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PubMed2003

Glutathione synthesis during in vitro maturation of buffalo (Bubalus bubalis) oocytes: effects of cysteamine on embryo development.

It was demonstrated that cysteamine supplementation during in vitro maturation (IVM) improves embryo development by increasing glutathione (GSH) synthesis in several species. An improved developmental competence of oocytes matured in the presence of cysteamine was also recorded in buffalo species. The purpose of this work was to investigate (1) if glutathione is de novo synthesized during in vitro maturation of buffalo oocytes, (2) if cysteamine improves buffalo embryo development via an increase in GSH synthesis, and (3) if the inhibition of glutathione synthesis by buthionine sulfoximide (BSO), in the presence or absence of cysteamine, affects subsequent embryo development and GSH synthesis.Cumulus-oocytes complexes (COCs), recovered from slaughtered animals, were matured in vitro in TCM199+10% fetal calf serum (FCS), 0.5 microg/ml FSH, 5 microg/ml LH and 1 microg/ml 17-beta-estradiol in the absence or presence of cysteamine (50 microM), with or without 5mM BSO. Glutathione content was measured by high-performance liquid chromatography (HPLC) and fluorimetric analysis in immature oocytes and in oocytes matured in the different experimental conditions. In a second experiment, the mature oocytes were in vitro fertilized and cultured for 7 days in order to assess development to blastocysts (BLs). It was demonstrated that buffalo oocytes synthesize glutathione during in vitro maturation and that cysteamine increases glutathione synthesis. Furthermore, the promoting effects of cysteamine on embryo development and GSH synthesis were neutralized by buthionine sulfoximide. These results indicate that glutathione plays a critical role on buffalo embryo development.

Animals↗
PubMed1976

Controlled trial of cysteamine in treatment of acute paracetamol (acetaminophen) poisoning.

A randomised controlled trial of the use of intravenous cysteamine in the treatment of severe paracetamol poisoning has been performed. Thirty-eight patients presenting 3-17 h after ingestion were admitted to the trial; of these eighteen received cysteamine. Two patients died from hepatic failure, one in each treatment group. Analysis of the series as a whole showed no advantage of cysteamine in preventing biochemical abnormalities of liver function except for aspartate aminotranferase and serum ferritin levels, which were significantly less after cysteamine therapy. Separate analysis of the patients treated within 9 h of paractamol ingestion and of those treated 9-17 h after paracetamol ingesion similarly showed no definite advantage of cysteamine. Histological evidence of liver damage showed a possible beneficial effect of cysteamine. Cysteamine therapy did not prevent renal or pancreatic damage.

Acetaminophen↗
PubMed1999

Intrahippocampal injections of cysteamine improve the retention of a bar-pressing task in mice.

Cysteamine was used as a tool aimed at investigating the role of central somatostatin (SS-14) and was shown to modulate learning in a task-dependent manner. However, direct arguments have not yet been provided to support the hypothesis that impairments and facilitation of learning produced by cysteamine are both mediated by the hippocampus. Mice were given daily intrahippocampal injections of artificial cerebrospinal fluid (CSF) or cysteamine at doses of either 2.5 microg/0.2 microl or 25 microg/0.2 microl 1 h prior to each learning session of a bar-pressing task, for which the acquisition was previously shown to be improved by systemic injections. The results showed that, with respect to CSF, the mice injected with cysteamine learned the bar pressing task faster whereas no evidence of changes in locomotor activity was provided. Moreover, the results showed that retention was specifically increased in the two groups injected with cysteamine. It is argued that the action of cysteamine on the hippocampus is sufficient to modulate specifically learning-memory processes in a task-dependent manner. In conclusion, the blockade of some hippocampal information processing function by cysteamine is discussed to understand the bidirectional effects of drugs on learning and memory.

Animals↗
PubMed1996

Effect of the sulfhydryl compound cysteamine on gamma-radiation-induced mutations in double-stranded M13 DNA.

Sulfhydryl compounds can protect DNA against free-radical-induced DNA damages not only by scavenging of radicals, but also by chemical non-enzymatic repair or modification of such damages by hydrogen-donation. To investigate the influence of chemical repair and modification on mutations, induced by gamma-radiation-generated free radicals (.OH, .H), phosphate-buffered aqueous solutions of double-stranded (ds) M13 DNA were exposed to gamma-rays under N2 in the presence of 5 mM cysteamine. The exposed DNA was subsequently transfected to wild-type E. coli and mutations in the mutational target were characterized. This target in fact contains three different target sequences, i.e., the lac promoter/operator, the lacZ alpha gene and a 144 bp inframe insert. The mutation spectrum obtained was compared with those in the absence of cysteamine under N2 and N2O. In the latter case, the ratio of .OH and .H available for reacting with DNA is about the same as under N2 + cysteamine. The results show that chemical repair and/or modification by cysteamine of potentially lethal lesions takes place, leading to a much higher survival of ds M13 DNA in the presence of cysteamine than could be expected on basis of scavenging of .OH and .H alone. This higher survival appeared to be accompanied with a higher mutation induction. However, the N2 + cysteamine mutation spectrum shows a remarkable resemblance with the N2O-spectrum. This holds for the total mutation target, as well as each of the three targets, although the mutations obtained in each of the three targets under the same irradiation conditions are quite different. Thus, it can be concluded that cysteamine is mainly effective on radiation-induced potentially lethal DNA lesions, and not so much on (pre)mutagenic damages. Moreover, the type of mutation appeared to be strongly dependent on the mutational target sequence.

Bacteriophage M13↗
PubMed1993

Improved renal function in children with cystinosis treated with cysteamine.

BACKGROUND: The lysosomal storage disease cystinosis results in renal failure at approximately 10 years of age. Although oral cysteamine therapy is recognized to preserve kidney function, the extent of renal benefit has not been determined. METHODS: Between 1960 and 1992, we determined 24-hour creatinine clearances in 76 children with cystinosis during 1081 admissions to the National Institutes of Health. Seventeen children were considered to have received adequate treatment with cysteamine, since they had depletion of cystine from leukocytes and began therapy before the age of 2 years; treatment lasted a mean of 7.1 years. Thirty-two children were considered to have received partial treatment, since they had poor compliance with therapy or began treatment after the age of 2; treatment lasted a mean of 4.5 years. Twenty-seven children were followed in the era before cysteamine therapy and thus never received cysteamine. RESULTS: Of the 27 children who never received cysteamine, 16 were followed at the National Institutes of Health until renal failure occurred; their mean (+/- SD) creatinine clearance was 8.0 +/- 4.8 ml per minute per 1.73 m2 of body-surface area at a mean age of 8.3 +/- 1.9 years. Of the 17 children who received adequate treatment, none had renal failure; their mean creatinine clearance was 57 +/- 20 ml per minute per 1.73 m2 at 8.3 +/- 3.8 years of age. The mean creatinine clearance of the children who received partial or adequate treatment with cysteamine increased with age up to the age of five years and then declined linearly with age at a normal rate. For the children who received adequate treatment, the mean creatinine clearance was predicted to reach 0 ml per minute per 1.73 m2 at the age of 74 years, as compared with 20 years of age for the children who received partial treatment. With no therapy, the mean creatinine clearance reaches 0 ml per minute per 1.73 m2 at 10 years of age. CONCLUSIONS: Children with cystinosis who are treated early and adequately with cysteamine have renal function that increases during the first five years of life and then declines at a normal rate. Patients with poorer compliance and those who are treated at an older age do less well.

Child↗
PubMed2002

In vitro maturation and glutathione synthesis of porcine oocytes in the presence or absence of cysteamine under different oxygen tensions: role of cumulus cells.

The present study was conducted to evaluate the effect of cumulus cells on the in vitro maturation (IVM) and glutathione (GSH) synthesis of porcine oocytes cultured in the presence or absence of cysteamine under different oxygen tensions, and on their subsequent male pronucleus formation after in vitro fertilization (IVF). Cumulus-oocyte complexes (COCs) and cumulus-denuded oocytes (DOs) were cultured for 45 h in modified TCM-199 supplemented with or without 150 microM cysteamine under a humidified atmosphere of 5% CO2 in air (20% O2) or 5% CO2, 5% O2 and 90% N2. When cultured in medium supplemented with cysteamine under 20% O2 tension, the rates of COC maturation to the metaphase II (MII) stage were significantly higher than those of DOs (P<0.05). Regardless of the addition of cysteamine and oxygen tension, the rates of male pronucleus formation in COCs after IVM and IVF were significantly higher than in DOs (P<0.05). The GSH content of oocytes was significantly increased by the addition of cysteamine to the maturation medium (P<0.05), with significantly higher GSH content in COCs than in DOs (P<0.05). However, the GSH content of COCs and DOs was not significantly different when cultured in medium without cysteamine. These results indicate that cumulus cells play an important role in nuclear maturation to MII, GSH synthesis in porcine oocytes cultured in the presence of cysteamine, and subsequent male pronucleus formation after IVF.

Animals↗
PubMed1987

Development and significance of cysteamine and propionitrile models of duodenal ulcer.

Cysteamine is widely used in rodents to induce duodenal ulcer. Herein, the pathogenesis of duodenal ulceration in its earliest stages was reviewed using findings from cysteamine- and propionitrile-induced duodenal ulcer in rodent models, especially taking into account changes in the secretion of gastric acid, duodenal and pancreatic bicarbonate as well as gastroduodenal motility. The effect of cysteamine-HCl in inducing ulcers in rats is circadian rhythm-dependent. The effect is greatest from just before the end of diurnal rest to just after the start of nocturnal activity. The chronobiologic effect may be in part due to the circadian rhythm-dependent increased gastric acid production from cysteamine. Titratable acidity was found to be twice as great in the gastric juice of rodents when cysteamine was given by injection at 2000 (just after the start of nocturnal activity) in comparison to when given at 0800 or 1200 (at the beginning or middle span of daily rest). Further studies have shown that adrenalectomy of rats 7 days before cysteamine administration obliterated the observed circadian susceptibility to ulcer formation. Duodenal ulceration, at least in the cysteamine model, appears to be under chronobiologic neuroendocrine control or influence, seemingly mediated by the adrenal glands.

Animals↗
PubMed1996

In vitro inhibition of the replication of human immunodeficiency virus type 1 by beta-mercaptoethylamine (cysteamine).

This study investigates the effects of cysteamine alone and in association with zidovudine or didanosine on the replication of human immunodeficiency virus type 1 (HIV-1). More than 90% viral inhibition was obtained by 200 microM cysteamine in lymphocytes and 100 microM cysteamine in macrophages against 4 primary isolates and 2 laboratory strains of HIV-1. Polymerase chain reaction analysis demonstrated that cysteamine interferes with early steps of HIV-1 replication, before proviral DNA formation. The use of cysteamine in conjunction with zidovudine or didanosine brought about an additive antiviral effect without concomitant increases in toxicity. The concentrations of cysteamine that are effective against HIV-1 in vitro have been well tolerated over long periods by patients under treatment for cystinosis, an inherited disorder. These observations suggest that cysteamine alone or in combination with zidovudine or didanosine could be a new potential treatment of HIV-1 infection.

Antiviral Agents↗
PubMed1983

Effect of cysteamine on gastroduodenal mucosal histamine in rat.

Cysteamine administration to rats is followed by a high incidence of peptic ulceration. The aim of the present study was to investigate the effect of cysteamine on gastric and duodenal mucosal histamine and gastric mucosal histamine formation capacity. After a four hour fast, cysteamine in doses of 50, 100, 200, 300, 400, and 500 mg/kg bodyweight was injected subcutaneously to male Wistar rats; saline injection was used as control. After 24 hours the animals were killed; the stomach and duodenum were removed and examined for ulceration. Mucosal biopsies were taken for histamine studies. Gastric and duodenal ulceration tended to appear with increasing incidence with higher doses. A direct correlation was found between the dose of cysteamine and gastric mucosal histamine (p less than 0.02), and duodenal mucosal histamine (p less than 0.05). Further, a direct relationship was found between gastric mucosal histidine decarboxylase activity and the dose of cysteamine (p less than 0.05). Gastric mucosal histamine and histidine decarboxylase activity showed a direct correlation (p less than 0.001). Gastric and duodenal mucosal histamine and gastric mucosal histamine formation capacity were higher in rats with ulcers than in controls and rats without ulcers. In rat, cysteamine induces dose related changes in mucosal histamine and histidine decarboxylase activity. These changes are related to ulcer formation; histamine may be involved in the pathophysiology of cysteamine induced ulcer formation.

Animals↗
PubMed1992

Cysteamine in combination with N-acetylcysteine prevents acetaminophen-induced hepatotoxicity.

N-Acetylcysteine (NAC) is protective against acetaminophen-induced hepatotoxicity primarily by providing precursor for the glutathione synthetase pathway, while cysteamine has been demonstrated to alter the cytochrome P-450 dependent formation of toxic acetaminophen metabolite. Mice administered acetaminophen (500 mg/kg) had elevations of serum alanine aminotransferase (ALT) to 273.0 +/- 37.5 and 555.8 +/- 193.4 U/mL at 12 and 24 h, respectively, after injection. Administration of cysteamine (100 mg/kg) or NAC (500 mg/kg) significantly reduced serum ALT activity (p less than 0.001). Reducing the dose of NAC or cysteamine by 50% greatly reduced their hepatoprotective effect while the co-administration of the reduced doses of NAC (250 mg/kg) and cysteamine (50 mg/kg) following acetaminophen overdose prevented elevation of serum ALT activity (39.2 +/- 1.17 and 32.5 +/- 5.63 U/mL at 12 and 24 h post-injection, p less than 0.001) and preserved normal mouse hepatic histology. Neither NAC (500 mg/kg), cysteamine (100 mg/kg), or the lower doses in combination of both agents were found to alter the half-life or peak levels of acetaminophen. Liver microsomal aryl hydrocarbon hydroxylase activity measured 24 h after drug administration was not significantly different between treatment groups and controls receiving only saline. These results indicate a possible role for the concomitant use of NAC and cysteamine in the prevention of hepatic necrosis following toxic doses of acetaminophen. Neither decrease in plasma acetaminophen levels nor depression of cytochrome P-450 enzyme activity appears to be the mechanism of protection when these doses of NAC, cysteamine, or both drugs together are administered with a toxic dose of acetaminophen in mice.

Acetaminophen↗
PubMed2005

Enhanced ghrelin secretion in rats with cysteamine-induced duodenal ulcers.

Ghrelin, produced and secreted by the A-like cells of the stomach, stimulates growth hormone secretion, gastric motility, and food intake. Cysteamine inhibits the release of somatostatin and induces the formation of duodenal ulcers in rats. The present study was conducted to investigate the dynamics of ghrelin secretion in rats treated with cysteamine. Male Wistar rats (7 wk old) were administered three doses of cysteamine (400 mg/kg) orally; at 50 h after the first dose, duodenal ulcers were induced, and the plasma level of somatostatin and gastric density of somatostatin-immunoreactive cells were significantly reduced. The plasma total and active ghrelin levels were significantly higher in the cysteamine-treated rats than in the control rats, whereas the gastric ghrelin levels, number of gastric ghrelin-immunoreactive cells, and preproghrelin mRNA expression levels were significantly lower. Even at the time points of 2 and 10 h after the first dose of cysteamine, at which time no significant ulcer formation or antral neutrophil accumulation was yet noted, a significant increase in the plasma ghrelin level and decrease in the gastric ghrelin level were observed. Furthermore, although lansoprazole treatment attenuated the duodenal ulceration induced by cysteamine, the increase in the plasma level of ghrelin could still be demonstrated. Because an inverse correlation was found between the plasma ghrelin and somatostatin levels, the inhibition of somatostatin secretion may be associated with the increased ghrelin secretion. In conclusion, an increase in the plasma ghrelin level precedes the formation of duodenal ulcers in rats treated with cysteamine.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1994

Abnormal glycosylation of duodenal membranous alkaline phosphatase induced by cysteamine in rats.

The membranous and soluble isoenzymes of alkaline phosphatase (AP-ase) were isolated from the duodenal mucosal cells in control and cysteamine-treated rats. Both the cytosolic and membranous isoenzymes of the AP-ase were drastically inhibited by a single subcutaneous injection of cysteamine-HCl, a potent duodenal ulcerogen. However, cysteamine did not change the isoenzyme distribution between the two compartments of the duodenal mucosal cells. Membranous isoenzyme of duodenal AP-ase in control rats was separated by concanavalin A (Con A) affinity chromatography into three fractions: unbound (65%), weakly bound (11%) and strongly bound (24%). The strongly bound fraction disappeared completely from duodenal mucosal cells of cysteamine-treated rats before any visible signs of ulcer formation. Since the strongly bound fraction of AP-ase contains high mannose-type sugar chains, we concluded that the ulcerogen affected the initial mannosylation (or glypiation) of membranous AP-ase which took place in the rough endoplasmic reticulum of the mucosal cells. In control rats, the Con A fractions of the membranous AP-ase were separated by gel filtration as tetramers of M(r) 420 and 340 kD and dimers of M(r) 185-200 kD. In cysteamine-treated rats, neither the strongly bound tetramers of 340 kD nor dimers of 185 kD were found by gel filtration. However, cysteamine did not change the total tetramer: dimer ratio. Judging by the decrease of Vmax values at the pH optimum, the different molecular forms of the AP-ase are selectively sensitive to cysteamine inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1995

Intravenous cysteamine therapy for nephropathic cystinosis.

A 4-y-old boy with nephropathic cystinosis and gastrointestinal dysmotility of unknown etiology was treated with i.v. cysteamine over a period of 10 mo. Thirty minutes after a dose of 10 mg/kg cysteamine free base, the leukocyte cystine value had fallen from 11.9 to 4.9 nmol of half-cystine/mg of protein. When cysteamine was given every 6 h, the leukocyte cystine concentration, measured 5-7 h after a dose, decreased with increasing cysteamine doses up to 17 mg/kg; at this dose the cystine value was 1.1 nmol of half-cystine/mg of protein, or 9% of the untreated value. Oral administration of approximately 16 mg/kg per dose every 6 h to this patient over the previous 3 y achieved similar leukocyte cystine depletion, to 1.2 nmol of half-cystine/mg of protein. The plasma cysteamine concentration 30 min after a dose of 10 mg/kg was 71 microM; 5-7 h after a dose of up to 20 mg/kg, the concentration was below 5 microM. Dimethylsulfide was elevated in the breath and urine of this boy after, but not before, the initiation of i.v. cysteamine therapy. Ten months after the start of therapy, the patient tolerated 250 mg (14 mg/kg) every 8 h. Adverse effects of this treatment included lethargy and increased nausea and vomiting when a schedule of therapy every 6 h was attempted. This investigation demonstrates that cysteamine given through a central venous catheter is effective in reducing leukocyte cystine levels.

Child, Preschool↗
PubMed1981

Somatostatin in rat tissues is depleted by cysteamine administration.

Administration of cysteamine (mercaptoethylamine) induces in rats severe perforating duodenal ulcers. Because the ulcerogenic properties of cysteamine are markedly reduced by treatment with somatostatin, we considered the possibility that cysteamine-induced duodenal ulcer might be mediated by depletion of tissue somatostatin, and thereby of its paracrine influences on gastrin and gastric acid secretion. To test this hypothesis, we measured the concentration of immunoreactive somatostatin (IR-somatostatin) in stomach and duodenal mucosa at intervals after administration of a single ulcerogenic dose (30 mg/kg by stomach tube). IR-somatostatin in these tissues fell rapidly to reach a minimum at 4 h (stomach 31%, duodenum 60% of control respectively). IR-somatostatin in hypothalamus and pancreas decreased gradually to a minimum at 7 h. Another duodenal ulcerogen, propionitrile (10 mg/100 g bw, s.c.) which is more toxic than cysteamine, and several stressful procedures including ether anesthesia, restraint and s.c. formalin did not lower stomach or duodenal IR-somatostatin. Gut, pancreas and hypothalamic VIP levels were not influenced by cysteamine. These findings suggest that cysteamine is a relatively specific depletor of tissue somatostatin. Because blood levels of somatostatin fell, and only trivial amounts of the peptide were found in the stomach lumen after cysteamine administration, it appears likely that this agent acts at the cellular level to cause breakdown of preformed somatostatin and/or to acutely reduce its synthesis.

Animals↗
PubMed1985

Blunted prolactin response to thyrotropin-releasing hormone stimulation in cystinotic children receiving cysteamine.

We investigated whether long term cysteamine therapy in cystinotic children altered their basal and stimulated serum PRL levels. Five subjects who had normal plasma PRL responses to TRH stimulation before cysteamine treatment each had a lower basal PRL level and a blunted PRL response during long term (19-59 months) cysteamine therapy. A blunted PRL response was not found in 12 cystinotic subjects of the same age and stage of disease who had not received cysteamine. The effect on PRL release was not found in 2 subjects who received short term (1-2 weeks) treatment with full-dose cysteamine (50 mg/kg . day). The TSH response to TRH stimulation was not blunted during long term cysteamine therapy. These findings suggest that cysteamine alters PRL secretion in humans.

Administration, Oral↗
PubMed1975

Influence of various factors and drugs on cysteamine-induced duodenal ulcers in the rat.

The cysteamine-induced duodenal ulcer reported by Selye et al. was investigated and the optimum conditions for the production of ulcers in rats were established. A single subcutaneous administration of cysteamine between 200 and 500 mg/kg produced ulceration in a dose-dependent manner in the duodenum within 18 hr. Female and older rats were more susceptible to cysteamine than male and younger ones, respectively. Atropine methylbromide inhibited duodenal ulcers induced by cysteamine dose-dependently and pyloric ligation immediately prior to cysteamine dosing completely inhibited ulceration. Tegragastrin or bethanechol increased the severity of cysteamine-induced ulceration. These data suggest that gastric juice may play an important role in the pathogenesis of cysteamine-induced ulcers. The present study provided an excellent animal model for studying the mechanism of duodenal ulcers and screening of antiulcer agents.

Aging↗
PubMed1987

The effect of verapamil on cysteamine-induced duodenal ulcer in the rat.

To determine the effect of verapamil on experimental duodenal ulcer, pathologic assessment and secretory study were performed in the rats with ulcerogenic dose of cysteamine. The cysteamine increased gastric acid secretion and produced double duodenal ulcers at the proximal protion of the duodenum. Intramuscular injection of verapamil, 3 hours later, produced a significant decreased in gastric acid secretion which lasted at least 4 hours (cysteamine vs. cysteamine+ verapamil; 63.5 +/- 18.4 muEq vs. 25.5 +/- 9.0 muEq during the 1st hour after verapamil administration, 83.1 +/- 24.2 muEq vs. 27.8 +/- 12.3 muEq during the 2nd hour, 110.9 +/- 14.4 muEq vs. 38.5 +/- 25.9 muEq during the 3rd hour, 116.4 +/- 12.1 muEq vs. 40.7 +/- 29.6 muEq during the 4th hour, p less than 0.001). However, cysteamine-induced duodenal ulcers were not alleviated by two doses of intramuscular verapamil administration (4 mg/kg x 2). It is presumed that suppression of gastric acid secretion may not be sufficient to reduce cysteamine-induced duodenal ulcer formation or that verapamil itself may have aggresive effects against duodenum. To illucidate the exact role of verapamil in cysteamine-induced duodenal ulcer, further studies would be needed.

Animals↗
PubMedDate not supplied

Effect of cysteamine on bile secretion in the rat.

The effect of cysteamine, a specific somatostatin depletor, on biliary secretion was studied in urethane-anesthetized rats. Different groups of rats received ip cysteamine at 25, 100 or 340 mg/kg just before bile collection commenced. Other groups of rats were pretreated with cysteamine (340 mg/kg ip) at 4 or 24 h prior to bile duct cannulation and bile collection. Bile secretions were collected at 30-min intervals for 4 h after bile duct cannulation. Total proteins, cholesterol, total lipids, glucose and several hepatic enzymes were assessed in bile. Results indicated that basal bile secretion was only slightly reduced and tended to decrease after drug administration (13% decrease after 340 mg/kg). Cysteamine induced dose-dependent decrease in protein secretion, and the maximum effect was reached at a dose of 340 mg/kg. The effect of cysteamine on protein secretion was prolonged, since it was still observed 24 h after the treatment with cysteamine. Cholesterol and lipid secretion was inhibited by 52.5 and 42.5%, respectively, by the drug, with the latter effect being evident 24 h after drug administration. In addition, the drug inhibited biliary glucose and aspartate aminotransferase concentrations, but increased that of alkaline phosphatase. The results suggest that acute administration of cysteamine inhibits protein, cholesterol and lipid secretion into bile.

Animals↗