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G F Wassermann

Publications and source records attributed to G F Wassermann.

At least 19 recordsLinked to original sources
PubMed2005

Localization of acid phosphatase activity in the testis of two teleostean species (Oreochromis niloticus and Odonthestes perugiae).

Acid phosphatase (AcP) activity was investigated in the testes of two species of teleosts in two seasons: summer and winter. AcP activity was detected in Sertoli cells from tilapia (Oreochromis niloticus) only during the nonreproductive period of its annual cycle, corresponding to the winter months. In kingfish (Odonthestes perugiae), the enzymatic reaction was identified during the non-reproductive period (summer) in epithelial cells of the efferent ducts but not in Sertoli cells. These data suggest that the enzyme is involved in the absorption of residual spermatid cytoplasm and as well as in the removal of spermatozoa remaining after the reproductive period. In kingfish, this heterophagous function is carried out by the efferent duct cells and not by Sertoli cells.

Acid Phosphatase↗
PubMed2005

Isoproterenol opens K+(ATP) channels via a beta2-adrenoceptor-linked mechanism in Sertoli cells from immature rats.

In the present study, we investigated the mechanism by which isoproterenol hyperpolarises membrane potential (MP) in Sertoli cells from seminiferous tubules of 15-day-old rat testes. Modification of MP and resistance (R0) was analysed using conventional intracellular glass microelectrodes. Isoproterenol (2 x 10(-6) M) induced an immediate and significant hyperpolarisation in the Sertoli-cell membrane. The beta2-AR antagonist, butoxamine (1 x 10(-6) M), nullified isoproterenol action. The effect of the beta1 antagonist, metoprolol (1 x 10(-6) M), was light and non-significant. Sulphonylurea glibenclamide inhibition of the K+(ATP) channels suppressed isoproterenol action, and testosterone, while depolarising Sertoli-cell MP closing the K+(ATP) channels through the PLC/PIP2 pathway, reduced beta-AR agonist-induced hyperpolarisation. Also, polycations LaCl3 and spermine reversed isoproterenol's hyperpolarisation effect, probably depolarising the membrane potential through ionic interaction neutralising the action of isoproterenol on K+(ATP) channels. Adenylate cyclase agonist forskolin (0.1 microM) rapidly hyperpolarised Sertoli-cell MP, mimicking the isoproterenol effect. These effects indicate that isoproterenol's action on K+(ATP) channel probably involves the known signalling cascade beta-AR/Gs/AC/cAMP/PKA. These results suggest that the isoproterenol-induced hyperpolarisation is mediated by the opening of K+(ATP) channels in Sertoli cells. This beta-adrenergic hyperpolarisation might play a physiological role in the modulation of MP.

ATP-Binding Cassette Transporters↗
PubMed2005

Testosterone rapidly stimulates insulin release from isolated pancreatic islets through a non-genomic dependent mechanism.

The action of testosterone on the 45Ca2+ uptake and insulin secretion was studied in short-term experiments using isolated pancreatic islets of Langerhans. Testosterone (1 microM) stimulated 45Ca2+ uptake within 60 seconds of incubation on similar proportion than tolbutamide. Also, the hormone rapidly increased insulin release (34%; 180 seconds) on the presence of non-stimulatory concentrations of glucose (3 mM). Impermeant testosterone-BSA significantly stimulated the secretion of insulin to a lower percentage (10%). The action of the hormone is specific--neither 17beta-E2 nor progesterone stimulated insulin secretion in the presence of 3 mM glucose. The action of testosterone on insulin secretion was dose-dependent, and at rat plasma physiological concentrations (25 nM), stimulus was 17% (p < 0.05). In conclusion, in isolated pancreatic islets experiments, physiological concentration of testosterone rapidly stimulate insulin secretion and 45Ca2+ uptake through a membrane bound mechanism.

Animals↗
PubMed2004

Testosterone modulates K(+)ATP channels in Sertoli cell membrane via the PLC-PIP2 pathway.

Testosterone at physiological intratesticular concentrations induces a dose-dependent depolarisation and an increase in input resistance together with an increment of 45Ca2+ uptake in the Sertoli cells from seminiferous tubules of immature rat. Previous studies have implicated K(+)ATP channels in these testosterone actions. This study demonstrates that testosterone and sulphonylureas (glibenclamide and tolbutamide) depolarise the membrane potential, augment resistance and 45Ca2+ uptake in the Sertoli cells of seminiferous tubules from 10-15 day-old rats. These actions were nullified by the presence of the K(+)ATP channel opener diazoxide. The depolarisation was also observed with the impermeant bovine serum albumin-bound testosterone. Testosterone actions were blocked by both pertussis toxin and the phospholipase C (PLC) inhibitor U73122 implying the involvement of PLC - phosphatidylinositol 4-5 bisphosphate (PIP2) hydrolysis via G protein in testosterone actions. Polycations, including spermine and LaCl3, depolarised the membrane potential and increased the resistance. Hyperpolarisation caused by EGTA was reversed by LaCl3 and by the presence of testosterone. This last effect was nullified by the presence of U73122. All of the above results indicate that the action of testosterone on the Sertoli cell membrane is exercised on the K(+)ATP channels through PLC-PIP2 hydrolysis that closes the channel, depolarises the membrane, and stimulates 45Ca2+ uptake.

Adenosine Triphosphate↗
PubMed2004

Testosterone action on the Sertoli cell membrane: a KIR6.x channel related effect.

This review focuses on the fast testosterone actions on the cell membrane principally on the Sertoli cells, its predominant effect, i.e. an increase in [Ca+]i and the possibility of its actions being mediated by KIR (ATP) channels. The regulation of the K+ATP channels by phosphatidylinositol-4,5-bisphosphate depletion on the cell membrane as a result of the action of testosterone, its putative receptors, and the phospholipase C--phosphatidylinositol-4,5-bisphosphate pathway are discussed. The electrostatic interaction between anionic and cationic charges on the K+ATP modulation is also considered, in the light of testosterone's effect on phospholipase C--phosphatidylinositol-4,5-bisphosphate hydrolysis. Thus, the interaction of testosterone with its putative receptors, phospholipase C, phosphatidylinositol-4,5-bisphosphate, and K+ATP channels (or other KIR channels) in the membrane may be one of the mechanism of rapid testosterone's physiological action on some classes of cells.

ATP-Binding Cassette Transporters↗
PubMed2002

Rapid effect of testosterone on rat Sertoli cell membrane potential. Relationship with K+ATP channels.

For this study, we investigated the changes in the electrophysiological parameters of Sertoli cells in seminiferous tubules from 17 - 19 day-old rats induced by testosterone. Using conventional intracellular microelectrode techniques, we analysed the membrane potential and its input resistance. The entire tubules were fixed in a superfusion chamber continuously perfused with Krebs-Ringer bicarbonate buffer (pH 7.4, 32 degrees C). Visual control of cell impalement was achieved using an inverted microscope. The parameters analysed were passed through an amplifier and recorded using a proprietary software system. The topical application of testosterone (0.1 to 10 microM) led to an immediate (within 30 seconds) and significant dose-dependent depolarization of the membrane potential of the cell at all concentrations used. Concomitantly, the input resistance of the cell membrane underwent a significant increment at 30 seconds. These changes returned to resting values after washout. Topical administration of 17beta-estradiol or progesterone (10 microM) did not change the membrane potential. The addition of the K +ATP channel agonist diazoxide to the perfusion buffer nullified the depolarization effect of testosterone at 30 seconds. This result suggests that the immediate action of testosterone is associated with the closing of K +ATP channels, thereby depolarizing the membrane.

Adenosine Triphosphate↗
PubMed2001

Steroid profiles in cultured female jundiá, the Siluridae Rhamdia quelen (Quoy and Gaimard, Pisces Teleostei), during the first reproductive cycle.

The jundiá Rhamdia quelen (Quoy and Gaimard) is a teleost species from the Siluridae family and is an important species for aquaculture in temperate and subtropical climates. Gonad and blood tissue samples were taken from cultured jundiá females between 1998 and 1999. Plasma concentrations of 17beta-estradiol (E(2)), testosterone (T), 11-ketotestosterone (11-KT), 17-hydroxy-4-pregnene-3,20-dione (17-P), 17,20beta-dihydroxy-4-pregnen-3-one (17,20beta-P), and 17,20beta,21-trihydroxy-4-pregnen-3-one (20beta-S) were measured by radioimmunoassay and potential correlations with the stage of oogenesis and sexual maturation examined. During the experimental period two spawning episodes were observed. Plasma concentrations of E(2) increased progressively during oocyte development, simultaneously with the appearance of yolk vesicles and increasing amounts of deposited yolk. In female jundiá, the T peak occurred in October and was coincident with the peak in gonadosomatic index. Two distinct peaks of progestogens were detected, corresponding to the two spawning episodes, suggesting that one or more of these steroids might act as the "maturational-inducing steroid" in jundiá. Unusually large amounts of 11-KT were also measured in the plasma of mature jundiá females. The identity of 11-KT was confirmed by thin-layer chromatography. Although the profiles of the other steroids are compatible with the roles proposed for the action of these hormones in other teleosts, the role of 11-KT, normally found only in males, is unknown.

Animals↗
PubMed2001

Reduction of large neutral amino acid levels in plasma and brain of hyperleucinemic rats.

Neurological dysfunction is common in patients with maple syrup urine disease (MSUD). However, the mechanisms underlying the neuropathology of this disorder are poorly known. In the present study we investigated the effect of acute hyperleucinemia on plasma and brain concentrations of amino acids. Fifteen-day-old rats were injected subcutaneously with 6 micromol L-leucine per gram body weight. Controls received saline in the same volumes. The animals were sacrificed 30--120 min after injection, blood was collected and their brain rapidly removed and homogenized. The amino acid concentrations were determined by HPLC using orthophtaldialdehyde for derivatization and fluorescence for detection. The results showed significant reductions of the large neutral amino acids (LNAA) L-phenylalanine, L-tyrosine, L-isoleucine, L-valine and L-methionine, as well as L-alanine, L-serine and L-histidine in plasma and of L-phenylalanine, L-isoleucine, L-valine and L-methionine in brain, as compared to controls. In vitro experiments using brain slices to study the influence of leucine on amino acid transport and protein synthesis were also carried out. L-Leucine strongly inhibited [14C]-L-phenylalanine transport into brain, as well as the incorporation of the [14C]-amino acid mixture, [14C]-L-phenylalanine and [14C]-L-lysine into the brain proteins. Although additional studies are necessary to evaluate the importance of these effects for MSUD, considering previous findings of reduced levels of LNAA in plasma and CSF of MSUD patients during crises, it may be speculated that a decrease of essential amino acids in brain may lead to reduction of protein and neurotransmiter synthesis in this disorder.

Amino Acids↗
PubMed1992

Biochemical factors involved in the FSH action on amino acid transport in immature rat testes.

Testes of 15-day-old rats preincubated and incubated during different times with various doses of FSH (0.2; 2.0 and 20.0 mU/ml) in Krebs-Ringer bicarbonate (KRb) buffer increase the uptake of [14C] methylaminoisobutyric acid and [14C] aminoisobutyric acid. The basal and FSH stimulated amino acid transport occurs at absolute lower levels when the protein or glycoprotein synthesis is inhibited by cycloheximide (350 mumol/l) or tunicamycin (12 mumol/l) or when the microtubules are depolymerized with colchicine (1.2 mumol/l). However, the proportional increase of amino acid transport produced by FSH was maintained. The blockage of the voltage-dependent Ca++ channels with verapamil or the competitive inhibition of the bivalent ion channels by Co++ or Ni++ nullified the stimulatory action of FSH on the amino acid transport. Also quinine, that blocks the ATP dependent K+ channels, abolished the FSH action. It was concluded that in immature rat testes FSH stimulates amino acid transport through a mechanism involving voltage-dependent Ca++ channels and ATP-sensitive K+ channel.

Amino Acids↗
PubMed1992

Electrophysiological changes of Sertoli cells produced by the acute administration of amino acid and FSH.

Electrophysiological studies were carried out using seminiferous tubules of "Sertoli cell enriched testes" of rats irradiated in utero. Sertoli cells were inserted with glass microelectrodes in a superfusion chamber continuously perfused with KRb buffer. The topical application of FSH (4.0 mU/ml) produced a biphasic effect characterized by a rapid hyperpolarization (less than 3 s) followed by depolarization. The depolarizing effect of FSH was prolonged and potentiated in the presence of 5 mmol/l alpha-methylamino-isobutyric acid in the bath medium of the superfusion chamber. Verapamil, at a dose (250 mumol/l) that nullified the stimulatory action of FSH in the amino acid transport, suppressed the depolarizing effect of FSH. It was concluded that in immature rat testes FSH produces electrophysiological changes that mediate the stimulatory action of the amino acid transport.

Amino Acids↗
PubMed1991

In vitro effect of insulin on the uptake of glucose and alpha-aminoisobutyric acid in the thyroid gland of the turtle (Chrysemys dorbigni).

The presence of specific insulin binding sites in the thyroid gland of the turtle Chrysemys dorbigni has been previously reported. The purpose of the present work was to investigate the probable action of insulin on the uptake of [14C]deoxy-D-glucose ([14C]DG) and [14C]alpha-aminoisobutyric acid ([14C]AIB) in turtle (C. dorbigni) thyroid glands in vitro. Thyroid fragments (+/- 40 mg) were incubated at 25 degrees in Krebs-Ringer-bicarbonate buffer containing 0.2 microCi of [14C]DG or [14C]AIB without or with bovine insulin at different periods of time. The uptake of [14C]DG and [14C]AIB increased with incubation time. The presence of insulin (7 x 10(-6) M) in the incubation medium during 240 min did not modify the [14C]DG uptake. However if the thyroid fragments were previously incubated with insulin (60 min) and then incubated (240 min) with the same concentration of the hormone, the [14C]DG uptake was markedly increased. This stimulatory effect of insulin was dose-dependent. In similar experimental conditions, insulin also produced a significant increase in the uptake of [14C]AIB. Therefore, these findings strongly support the hypothesis that insulin might exert a direct action on the thyroid function.

Aminoisobutyric Acids↗
PubMed1985

Amino acid uptake and protein synthesis in rat testes: stimulation by dissociable factors.

Low concentration (25 mM) of sodium in the incubation medium produced a decrease in the amino acid uptake by the testis tissue as well as a reduction in the response to FSH. In this experimental condition, the basal protein synthesis and the stimulatory effect of FSH was not modified. The subcutaneous administration of testosterone to 15 day old rats increased the protein synthesis in the testis without any modification in the amino acid uptake. The addition of DBcAMP (1 mM) or glucose (14 mM) to the incubation medium increased the protein synthesis in the testes of immature (12 day-old) or prepubertal (32 day-old) rats respectively. The amino acid uptake was not modified. In immature rat testes, with protein synthesis completely inhibited by cycloheximide, the restoration of the sodium concentration in the incubation medium to normal levels produced an increase in amino acid uptake. The results above seem to indicate that protein synthesis and amino acid uptake in rat testes tissue can be regulated, at least partially, by different factors.

Amino Acids↗
PubMed1985

Identification of amino acid transport systems stimulated by FSH in rat testes.

Testes of 12-day-old rats preincubated (90 min) and incubated (60 min) with FSH in Krebs-Ringer bicarbonate buffer (KRB) increased their uptake of [14C]methylaminoisobutyric acid and [14C]aminoisobutyric acid. The hormone was ineffective in sodium-free KRB. Transport of [14C]aminoisobutyric acid in the presence of methylaminoisobutyric acid (MeAIB; 30 mmol/l) was not stimulated by FSH, and uptake of [14C]cycloleucine was not increased by FSH in any of the experimental conditions used. It was concluded that in immature rat testes FSH affects only the sodium-dependent system which permits the transport of MeAIB (transport system A) and has no effect on the sodium-independent system which prefers leucine (system L) or the sodium-dependent system which does not transport MeAIB (system ASC).

Amino Acids↗
PubMed1984

Insulin binding sites and action in the adrenal glands from normal and streptozotocin diabetic rats.

Insulin binding to rat adrenal glands was studied in vivo by i.v. injection of 125I-insulin either alone or together with an excess of unlabelled hormones (insulin, glucagon, prolactin, or growth hormone). In addition, isolated glands from normal or streptozotocin diabetic rats (STZ) were incubated in vitro with 125I-insulin and varying concentrations of unlabelled insulin. Both experiments showed specific binding sites in the adrenal glands. Furthermore the glands from diabetic rats bound more insulin than the glands from controls. The insulin stimulatory effect on the deoxyglucose (14C-DG) uptake was examined in isolated glands from normal and STZ rats. Adrenal glands from control rats exhibited higher basal values of 14C-DG uptake than glands from STZ rats. Insulin induced a stimulatory effect on the 14C-DG transport in glands from both control and diabetic rats. Adrenal glands from STZ rats responded much earlier to exogenous insulin, however the maximal stimulating concentration of the hormone did not restore the 14C-DG uptake to control values. The lowest concentration of insulin that increased the 14C-DG transport was 3 X 10(-8) M. The adrenal gland must be considered a target organ for insulin by both criteria, insulin specific binding and stimulatory action on the deoxyglucose transport.

Adrenal Glands↗
PubMed1981

Amino acid transport in rat Sertoli cell enriched testes: studies on the mechanism of action of follicle stimulating hormone.

1. The in vivo administration of ovine Follicle Stimulating Hormone (FSH) (15 mu g/rat, 1 h before measurements) enhanced the transport of Alpha [3-14C]-aminoisobutyric acid ([14C]-AIB) in Sertoli cell enriched testes of 10, 15 and 20-day-old rats. The effect was not observed in 5 or 25-day-old rats. 2. Increasing the intracellular concentration of cyclic AMP by means s cholera toxin, exogenous cyclic AMP or 1-methyl-3-isobutylxanthine did not change either the control or the FSH-stimulated uptake of [14C]-AIB. 3. The inhibition of glycoprotein synthesis by tunicamycin decreased the uptake of [14C]-AIB in controls and significantly reduced (24%) the effect of FSH on [14C]-AIB transport in Sertoli cell enriched testes.

Adenylyl Cyclases↗
PubMed1977

Changes in protein kinase activity in rat testes during development.

Protein kinase activity in rat testes remained fairly constant from day 16 1/2 of embryonic life up to 10 days after birth. At the 21st postnatal day a nadir of activity was observed, and after an increase at 35 days of age a decrease in activity at 60 days was seen. The enzyme reached maximal specific activity in the testes of 90-day-old rats.

Animals↗