The thyroid stimulating hormone (TSH) content (2.45 +/- 0.31 mIU/L) was significantly decreased by 21.63% (P < 0.01) on day 1, and 18.37% (P > 0.05) on day 3 and day 5. Comparing with control phase (5.41 +/- 0.98 microg/L), T4 contents were elevated by 60.26% (P < 0.01), 43.25% (P < 0.01), 37.15% (P < 0.01) and 16. 82% (P < 0.01) respectively on day 1, 3, 5, 7. T3 level was (1.05 +/- 0.06) microg/L in control phase, whereas the levels was significantly increased by 36.19% (P < 0.01) on day 3. Also, the insulin concentration was higher than that of control (4.43 +/- 0.41 mU/ L) by 18.28% (P < 0.05) on the day 5.

CONCLUSIONThese results indicate that CS can decrease the plasma SS and TSH levels, whereas increase the levels of T4, T3 and insulin, therefore change metabolism, improve the nutrition transform and accelerate the growth in geese.

Animals ; Cysteamine ; pharmacology ; Diet ; Geese ; Insulin ; blood ; Somatostatin ; blood ; Thyrotropin ; blood ; Thyroxine ; blood ; Triiodothyronine ; blood

Treatment of rabbits with thyroxine 1 mg/kg daily for three to six days produced a hyperthyroid state as evidenced by increase in the heart rate and PBI. The hyperthyroid animals exhibited a significant shortening of the atrial refractory period. Beta adrenergic receptor blocking agents, propranolol (l0(-6)M pronethalol (5 X 10(-5)M) or MJ-1999 (5 X 10(-4)M), completely blocked the shortening of the atrial refractory period produced by the treatment with thyroxin, and with norepinephrine. Consequently, the shortening of the atrial refractory period of rabbits treated with thyroxin appears to bs mediated through stimulation of the beta adrenergic receptor in the heart. From these results, it may be concluded that the stimulation of the beta adrenergic receptor plays an important role in the alteration of cardiac function found in hyperthyroidism, and that the beta adrenergic blocking agents may be useful in treatment of the cardiac complications of hyperthyroidism.
Adrenergic beta-Antagonists/pharmacology ; Animals ; Female ; Heart Atria/*drug effects/physiopathology ; Hyperthyroidism/chemically induced/*physiopathology ; Male ; Rabbits ; Sympatholytics/*pharmacology ; Thyroxine

The influence of thyroxine upon n the cardiac uptake of catecholamines was investigated in rabbits. A single injection of thyroxine(1.0m/kg) into rabbits did not affect the concentration of myocardial catecholamines. However, this dose of thyroxine greatly increased the cardiac uptake of catecholamine following injection of 2.0mg of norepinephrine as compared to that of untreated normal animals and it remained elevated for several hours. Similarly thyroxine also enhanced the accumulation of myocardial catecholamines following administration of dopa(60-80mg/kg) and epinephrine(1.0-1.5mg/kg).
Animal ; Catecholamines/metabolism* ; Epinephrine/metabolism ; Heart/drug effects* ; Male ; Myocardium/metabolism* ; Norepinephrine/metabolism ; Rabbits ; Thyroxine/pharmacology* ; Tritium

Animals ; Apoptosis ; Brain/metabolism* ; Male ; Phosphatidylinositol 3-Kinases/metabolism* ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage/drug therapy* ; Thyroxine/pharmacology*

OBJECTIVETo study the effects of excess iodine intake on neurogranin expression in cerebrum of filial mice and the intervention of selenium.

METHODSSixty BALB/c mice were divided randomly into four groups with different drinking water: control group (tap water, NC), excess iodine group (3000 microg/L I, EL +), supplementing selenium group (200 microg/L Se, Se +) and the excess iodine plus selenium (3000 microg/L + I 200 microg/L Se, EI + Se +) group. The mice were mated at the end of the fourth month. Serum T4 and T3 were determined on postnatal day 14 and 28. The expression level of neurogranin in filial cerebrum was measured by immunohistochemistry and Western blot.

RESULTSSerum T4 level in EI (68.78 +/- 11.10 nmol/ L) + was lower significantly than that in NC (100.85 +/- 11.47 nmol/ L) and EI + Se + (93.15 +/- 12.10 nmol/ L) on postnatal day 14. Western blot analysis showed that the relative level of neurogranin in EI + (0.621 +/- 0.041) was lower than that in NC (0.841 +/- 0.039) and EI + Se + (0.781 +/- 0.029) on postnatal day 14 (P < 0.05). No significant difference in serum T4 and neurogranin level between four groups on postnatal day 28.

CONCLUSIONExcess iodine intake might change the expression of neurogranin in filial cerebrum and the selenium supplementation might alleviate it.

Animals ; Female ; Iodine ; adverse effects ; Male ; Mice ; Mice, Inbred BALB C ; Neurogranin ; biosynthesis ; Selenium ; pharmacology ; Telencephalon ; metabolism ; Thyroxine ; blood ; Triiodothyronine ; blood

AIMTo determine whether 7-oxo-dehydroepiandrosterone (7-oxo-DHEA) can reverse the hypoimmunity in BALB/c mice exposed to chronic mild stress.

METHODSA chronic mild stress animal model was established by subjecting BALB/c mice to a stressful regimen arranged in an unpredicted manner for 4 consecutive weeks. Immunological function alternations under chronic mild stress were assessed by lymphocytes proliferative response to mitogens and NK cell lysis activity test.

RESULTSThe studies showed the correlation between the state of depression and abnormalities in the immune response, such as a decrease of T lymphocytes proliferative response to Con A and suppression of cytotoxic of NK cell. Meanwhile, significant decrease of T3 and T4 levels was also observed. When stressed mice were daily given 7-oxo-DHEA 15 mg.kg-1, lymphocyte proliferative response and the NK cell activity were significantly enhanced and the decreased levels of T3 and T4 were restored in the stressed mice.

CONCLUSION7-oxo-DHEA can improve the depressive symptoms and hypoimmunity of BALB/c mice induced by chronic mild stress as its parent DHEA.

Adjuvants, Immunologic ; pharmacology ; Animals ; Antidepressive Agents ; pharmacology ; Cell Division ; drug effects ; Chronic Disease ; Dehydroepiandrosterone ; analogs & derivatives ; pharmacology ; Killer Cells, Natural ; immunology ; Male ; Mice ; Mice, Inbred BALB C ; Stress, Physiological ; blood ; immunology ; T-Lymphocytes ; immunology ; pathology ; Thyroxine ; blood ; Triiodothyronine ; blood

Ammonium perchlorate (AP), mainly used as solid propellants, was reported to interfere with homeostasis via competitive inhibition of iodide uptake. However, detailed mechanisms remain to be elucidated. In this study, AP was administered at 0, 130, 260 and 520 mg/kg every day to 24 male SD rats for 13 weeks. The concentrations of iodine in urine, serum thyroid hormones levels, total iodine, relative iodine and total protein, and malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) activity in thyroid tissues were measured, respectively. Our results showed that high-dose perchlorate induced a significant increase in urinary iodine and serum thyroid stimulating hormone (TSH), with a decrease of total iodine and relative iodine content. Meanwhile, free thyroxine (FT4) was decreased and CAT activity was remarkably increased. Particularly, the CAT activity was increased in a dose-dependent manner. These results suggested that CAT might be enhanced to promote the synthesis of iodine, resulting in elevated urinary iodine level. Furthermore, these findings suggested that iodine in the urine and CAT activity in the thyroid might be used as biomarkers for exposure to AP, associated with thyroid hormone indicators such as TSH, FT4.
Analysis of Variance ; Animals ; Catalase ; metabolism ; Dose-Response Relationship, Drug ; Homeostasis ; drug effects ; Iodine ; metabolism ; urine ; Male ; Malondialdehyde ; metabolism ; Perchlorates ; pharmacology ; Quaternary Ammonium Compounds ; pharmacology ; Radioimmunoassay ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism ; Thyroid Gland ; metabolism ; Thyrotropin ; blood ; Thyroxine ; blood ; Triiodothyronine ; blood

OBJECTIVETo investigate the effect of selenium supplementation on the selenium status and selenoenzyme, especially the activity and mRNA expression of type 1 deiodinase (D1) in mice with excessive iodine (EI) intake and to explore the mechanism of selenium intervention on iodine-induced abnormities.

METHODSWeanling female BALB/c mice were given tap water or 3 mg/L of iodine or supplemented with 0.5 mg/L or 1.0 mg/L of selenium in the presence of excessive iodine for 5 months. Selenium status, thyroid hormone level, hepatic and renal D1 activity and mRNA expression were examined.

RESULTSExcessive iodine intake significantly decreased the selenium concentration in urine and liver, and the activity of glutathione peroxidase (GSH-Px) in liver. Meanwhile, serum total T4 (TT4) increased while serum total T3 (TT3) decreased. Hepatic D1 enzyme activity and mRNA expression were reduced by 33% and 86%, respectively. Renal D1 enzyme activity and mRNA were reduced by 30% and 55%, respectively. Selenium supplementation obviously increased selenium concentration, activity of GSH-Px and Dl as well as mRNA expression of D1. However, increasing the supplementation of Se from 0.5 to 1.0 mg/L did not further increase selenoenzyme activity and expression.

CONCLUSIONRelative selenium deficiency caused by excessive iodine plays an essential role in the mechanism of iodine-induced abnormalities. An appropriate dose of selenium supplementation exercises a beneficial intervention.

Animals ; Antioxidants ; pharmacology ; Creatinine ; metabolism ; urine ; Dietary Supplements ; Female ; Iodide Peroxidase ; genetics ; metabolism ; Iodine ; toxicity ; urine ; Kidney ; metabolism ; Liver ; metabolism ; Mice ; Mice, Inbred BALB C ; RNA, Messenger ; metabolism ; Selenium ; pharmacology ; urine ; Thyroxine ; blood ; Triiodothyronine ; blood

The effects of thyroid hormone on hepatic and gastric alcohol dehydrogenase (ADH) activities (nM of NADH/min/mg of cytosolic protein) have been investigated in male Sprague Dawley rats treated with thyroxine (1 mg/kg, po) for 14 days. Whereas hepatic ADH activity in thyroxine-treated rats decreased by 61.3% of control rats (26.4 vs 43.2, p<0.001), gastric ADH activity increased by 262.9% of control rats (4.9 vs 1.9, p<0.001). As for the activities of the lung and kidney, thyroxine treatment did not produce any statistically significant changes. These data suggest that thyrotoxicosis causes a decrease of hepatic alcohol metabolism, and that the increase of gastric ADH activity in thyrotoxic rats can partly restore the first-pass metabolism of ethanol.
Alcohol Dehydrogenase/*metabolism ; Animal ; Gastric Mucosa/enzymology ; Kidney/enzymology ; Liver/drug effects/*enzymology ; Lung/enzymology ; Male ; Rats ; Rats, Sprague-Dawley ; Stomach/drug effects/*enzymology ; Thyrotoxicosis/chemically induced/metabolism ; Thyroxine/administration & dosage/*metabolism/pharmacology

OBJECTIVETo explore the effects of thyroid hormone (TH) on cardiac function and peripheral lymphocyte beta-adrenoceptors (beta-ARs) of patients with chronic congestive heart failure (CHF).

METHODSTwenty-eight patients with class III or IV advanced CHF due to dilated cardiomyopathy (DCM) or ischemic cardiomyopathy (ICM) were randomly divided into groups A and B. L-thyroxine (L-T(50)) was administered to group B. Exercise tolerance, chest X-rays, and echocardiographic parameters were obtained before and after one month of treatment, Ficoll-hypaque solution was used to separate peripheral lymphocytes, and (125)I-pindolol radioligand binding was used to measure beta-AR levels in peripheral lymphocytes.

RESULTSL-T(50) therapy improved cardiac output [CO, (2.98 +/- 0.31)L/min vs (3.24 +/- 0.28) L/min, P < 0.01], left ventricular ejection fraction (LVEF, 26.21% +/- 3.21% vs 37.93% +/- 9.01%, P < 0.01), and decreased isovolumetric relaxation time (IVRT, 0.12 +/- 0.04 vs 0.10 +/- 0.02, P < 0.01). Serum TH levels and the maximal number of beta-AR binding sites (beta(max)) in peripheral lymphocytes were lower in patients with CHF than in normal healthy people, but L-T(50) administration induced a beta-AR up-regulation on peripheral lymphocyte surfaces. L-T(50) was well tolerated without episodes of ischemia or arrhythmia. There was no significant change in heart rate or metabolic rate.

CONCLUSIONTH administration improves cardiac function and beta-AR expression in peripheral lymphocytes of patients with CHF.

Adult ; Aged ; Blood Pressure ; drug effects ; Chronic Disease ; Echocardiography ; Female ; Heart ; drug effects ; physiology ; Heart Failure ; physiopathology ; Heart Rate ; drug effects ; Humans ; Lymphocytes ; chemistry ; Male ; Middle Aged ; Receptors, Adrenergic, beta ; analysis ; Thyroxine ; pharmacology