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PubMed1997

The thyroid hormone, 3,5,3'-triiodothyronine, is a negative modulator of domestic fowl (Gallus gallus domesticus) adrenal steroidogenic function.

Previous work with chickens (Gallus gallus domesticus) suggests a relationship between depressed thyroid hormone status and enhanced adrenal steroidogenic function. In addition, in hypophysectomized chickens, replacement of the thyroid hormone, 3,5,3'-triiodothyronine (T3), maintains chicken adrenal steroidogenic cell sensitivity to adrenocorticotropin (ACTH) but decreases steroidogenic capacity further than that due to hypophysectomy alone. The present in vivo and in vitro studies were conducted to determine the influence of thyroid status and T3 per se on avian adrenal steroidogenic function. Chicks (1 day old) were thyroidectomized using combined surgical and chemical (6-propyl-2-thiouracil) treatments and were administered a replacement dose of T3 (0, 1.5, 4.5, 15, and 45 microg/kg body wt/day) for 5 weeks. Whereas thyroidectomy (TX) decreased adrenal weight (-20%), it increased relative adrenal weight (mg/100 g body weight) (+171%), trunk plasma corticosterone (+880%), and aldosterone (+124%). In addition, TX increased basal, maximal ACTH-induced, maximal 8-bromo-cyclic AMP-induced, and maximal 25-hydroxycholesterol-supported corticosterone production (+520, +93, +124, and +195%, respectively) and aldosterone production (+578, +288, +280, and +275%, respectively) by isolated adrenal steroidogenic cells. T3, in a dose-dependent manner, reversed the effects of TX on these in vivo and in vitro parameters of adrenal steroidogenic function. Restoration of most of these parameters to those in the sham-treated control was attained with 4.5-15 microg/kg body wt/day. Although some of the effects of TX and T3 replacement on adrenal steroidogenic function may have been mediated through changes in circulating levels of ACTH, other data suggest a direct effect on adrenal steroidogenic cell function. Adrenal steroidogenic cells from sham-treated and TX birds were preincubated (0, 4, and 12 hr) with various concentrations of T3 (0, 0.3, 3, and 30 nM), washed, and then incubated for an additional 2 hr in medium containing the same respective concentrations of T3, with or without a maximal steroidogenic concentration of ACTH (100 nM). T3 had no acute effects on TX-dependent enhancement of adrenal steroidogenic cell function (2-hr incubation). However, with preincubation (4 and 12 hr), T3 inhibited basal and maximal ACTH-induced corticosterone production in a dose-dependent manner. This concentration-dependent, direct effect of T3 was not observed with cells from sham-treated birds. In addition, the ostensibly inactive thyroid hormone metabolite, 3,3',5'-triiodothyronine [reverse T3; 30 nM], was without effect. Taken collectively, these studies indicate that T3 is a direct negative modulator of avian adrenal steroidogenic function.

Adrenal Cortex Hormones↗
PubMed1999

Characterization of thyroid hormone 5'-monodeiodinase activity in the turtle (Trachemys scripta).

Thyroid hormone metabolism by 5'-monodeiodinase enzymes (5'MD) was characterized in peripheral tissues of the turtle, Trachemys scripta, and compared with activity measured in the rat. Based on differences in pH dependence, sensitivity to inhibitors, substrate affinity, and cofactor requirements, at least two types of enzyme activities have been identified in the turtle. A 5'MD activity was measured in liver and kidney microsomal fractions that exhibits inhibition by 2n-propyl-6-thiouracil (PTU), a higher affinity for rT3 (Km = 2 microM) than for T4 (Km = 6.5 microM), a low cofactor dependence, and a high pH optimum for T4 metabolism. The characteristics of this turtle low affinity T4 activity correspond to the mammalian type I monodeiodinase. A second type of monodeiodinase (MD) activity that is less sensitive to PTU, has a higher affinity for T4 (Km = 1 nM), a higher cofactor requirement, and a lower pH optimum was colocalized with the first form. Both turtle MD activities remain active over a range of temperatures, allowing for activity at the preferred body temperature of this species (28 to 37 degrees C compared to the 37 degrees C optimum in the rat). Based on limited comparative data of MD systems from several fish and birds, the turtle most closely resembles avian species. Like birds, turtles possess a mammalian-like type I activity and have colocalized MD forms in the liver. However, the second turtle MD form (MDH) is not comparable to the mammalian or avian MDII-like activity. Analysis of the deiodinase products from both turtle MDs by high-performance liquid chromatography confirmed that the putative turtle MDI produces T3 from T4 as expected. The MDH produces rT3 from T4 as does the mammalian type III form, but MDH has a wider tissue distribution (kidney, liver, pancreas, heart, ovary, and brain) and distinct enzyme kinetics. Moreover, MDH activity in the turtle kidney is 100-fold higher than in the liver, indicating that the kidney may play a critical role in the metabolism of thyroid hormones in the turtle; this high renal activity distinguishes the turtle from all other vertebrates studied.

Animals↗
PubMed2000

Hepatic outer-ring deiodinase in a Mexican endemic lizard (Sceloporus grammicus).

The kinetic characterization of the outer-ring deiodination pathway using rT(3) (rT(3)-ORD) in male, female, and pregnant female livers of an endemic lizard, Sceloporus grammicus, is reported. The ORD pathway does not have the characteristics of deiodinase type II; it is exclusively carried out by deiodinase type I (DI). DI enzymatic activity in lizard liver contains one of the highest activities reported in vertebrates. This activity is sexually dimorphic, with males presenting the highest activity during the reproductive season. The properties of this enzyme correspond to those described in mammals, such as specificity for rT(3), susceptibility to inhibition by 6-n-propyl-2-thiouracil and gold-thioglucose, cofactor requirement, and kinetic pattern. Unlike other vertebrates, the lizard DI exhibits conspicuous stability in the thermal range of 15 to 42 degrees C and in the pH range of 5.0 to 9.0. Male true kinetic constants exhibit a direct correlation with temperature. This is in agreement with short-term adaptation to microenvironmental changes and the feasible expression of enzymatic forms/variants which, together, endow this lizard species with a greater adaptation to natural daily ambient thermal fluctuations.

Animals↗
PubMed1997

Effects of maternal exposure to 3,3',4,4'-tetrachlorobiphenyl or propylthiouracil in rats trained to discriminate apomorphine from saline.

In the present experiment drug discrimination was examined in rats after maternal exposure to 3,3',4,4'-tetrachlorobiphenyl (PCB 77) using apomorphine (APO) as the training drug at a dose reported to act on dopamine D2 receptors. A group with maternal exposure to 6n-propyl-2-thiouracil (PTU) was included as a positive control for effects induced by PCB 77 on thyroid hormones. On gestational day (GD) 19 reduced levels of free and total thyroxine (FT4, TT4) and free triiodothyronine (FT3) were detected in dams exposed to PCB 77 or PTU. In the offspring decreases in levels of FT4 and TT4 were found in both treated groups on postnatal day (PND) 21, while reductions of FT3 were observed only in the PTU group. PTU-treated rats needed more daily sessions for successful discrimination between apomorphine and saline. There were no differences between groups in generalization tests and sessions with the D2/D3 agonist quinpirole, the D2 antagonist haloperidol plus APO, or with the GABAergic drug pentobarbital and only minor differences in sessions with the D1 agonist SKF-38393. Differences between controls and groups exposed to PCB 77 or PTU were detected in a blocking test using the mixed serotonin 5-HT1A agonist and partial D2 antagonist buspirone. This outcome suggests long-lasting effects by developmental exposure to PCB 77 on the interaction between dopaminergic and serotonergic processes which may be mediated by effects on thyroid hormone levels.

Animals↗
PubMed1988

The origin of hydrogen cyanide in breath.

The excretion of hydrogen cyanide in breath and blood concentrations of cyanide were measured in eight normal subjects. There was no correlation between breath and blood levels of cyanide. Furthermore, breath cyanide concentrations calculated from blood values were much lower than measured values, which suggested a local production of hydrogen cyanide in the oropharynx. When saliva was incubated at 37 degrees C hydrogen cyanide was formed in the presence of air but not in a nitrogen atmosphere. No hydrogen cyanide was formed with boiled saliva and the production of hydrogen cyanide by native saliva was inhibited by catalase and by 6-n-propyl-thiouracil. Centrifugation of saliva resulted in a supernatant and a sediment, which were both required for the formation of hydrogen cyanide. Dialysis of the supernatant abolished its cyanide forming ability, which could be restored by addition of thiocyanate. We conclude that most of the hydrogen cyanide found in breath from normal human beings originates from oxidation of thiocyanate by salivary peroxidase in the oropharynx. As a consequence measurements of breath hydrogen cyanide can only be used to detect heavy exposure to cyanide.

Adult↗
PubMed1992

Thyroid control of contractile function and calcium handling in neonatal rat heart.

Newborn rats were rendered hyperthyroid (daily subcutaneous injections of L-triiodothyronine, 10 micrograms 100 g-1 body weight) or hypothyroid (0.05% 6-n-propyl-2-thiouracil in drinking water to nursing mothers) during the first 3 weeks of postnatal life. Compared with the euthyroid group, hyperthyroidism resulted in: (1) cardiac enlargement with right ventricular preponderance, (2) increased cardiac contractile function, (3) increased Ca2+ uptake by the sarcoplasmic reticulum (SR), (4) decreased sensitivity to the negative inotropic effect of verapamil and (5) greater inhibition of contractile function by ryanodine. Hypothyroidism generally resulted in opposite changes. The data suggest that the development of the heart and its contractile function during early postnatal life depends on the plasma level of thyroid hormones. In particular, the relative contribution of the SR and sarcolemmal Ca2+ transport to the control of cardiac contractility seems to be markedly affected by altered thyroid states. The postnatal maturation of the SR function is accelerated in hyperthyroidism but retarded in hypothyroidism. Consequently, hyperthyroid hearts appear to be less dependent and hypothyroid ones more dependent on trans-sarcolemmal Ca2+ fluxes when compared with age-matched euthyroid animals.

Animals↗
PubMed1985

Thyroid-dependent alterations of myocardial adrenoceptors and adrenoceptor-mediated responses in the rat.

Cardiovascular alterations in hypo- and hyperthyroidism have been ascribed to changes of noradrenergic neurotransmission. In the present study the influence of thyroid hormones on adrenoceptors in the rat heart was further characterized. The effect of artificial hypothyroidism (induced by feeding 6-propyl-2-thiouracil, PTU) and hyperthyroidism (induced by daily injections of triiodothyronine, T3) on myocardial adrenoceptor binding, catecholamines, some physiological responses, and their interdependence was examined. The density of myocardial beta-adrenergic binding sites (3H-dihydroalprenolol, 3H-DHA) was reduced after PTU (by 38%) and enhanced after T3 treatment (by up to 82%). The increase was dose- and time-dependent and reversible within 4 days. No changes of the affinity of 3H-DHA to its binding sites were observed. Only L-T3 and L-T4 proved to be active, D-T3 and reverse T3 had no effect. The rise in beta-adrenoceptor density caused by T3 was prevented by concomitant administration of cycloheximide, indicating its dependence on protein synthesis. The density of myocardial alpha 1-adrenergic binding sites (3H-prazosin) was significantly reduced in the PTU group (by up to 28%) and even more distinctly by T3 treatment (by up to 50%). KD values remained unaltered. The noradrenaline content and turnover of rat hearts was significantly reduced by T3-induced hyperthyroidism. PTU treatment had no influence on content and turnover of noradrenaline. Plasma noradrenaline as well as adrenaline levels in freely moving rats were increased by PTU treatment 9- and 5-fold, respectively. In T3-injected animals no significant changes were measured. The density of adrenoceptors is known to be inversely correlated with catecholamine levels in several organs. Neither alpha- nor beta-adrenoceptor changes in the myocardium of dysthyroid rats could be attributed to such a homologous regulation, since they still occurred after chemical sympathectomy with 6-hydroxydopamine and adrenalectomy.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Regulation of vasopressin gene expression: changes in the level, but not the size, of vasopressin mRNA following endocrine manipulations.

1. Regulatory interactions between the hypothalamoneurohypophyseal vasopressin (VP) axis and the endocrine systems of the anterior pituitary have been investigated in the rat by observing changes in VP mRNA expression following endocrine manipulations. 2. An increase in the level, but not size, of VP mRNA was found in the supraoptic (SON) and paraventricular nuclei (PVN) of the hypothalamus and in the neurointermediate lobe (NIL) of the pituitary following hypothyroidism (induced by drinking 6-n-propyl-2-thiouracil; PTU) and adrenalectomy. Hypothyroidism induced by alternative procedures (surgical thyroidectomy or PTU injections) did not exert similar effects. 3. Treatment with the dopamine agonist bromocriptine to reduce prolactin secretion raised levels of VP mRNA in the NIL only. Castration did not up-regulate VP mRNA levels. 4. Since the observed effects on VP mRNA levels occur in the absence of changes in plasma osmolality, these results provide evidence of nonosmotic regulation of VP gene expression, an effect which is observed most clearly in the NIL pool of VP mRNA. Furthermore, the effects are distinct from changes in VP mRNA levels associated with raised plasma osmolality since the VP mRNA size was not increased.

Adrenalectomy↗
PubMed1994

Effect of propylthiouracil-induced hypothyroidism on cerebral cortex of young and aged rats: lipid composition of synaptosomes, muscarinic receptor sites, and acetylcholinesterase activity.

The effect of hypothyroidism on the lipid composition of synaptosomes, density and affinity of muscarinic receptor sites, and acetylcholinesterase activity in the cerebral cortex of young and aged rats was investigated. The animals were made hypothyroid by adding 0.05% propyl-2-thiouracil to their drinking water for four weeks. This pathological state induced an increase in the relative percentage of sphingomyelin in young rats. In aged rats hypothyroidism induced a decrease of sphingomyelin and glycerophosphocholine and an increase of cholesterol. The effect of hypothyroid state on cerebral cortex resulted in an increase of acethylcholinesterase activity both in young and aged rats and was also reflected in an increase of density of M1-AChRs but only in the former.

Acetylcholinesterase↗
PubMed1977

Modification of adriamycin toxicity in rats fed a high fat diet.

Rats fed a diet containing a high percentage of butter, cholesterol, cholic acid and proply thiouracil (HFD) showed weight loss and developed hyperlipidemia, marked fatty infiltration of the liver, moderate elevation of SGPT, degenerative changes of the heart muscle, bradycardia, alterations of the QRS complex in the electrocardiogram, and initial hemoconcentration followed by moderate anemia. Treatment with adriamycin (18 X 1 mg/kg i.p.) resulted in significant augmentation of the cardiotoxic effects of this drug demonstrated by electrocardiographic measurements and myocardial histopathology. Adriamycin-induced atrophy of the lymphatic tissue was seen only in rats fed HFD and not in animals receiving ground chow. Adriamycin levels in the heart after single i.p. injection were higher in rats receiving HFD. This effect was present already after 10 days on HFD. At this time histopathological liver changes were present and SGPT was elevated. It is concluded that the increase in adriamycin toxicity is, at least in part, due to diminished excretion by the liver. These experimental findings are in accordance with clinical observations which have identified liver disease as one of the important risk factors for the development of adriamycin cardiomyopathy.

Alanine Transaminase↗
PubMed1993

Effect of propylthiouracil-induced hypothyroidism on membranes of adult rat brain.

The effect of hypothyroidism on the lipid composition of myelin and synaptosomes isolated from adult rat brain was investigated. The animals were made hypothyroid by adding 0.05% propyl-2-thiouracil to their drinking water for four weeks. This pathological state resulted in a significant increase in the relative percentage of choline glycerophospholipids in synaptosomes with a concomitant decrease in ethanolamine glycerophospholipids as compared to controls. In myelin, hypothyroidism significantly influenced only the relative percentage of sulfatides. The effect of the hypothyroid state on mature brain was also reflected in changes in the membrane fatty acid composition. Myelin and synaptosomes showed an increase in arachidonic (20:4) and eicosatrienoic (20:3) acids and an increase in the fatty acid unsaturation index. Furthermore, the 20:4/20:3 and 20:3/18:2 ratios were lower and higher, respectively, in treated animals. The data indicate that hypothyroidism affects the lipid composition of synaptosomes and myelin even though the effects were less pronounced in myelin. The lipid changes observed in hypothyroidism may be of physiological significance, as it is well known that lipid composition modulates various membrane-bound enzymes, transporters and receptors.

Animals↗
PubMed2003

Effect of thyroid hormone on the development and gene expression of hormone receptors in rat testes in vivo.

Thyroid hormone is known to play a pivotal role in the regulation of prepuberal rat testes development and function with specific influence on the differentiation of Sertoli cells, the only cell type that expresses thyroid hormone receptors in testes. To explore in vivo effects of thyroid hormone on testes development and the regulation of testicular gene expression, the hyper- and hypothyroid rat models were established by T3 injection to pups (ip 100 microg/kg bw) and by oral administration of 6-N-propyl-2-thiouracil (PTU) to the lactating mother from days 1 to 21 post-delivery. Half of the rats from each group were sacrificed at 21 days of age, and the other half were allowed to recover with discontinued treatments from day 22 to day 50. At 21 days of age, a significantly elevated serum T3 level was observed in hyperthyroid rats (179.5 ng/dl) vs controls (97.5 ng/dl), and in hypothyroid rats a significantly lower level of T3 was detected (26.1 ng/dl). However, serum T4 concentration was significantly lower in both hyper- (0.105 microg/dl) and hypothyroid (0.058 microg/dl) rats compared to the controls (2.48 microg/dl). In recovered rats in which the serum T3 and T4 were restored to normal, the serum T levels remained remarkably lower in both hyper- and hypothyroid rats. The significantly decreased body and testes weights observed in both hyper- and hypothyroid rats at 21 days of age were not restored by the time they were 50 days old. Histological analyses of testes of 21-day-old hypothyroid rats revealed smaller-sized seminiferous tubules, incomplete lumen formation and delayed germ cell differentiation and in hyperthyroid rats an increased number of early stage spermatocytes was found. Testicular mRNA levels of follicle-stimulating hormone receptor (FSH-R), luteinizing hormone receptor (LH-R) and androgen binding protein (ABP) were studied by Northern blot hybridization. At 21 days of age data showed that FSH-R mRNA levels were significantly higher in both hyper- and hypothyroid rat testes compared to controls, but no differences were detected in recovered 50-day-old rats. Significantly decreased ABP mRNA levels were detected only in hypothyroid rat testes compared to those in both the hyperthyroid and control groups at 21 days of age, but no significant change was observed in recovered 50-day-old rats. To further evaluate the effect of thyroid hormone on the Leydig cell function, the 2.3/2.6 kb specific LH-R hybridization bands were detected with rat LH-R cRNA probe. Significant suppression of LH-R mRNA levels was only observed in the hypothyroid rat testes at 50 days of age. The testicular thyroid hormone receptors (TRs) and the regulation of TR by thyroid hormone were investigated using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) assays. Both TRalpha and TRbeta mRNAs were identified in the testes from 21- and/or 50-day-old rats. TRalpha mRNA levels were significantly increased in hypothyroid rat testes and were suppressed in hyperthyroid rats at 21 days of age and no changes of TRalpha mRNA were found in recovered animals. Our in vivo data strongly suggest that the thyroid hormone directly affects the development of prepuberal testes and the regulation of FSH-R and ABP gene expression in Sertoli cells, as well as the LH-R mRNA levels in Leydig cells, which may lead to further modulating the effect of gonadotropins on testes function.

Androgen-Binding Protein↗
PubMed1990

Neuroendocrine-thymus interactions. I. In vitro modulation of thymic factor secretion by thyroid hormones.

Several in vivo experimental and clinical studies suggest that the production of thymic hormones, such as thymulin (Zn-FTS), is modulated by thyroid hormones. It was not determined in these studies, however whether such modulation is exerted directly on the thymic epithelial cells which synthesize and secrete thymic hormones. In order to discriminate between direct and indirect modulation, the effect of thyroid hormones on the in vitro production of thymulin by whole thymic organ culture, as detected by the rosette inhibition assay, has been investigated. Donors of thymuses were young 6N-propyl-2 thiouracil (PTU)-treated hypothyroid Balb/c mice and normal littermates. Thymuses from hypothyroid mice were shown to produce concentrations in vitro nearly undetectable of thymic hormone, when compared to thymuses from normal mice. The in vitro addition of triiodothyronine (T3) caused a complete recovery of the thymic hormone production by thymuses from hypothyroid mice and an increased synthesis even by normal thymuses over control values. The complete blockade of in vitro thymic hormone production with cycloheximide, which inhibits mRNA and protein synthesis but not thyroid hormone permissive actions, suggests that the T3 induced increment of thymic hormone level in the supernatant is due to de novo synthesis. Furthermore, the number of thymulin-producing cells, as detected by immunofluorescence using a specific antithymulin monoclonal antibody, which is quite low in thymuses from hypothyroid mice, is completely regained after in vitro incubation with T3. These findings support the idea that the modulation of thyroid hormones on thymic endocrine activity is directly exerted at thymic level.

Animals↗
PubMed2001

Over-production of hydantoinase and N-carbamoylamino acid amidohydrolase enzymes by regulatory mutants of Agrobacterium tumefaciens.

While the hydantoin-hydrolysing enzymes from Agrobacterium strains are used as biocatalysts in the commercial production of D-p-hydroxyphenylglycine, they are now mostly produced in heterologous hosts such as Escherichia coli. This is due to the fact that the activity of these enzymes in the native strains is tightly regulated by growth conditions. Hydantoinase and N-carbamoylamino acid amidohydrolase (NCAAH) activities are induced when cells are grown in the presence of hydantoin or an hydantoin analogue, and in complete medium, enzyme activity can be detected only in early stationary growth phase. In this study, the ability of Agrobacterium tumefaciens RU-OR cells to produce active enzymes was found to be dependent upon the choice of nitrogen source and the presence of inducer, 2-thiouracil, in the growth medium. Growth with (NH4)2SO4 as the nitrogen source repressed the production of both enzymes (nitrogen repression) and also resulted in a rapid, but reversible loss of hydantoinase activity in induced cells (ammonia shock). Mutant strains with inducer-independent production of the enzymes and/or altered response to nitrogen control were isolated. Of greatest importance for industrial application was strain RU-ORPN1F9, in which hydantoinase and NCAAH enzyme activity was inducer-independent and no longer sensitive to nitrogen repression or ammonia shock. Such mutants offer the potential for native enzyme production levels equivalent to those achieved by current heterologous expression systems.

Agrobacterium tumefaciens↗
PubMed1996

Effect of hypothyroidism on satellite cells and postnatal fiber development in the soleus muscle of rat.

The effect of hypothyroidism, induced by 4-propyl-2-thiouracil, on muscle satellite cells in vivo and in vitro, and on postnatal muscle fiber development in the soleus muscle of rats during the first 40 days of postnatal life was analyzed. The proliferative activity of satellite cells was determined by means of bromodeoxyuridine incorporation. Creatine kinase activity was used as a marker for differentiation. In vivo, hypothyroidism resulted in smaller fibers in which the amount of sarcoplasm remained in balance with the number of myonuclei. The in vivo labeling data of satellite cells did not indicate a decreased proliferative activity, but the in vitro experiments showed that the hypothyroid rat muscles contained fewer satellite cells that were less active in proliferation and differentiation at the start of culture. Despite this, the bromodeoxyuridine signal increased in time at a similar rate as that in control cultures. From this and because the cells resembled control cells in their response to bFGF, we conclude that hypothyroid satellite cells remain responsive to proliferation stimuli. However, in hypothyroid cultures, the activity of creatine kinase is lower, even at longer culture times. We therefore conclude that hypothyroid status affects muscle precursor cells mainly by depressing their ability to differentiate and fuse with existing myofibers.

Animals↗
PubMed2006

Upregulation of the alpha1-adrenoceptor-induced phosphoinositide and inotropic response in hypothyroid rat heart.

In this study, we examined changes in the biochemical and inotropic events of the alpha(1)-adrenoceptor signaling pathway in hypothyroid rat hearts. Hypothyroidism was induced by treating experimental animals with 0.05% 6-n-propyl-2-thiouracil (PTU) in drinking water for 7 weeks. A significant decrease of beta- and an increase in alpha(1)-adrenoceptor density as well as an increase in the basal activity of the phosphoinositide (4,5) bisphosphate hydrolyzing phospholipase C was observed in sarcolemmal membranes purified from hypothyroid hearts as compared to age-matched euthyroid controls. Following stimulation with 10 microM phenylephrine (in the presence of 10 microM atenolol), the increase of contractile parameters over baseline values was significantly higher in hypo- than euthyroid hearts, while the opposite occurred under beta-stimulation with 0.1 microM isoproterenol. Interestingly, the increase in phenylephrine-mediated positive inotropy was accompanied by a significant increase in the sarcolemmal phospholipase C activity and in the inositol 1,4,5-trisphosphate content in hypothyroid as compared to euthyroid controls. Our results suggest that cardiac alpha(1)-adrenoceptor and its associated phosphoinositide signaling pathway may act as a reserve for catecholamine inotropic response in hypothyroidism, where the beta-adrenoceptors are compromised.

Animals↗
PubMed1990

Catalase HPI influences membrane permeability in Escherichia coli following near-UV stress.

The katG gene in Escherichia coli encodes catalase HPI, which is involved in membrane transport and protects the cell during oxidative stress. Hydrogen peroxide (H2O2) induces synthesis of HPI. We examined the role of HPI in membrane permeability (proline uptake) following exposure to near-ultraviolet radiation (NUV). We found that NUV resulted in the same type of induction as H2O2. KatG::Tn10 cells experienced a large drop in uptake after NUV exposure, and levels remained low following incubation. A strain carrying a katG+ plasmid, however, showed considerably less decrease in uptake after NUV, and uptake quickly resumed upon incubation. Further, in an srd mutant which lacks 4-thiouracil, NUV resulted in only a small drop in proline uptake, which was immediately resumed.

Catalase↗
PubMed1992

Iodothyronine 5-deiodinase in rat posterior pituitary.

We first describe the presence of iodothyronine 5-deiodinase (5D) in the neural lobe of rat pituitary. 6-n-Propyl-2-thiouracil (PTU), a specific inhibitor of type-I deiodinase, had no effect, showing that 5D in neurohypophysis is of type-III isozyme, which is specific for 5-deiodination and has been found only in the brain, placenta and skin. The presence of 5D (type-III) together with our previous report of 5'-deiodinase (type-I in euthyroidism and type-II in hypothyroidism) shows that the isozymes of deiodinases in the neurohypophysis are quite similar to those in the brain. These data suggest a previously unrecognized role of thyroid hormone in posterior pituitary physiology.

Animals↗