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PubMed1986

Thiol regulation of depletion-transformation and release of prolactin by the pituitary of the lactating rat.

We investigated the possibility that thiol-disulfide interchange mechanisms are involved in depletion-transformation (loss of tissue PRL detectability) and release of PRL from adenohypophyses (AP) of lactating rats. The influence of pH, bicarbonate, and Triton X-100 as well as thiol-related compounds on these processes was assessed. Tissue PRL was depleted-transformed by the use of three different conditions: 1) 30 min of suckling after 8 h of nonsuckling; 2) in vitro incubation of APs for 2 h; or 3) in vivo cysteamine (CSH) treatment. Lactating rats nonsuckled for 8 h served as controls (no depletion-transformation). The depletion-transformation phenomenon was unchanged by extraction with Tris-HCl-0.1% Triton X-100 buffers but reversed either by extraction with bicarbonate buffer (pH 8.2 or 9.7) or by incubation of pH 8.2 homogenates for 3 h at 37 C. Reduced glutathione (GSH) added to these homogenates further enhanced PRL detectability. At pH 6.5, however, incubation with or without GSH had the opposite effect and decreased PRL detectability. In AP incubations, depletion was increased in a dose- and time-dependent fashion by the aminothiol CSH, and by GSH, dithiothreitol, or mercaptoethanol but not sodium ascorbate. These agents also inhibited PRL release. Similar results were obtained after injection of CSH (20-120 mg/kg BW) 4 h before death. Depletion and release of PRL in incubated APs were prevented by iodoacetamide and N-ethylmaleimide (0.1-5 mM); GSH or CSH counteracted these effects. In contrast to the alkylating agents, oxidized glutathione and 5,5'-dithio-2-nitrobenzoic acid inhibited PRL depletion but stimulated PRL release. Thus, thiols and aminothiols may preferentially lead to depletion-transformation of PRL, whereas disulfides may inhibit depletion and facilitate PRL release. Although in some experiments increased depletion was dissociated from increased release, nonetheless the data support the concept that shifts in PRL detectability during depletion-transformation, repletion, and release involve thiol-disulfide interchange mechanisms.

Animals↗
PubMed1986

Reversal by thiols of dopamine-, stalk-median eminence-, and zinc-induced inhibition of prolactin transformation in adenohypophyses of lactating rats.

Depletion-transformation of PRL is a decrease in tissue PRL detectability which precedes and may often be required for increased PRL release. The present studies were designed to determine whether thiol-disulfide interchange mechanisms may be involved in PRL transformation and release by the pituitary of the lactating rat. Thirds of 8-h nonsuckled lactating rat adenohypophyses were incubated with or without thiols (reduced glutathione, the aminothiol cysteamine, or mercaptoethanol), in the presence of known inhibitors of transformation and release such as dopamine (DA), stalk median eminence (SME) extract, or Zn++. PRL concentrations in pre- and postincubated tissues, as well as the amount of released PRL, were determined by polyacrylamide gel electrophoresis and densitometry. In 30-min incubations without additions, 12-22% of the tissue PRL was depleted; however, in the presence of 17-50 microM DA, all doses of SME extracts tested (0.5-2.0 eq), or 0.1 mM Zn++, depletion was partially or totally prevented and PRL release was inhibited 25-60%. On the other hand, when thiols were added in addition to the above agents, a complete, dose-related, restoration of PRL depletion was obtained. In 120-min incubations, thiols similarly reversed the effects of 0.05 mM DA on depletion, but thiols did not reverse the inhibition of PRL release caused by DA, SME, or Zn++. Other data indicate that thiols alone may inhibit rat PRL release and also facilitate or induce PRL depletion; in bovine PRL granules, thiols reverse Zn++ inhibition of PRL release and detectability. These data suggest that thiol-disulfide interchange reactions may be importantly involved in both depletion-transformation and in secretion. The precise thiol sensitivity of the two processes does not appear identical, secretion being more sensitive to DA and less sensitive to thiols than depletion-transformation.

Animals↗
PubMed1999

Characterization of dopamine receptor subtypes involved in experimentally induced gastric and duodenal ulcers in rats.

There are conflicting reports about the role of dopamine in gastric and duodenal ulcers. This investigation was undertaken to characterize the specific subtypes of dopamine receptor involved in gastric and duodenal ulceration. Administration of dopamine D1 agonist fenoldopam and dopamine D2 antagonist sulpiride elicited a significant decrease in acid secretion, total acid output, pepsin output and histamine content in the gastric juice, and reduced ulcer-index values, in pylorus-ligated rats. However, dopamine D1 receptor antagonist SCH 39166 ((-)-trans-6,7,7a,8,9,13b-hexahydro-3-chloro-2-hydroxy-N-methyl-5H -benzo (d) naptho -(2,1-b) azepine) and the D2 receptor agonist quinpirole led to significant augmentation of these parameters compared with respective controls. In the restraint plus water-immersion stress model the score for intraluminal bleeding and the cumulative gastric lesion length was significantly lower for rats treated with fenoldopam and sulpiride. The opposite effects were observed after pretreatment of rats with SCH 39166 and quinpirole. In the cysteamine-induced duodenal ulcer model the mean ulcer area and the score for intensity were significantly lower for fenoldopam and sulpiride and higher for SCH 39166 and quinpirole. Our data suggest that the dopamine D1 and D2 receptors have opposite effects on gastric and duodenal ulcers. Whereas stimulation of dopamine D1 receptors inhibits the formation of gastric and duodenal ulcers, stimulation of dopamine D2 receptors has a pro-ulcerogenic effect.

Animals↗
PubMed1992

Studies on chemical protectors against radiation. XXXV. Effects of radioprotective Chinese traditional medicines on radiation-induced lipid peroxidation in vivo and in vitro.

The fluctuation of lipid peroxidation (LP) in 9 tissues was investigated in mice for 7 d after whole-body X-irradiation with a lethal dose of bone marrow death. LP increased significantly in bone marrow, thymus, spleen and liver following irradiation, and slightly in brain and testis, but not in blood plasma, submaxillary gland or kidney. The effects of 7 radioprotective Chinese traditional medicines (CTMs) and cysteamine (MEA) on the radiation-induced LP in 4 tissues were studied by i.p. injection before or after irradiation and their LP content in tissues was measured 2 d after irradiation. Most CTMs showed significant inhibition of radiation-induced LP in bone marrow and liver, especially when injected prior to irradiation. Some CTMs also showed such inhibition in spleen. MEA only inhibited the increase of LP in liver when injected before irradiation, but enhanced the increase of LP in spleen. None of these radioprotectors including MEA was recognized to inhibit radiation-induced LP in thymus. The in vitro experiments were carried out using mouse liver microsomal suspensions (MS). The MS were prepared from normal (non-irradiated) mice. Each of the 8 radioprotectors was added to MS before or after irradiation and then post-irradiation-incubated at 37 degrees C. All markedly inhibited radiation-induced LP if added before irradiation, but were slightly less effective if added after.

Animals↗
PubMed1991

Pharmacological studies on lappaconitine: antinociception and inhibition of the spinal action of substance P and somatostatin.

The pain response of mice to an injection of 0.5% formalin into the dorsal surface of a hindpaw is biphasic, with a first phase lasting for 5 min and a second phase lasting from 10 to 30 min post-injection. Intrathecal (i.t.) injection of [D-Pro2, D-Trp7,9]-substance P inhibited the first phase, and i.t. cysteamine inhibited the second phase. Lappaconitine (LA) and morphine (MOR) inhibited both phases equally in a dose-dependent manner. Diclofenac inhibited both phases, but the second phase was inhibited by lower doses. An i.t. injection of substance P (SP) or somatostatin (SOM) produced a characteristic behavioral response (scratching, biting, and licking). This behavioral response to SP and SOM was inhibited by s.c., intracerebroventricular (i.c.v.), or i.t. injection of MOR. In contrast, LA inhibited the SP- and SOM-induced response when injected s.c. or i.c.v., but had no effect when injected intrathecally. These results indicate that LA may act supraspinally to inhibit the transmission of nociceptive information by SP and/or SOM.

Aconitine↗
PubMed1994

A screening concept based on a hypothesis led to the development of a putative cognitive enhancer that stimulates penile erection.

Starting from the hypothesis that drugs which specifically activate the hippocampal cholinergic nerve activity may ameliorate memory impairments, we carried out a series of evaluations for a novel cognitive enhancer using enhancement of penile erection as a sign of cholinergic activation, and found FR64822. The compound facilitated penile erection in naive rats, and it ameliorated scopolamine-induced amnesia of rats in passive avoidance tasks with bell-shaped dose-response curves, while it dose-dependently reduced body weight gain in Zucker fatty rats. Pretreatment with sulpiride (32 mg/kg, p.o.) hardly affected the former two activities, but significantly reduced the anorectic activity in Zucker rats. Further evaluation of FR64822 derivatives characterized a second compound, FR121196, which induces penile erection and memory enhancement, but not body weight reduction. Memory enhancing and erection stimulating activities of FR121196 were abolished in rats treated with either cysteamine (200 mg/kg, s.c.), a somatostatin depletor, or lesioning of the serotonergic raphe nuclei. Thus, classic whole animal studies based on a hypothesis proved to be efficient for reaching our objective, the discovery of a new drug. They also gave us insight into the common somatostatinergic and serotonergic mechanisms underlying penile erection and memory improvement.

Animals↗
PubMed1997

Single-strand breaks in oligodeoxyribonucleotides induced by fission neutrons and gamma radiation and measured by gel electrophoresis: protective effects of aminothiols.

The technique of high-resolution gel electrophoresis using oligodeoxyribonucleotides of known composition as model systems, offers a simple quantitative estimate of DNA damage in aqueous solution induced by ionizing radiation. The fraction of damaged DNA can be quantitatively defined in terms of the increased electrophoretic mobilities of the damaged oligonucleotides, relative to the mobility of the unirradiated and intact oligonucleotides. The usual direct strand breaks can be observed at gamma-ray dosages of 200 Gy. However, at a gamma-ray dosage of 400 Gy, only a broad background, attributed to heterogeneously and multiply damaged oligonucleotide fragments with overlapping and varying electrophoretic mobilities, can be distinguished. On the other hand, individual bands due to resolvable DNA fragments are evident even at dosages as high as 400 Gy for fission neutrons. When double-stranded oligonucleotides are exposed to gamma-ray dosages of 200 Gy, the fraction of damaged DNA approaches 30-40%. This damage can be almost completely suppressed (> 99%) if the irradiations are conducted in aqueous solutions in the presence of 0.5-1.0 mM concentrations of the thiols cysteamine or 3-(3-methylaminopropylamino)propanethiol (WR-151326). The rate constant of reaction of OH radicals with small double stranded oligonucleotides 16 base pairs long, KDNA, is found to be closer to the diffusion-controlled value (> 3 x 10(9) M-1 s-1) than the magnitudes of KDNA for the higher molecular weight, native DNA reported in the literature. These observations suggest that oligonucleotides represent more simple model systems than native DNA in solutions for studying the mechanisms of radioprotection exerted by thiols of different structures.

Amino Acids↗
PubMed1992

An effective method for the synthesis of neoglycoproteins and neogangliosideproteins by use of reductively aminated sulfhydryl-containing carbohydrate conjugates.

A highly effective method for the synthesis of neoglycoconjugates has been developed. The technique is based on two steps. First, a sulfhydryl group is introduced into the carbohydrate by reductive amination with cysteamine, and secondly the sulfhydryl group carrying carbohydrate is coupled to a protein or carrier via a disulfide bridge. The method was used to couple sialic acid-containing carbohydrates such as N-acetylneuraminyllactose and the carbohydrate moieties of gangliosides (GM1, GM3 and GD1b) to bovine serum albumin. Biological functionality of the generated GM1- and GD1b-neoglycoprotein was demonstrated by a choleratoxin-binding assay and an immunoassay, respectively. The applicability of neoglycoconjugates for the quantification of gangliosides in solution by a competitive assay is shown.

Amination↗
PubMed1986

Cholinergic agonist and antagonist drugs modulate the growth hormone response to growth hormone-releasing hormone in the rat: evidence for mediation by somatostatin.

Recently, data have been presented showing that muscarinic cholinergic agonists or antagonists can modulate, in opposite ways, GH-releasing hormone GHRH)-induced GH release in man. The aim of the present study was, first, to confirm these findings in the rat and, secondly, if confirmed, to investigate the mechanism(s) subserving the effect of cholinergic drugs. In adult male rats bearing chronic indwelling atrial cannulae, pretreatment with the cholinergic antagonists pirenzepine (0.5 mg/kg, i.v.) or atropine (0.5 mg/kg, i.v.) significantly reduced the rise in plasma GH induced by GHRH (2 micrograms/kg, i.v.), while pretreatment with the cholinergic agonist pilocarpine (3 mg/kg, i.v.) potentiated it. In rats with hypothalamic somatostatin (SRIF) depletion, i.e. rats with anterolateral deafferentation of the mediobasal hypothalamus or rats treated with cysteamine, the modulatory action of cholinergic drugs on the neuroendocrine effect of GHRH was completely lacking. In these two experimental models, an antiserum raised against SRIF failed to elicit a rise in plasma GH and measurement of hypothalamic SRIF content revealed a clear-cut reduction of the neuropeptide. Atropine (1 mumol/l) and pilocarpine (1 mumol/l), added to pituitary cells in vitro, failed to alter GHRH-induced GH release. The present results indicate that muscarinic cholinergic agonists and antagonists modulate GHRH-induced GH release in the rat and suggest that the effect of cholinergic modulation takes place through SRIF.

Afferent Pathways↗
PubMed1988

Involvement of the somatostatin and cholinergic systems in the mechanism of growth hormone autofeedback regulation in the rat.

The involvement of the cholinergic system in GH secretion has recently acquired increasing importance. Data have been presented suggesting that in rats the effect of cholinergic modulation on GH secretion takes place through inhibition or stimulation of hypothalamic somatostatin (SRIF) release. To investigate further the significance of cholinergic-SRIF link and its role in the regulation of GH secretion, the action of cholinergic agonist and antagonist drugs in the GH short-loop feedback mechanism mediated by SRIF was investigated. Intracerebroventricular (i.c.v.) infusion of 0.2 or 2.0 micrograms GH/rat into the lateral brain ventricle of adult male rats induced a significant reduction in the GH-releasing hormone (GHRH; 2 micrograms/kg, i.v.)-induced peak GH rise, but only the 2.0 micrograms dose reduced also the GH-integrated area after administration of GHRH. This effect was absent after central administration of 20.0 micrograms GH/rat, due probably to leakage of some GH from the cerebral ventricle into the systemic circulation. Pretreatment with cysteamine (300 mg/kg, s.c.), a known depletor of hypothalamic SRIF, or with anti-SRIF serum (0.5 ml/rat) completely counteracted the lessening of the GH response to GHRH induced by 2.0 micrograms GH injected i.c.v. Similarly, pretreatment with the cholinergic agonist pilocarpine (3 mg/kg, i.v.) completely antagonized the inhibitory effect of central infusion of GH on the GHRH-induced GH response. Atropine (1.0 mg/kg, i.v.), a muscarinic cholinergic antagonist, strikingly inhibited the GHRH-induced GH rise, but when given in combination with i.c.v. infusion of GH there was no additive inhibitory effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Cysteine analogues potentiate glucose-induced insulin release in vitro.

In rat pancreatic islets, cysteine analogues, including glutathione, acetylcysteine, cysteamine, D-penicillamine, L-cysteine ethyl ester, and cysteine-potentiated glucose (11.1 mM) induced insulin secretion in a concentration-dependent manner. Their maximal effects were similar and occurred at approximately 0.05, 0.05, 0.1, 0.5, 1.0, 1.0 mM, respectively. At substimulatory glucose levels (2.8 mM), insulin release was not affected by these compounds. In contrast, thiol compounds, structurally different from cysteine and its analogues, such as mesna, tiopronin, meso-2,3-dimercaptosuccinic acid (DMSA), dimercaprol (BAL), beta-thio-D-glucose, as well as those cysteine analogues that lack a free-thiol group, including L-cystine, cystamine, D-penicillamine disulfide, S-carbocysteine, and S-carbamoyl-L-cysteine, did not enhance insulin release at stimulatory glucose levels (11.1 mM); cystine (5 mM) was inhibitory. These in vitro data indicate that among the thiols tested here, only cysteine and its analogues potentiate glucose-induced insulin secretion, whereas thiols that are structurally not related to cysteine do not. This suggests that a cysteine moiety in the molecule is necessary for the insulinotropic effect. For their synergistic action to glucose, the availability of a sulfhydryl group is also a prerequisite. The maximal synergistic action is similar for all cysteine analogues tested, whereas the potency of action is different, suggesting similarity in the mechanism of action but differences in the affinity to the secretory system.

Acetylcysteine↗
PubMed1987

Disposition of new sulphur-containing 2-(chloroethyl)nitrosoureas in rats.

N'-(2-Chloroethyl)-N-[2-(methylsulphinyl) ethyl] and N'-(2-chloroethyl)-N-[2-(methylsulphonyl) ethyl]-N and N'-nitrosoureas (CMSOEN1, CMSO2EN1, CMSOEN2 and CMSO2EN2) are new nitrosoureas derived from cysteamine. Two of them (CMSOEN2 and CMSO2EN2) have shown excellent efficacy against several murine tumours. The inactive agents (CMSOEN1 and CMSO2EN1) display low alkylating activity but high carbamoylating activity. In contrast, the active agents (CMSOEN2 and CMSO2EN2) are strong alkylating agents but relatively weak carbamoylators. The disposition of CMSOEN2 and CMSO2EN2 was studied in rat, using two differently labelled species of each compound, administered i.v. (60 mumol/kg). Plasma disappearance, tissue distribution (with the exception of the brain) and elimination of radioactivity are similar for the two compounds similarly labelled. In contrast, these parameters are strongly influenced by the label position used. Plasma disappearance of unchanged CMSOEN2 and CMSO2EN2 follows a first-order kinetic process with the same half-life for both compounds (30-31 min). More unchanged CMSO2EN2 is found in brain compared to its congener (55 nmol/g and 37 nmol/g respectively at five minutes). This is most likely the consequence of the higher lipophilic character of the former compound. The breakdown product 2-chloroethanol was identified in plasma.

Alkylation↗
PubMed1987

Ocular changes in long-term evolution of infantile cystinosis.

Infantile cystinosis is an autosomal recessive lysosomal disorder of aminoacid metabolism leading to a storage of cystine crystals in the cells of many tissues, but mainly in the kidney and the eye. The ocular symptoms and long term evolution were studied in a series of 25 patients at the Enfants Malades Hospital. The follow-up over 26 years demonstrated that infantile cystinosis affected mainly corneal and retinal epithelium just as it affected the kidney epithelium. Corneal involvement was a constant finding after one year of age. It induced photophobia, which appeared between three and four years when a superficial punctate keratopathy appeared. A characteristic retinopathy was observed as early as three years of age. It was constantly present at seven years of age and caused loss of vision. When ERG results were compared to the most recent measurement of visual acuity, a correlation was observed between retinopathy and visual defect. For this reason, no corneal grafts were performed. The use of topic cysteamine appeared promising but no definitive conclusions could be made.

Adolescent↗
PubMed1977

Acetaminophen.

Acetaminophen is an effective mild analgesic and antipyretic agent. In double-blind, controlled experimental pain studies of short duration, acetaminophen is superior to placebo and produces analgesia comparable to that produced by aspirin. The frequency of adverse reactions to therapeutic doses of acetaminophen is low, as is that of aspirin. Overdosage with acetaminophen, however, may result in irreversible hepatotoxicity. Since clinical manifestations of intoxication can be of slow onset, physicians may tend to delay initiation of definitive therapy. Intravenous cysteamine, and possibly oral methionine, appear to be effective in preventing hepatotoxicity if they are administered with 10 h of drug ingestion. Physicians should be aware of the potential danger of acetaminophen overdosage and alerted to its clinical manifestations.

Acetaminophen↗
PubMed1980

Genetic disorders of glutathione and sulfur amino-acid metabolism. New biochemical insights and therapeutic approaches.

Important insights have recently been derived from studies of inborn human defects of sulfur metabolism. Metabolic lesions responsible for homocystinuria have been elucidated, with possible implications for understanding atherogenesis in the general population. The cause of cystinosis remains enigmatic, but important information has been gained on the origin of some stored cystine from degraded protein. Cysteamine and ascorbic acid deplete the cystine content of cystinotic fibroblasts in vitro, and clinical trials with these agents have been undertaken. Studies of patients with glutathione synthetase deficiency have provided new understanding of the roles of glutathione as in antioxidant and as a modulator of microtubule-related processes. Studies of patients with this disorder and glucose-6-phosphate dehydrogenase deficiency, in which the capacity to maintain glutathione in the reduced state is compromised, indicate that pharmacologic doses of vitamin E can correct certain functional consequences of an inadequate supply of reduced glutathione both in erythrocytes and polymorphonuclear leukocytes. Much remains to be learned about the mechanisms of membrane damage in these states of enhanced oxidative susceptibility.

Amino Acid Metabolism, Inborn Errors↗
PubMed2000

Role of cytoprotectants and nitric oxide inhibition in nonsteroidal anti-inflammatory drug-induced gastroduodenal injury in the rat.

BACKGROUND AND PURPOSE: Nonsteroidal anti-inflammatory drugs (NSAIDs) induce gastroduodenal injury and ulceration. The pathogenesis is uncertain, although reductions in cytoprotective prostaglandins and nitric oxide (NO) have been proposed. The effects of several cytoprotective agents on inhibition of gastroduodenal ulcerogenesis induced by CI-987, a novel NSAID, were evaluated in Wistar rats. METHODS: Male Wistar rats were given CI-987 orally (p.o.) at a dosage of 300 or 450 mg/kg of body weight or subcutaneously (s.c.) (3 x 50 mg/kg), alone or with misoprostol pretreatment (2 x 1 mg/kg, p.o.). In a second experiment, rats were pre-treated with 2 ml of gelusil p.o., 500 mg of sucralfate/kg, p.o., 100 mg of ranitidine/kg s.c., or 200 mg of N omega-nitro-L-arginine methyl ester (L-NAME)/kg, s.c.. Duodenal injury was induced by administration of 450 mg of CI-987/kg, p.o., 3 x 50 mg of CI-987/kg, s.c., or 300 mg of cysteamine/kg, s.c. Animals were euthanized within 24 to 48 hours, and the gastrointestinal tract was examined for evidence of gross or microscopic change. RESULTS: The L-NAME significantly reduced the incidence and severity of gastroduodenal injury induced by CI-987 and cysteamine. Prostaglandin ameliorated duodenal lesions induced by CI-987 given s.c., and Gelusil, ranitidine, and sucralfate were without effect on duodenal lesions induced by NSAID. CONCLUSIONS: Preemptive blockade of NO synthase is important in preventing NSAID-induced duodenal injury in rats. Inhibition of cytoprotective prostaglandins and enhanced acid-induced damage are unlikely to be primary mechanisms underlying NSAID-induced duodenal injury in rats.

Administration, Oral↗
PubMed1975

13C NMR or coenzyme A and its constituent moieties.

Natural abundance 13C nuclear magnetic resonance spectra, in D2O, were obtained for the following: pantoyl lactone, beta-alanine, cysteamine hydrochloride, cystamine dihydrochloride, calcium pantothenate, beta-aletheine oxalate, pantetheine, pantethine, pantetheine 4'-phosphate, oxypantetheine 4'-phosphate, desulfopantetheine 4'-phosphate, N-acetyl-aminodesthiopantetheine 4'-phosphate, adenosine 2',5'-diphosphate, adenosine 3',5'-diphosphate, and coenzyme A. A complete assignment of the 13C chemical shifts in the NMR spectrum of CoA is reported. Comparison of spectra indicates that CoA most likely exists in an extended conformation.

Adenosine Diphosphate↗
PubMed2001

Taurine and hypotaurine in spermatozoa and epididymal fluid of cats.

Taurine and hypotaurine have been found in spermatozoa and seminal plasma of numerous species and are known to have beneficial effects on sperm characteristics in mammals. Taurine is considered an essential dietary constituent in cats. Dietary deficiency has been associated with a range of serious clinical disorders. Quantification of taurine and hypotaurine in the genital tracts of male cats has not been reported. In this study, the concentrations of taurine and its precursors were measured in serum, spermatozoa, epididymal fluid and seminal plasma from cats. The concentrations of taurine measured in serum samples confirmed that the cats were not deficient in taurine. Significant amounts of taurine and hypotaurine were found in spermatozoa, seminal plasma and epididymal flushing fluid. Hypotaurine was not detected in serum samples. These results indicate that hypotaurine may be synthesized in cat testes or epididymides. Cysteamine was not detected in any of the samples.

Animals↗