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At least 343 records · Page 19Linked to original sources
PubMed1995

Cysteamine-induced depletion of somatostatin in sheep: time course of depletion and changes in plasma metabolites, insulin, and growth hormone.

Eight crossbred wethers (51 +/- 2 kg BW), surgically fitted with abomasal cannulas, were used to determine the extent and time course of cysteamine (CSH)-induced depletion of somatostatin (SRIF) in abomasal tissue and associated changes in plasma metabolites, insulin, and growth hormone (GH). Cysteamine was administered as a single i.v. bolus (50 mg.kg BW-1 x 10 min-1) on d 0. Abomasal biopsies were obtained on d -7, -3, 0, 1, 3, and 10. On d 0, additional biopsies were taken at 2, 4, and 8 h after CSH administration. Jugular blood samples were collected over 8 h at 15-min intervals on d -2, 0, and 1. Cysteamine administration decreased (P < .05) tissue SRIF on d 0 (2, 4, and 8 h), 1, and 3; maximal depletion (42 to 55% of Pre-treatment; Pre-trt) occurred during the initial 24 h, returning to Pre-trt by d 10. Gel chromatography of pooled -7 d abomasal tissue extracts showed five peaks of SRIF immunoreactivity; the predominate peak eluted in the same position as synthetic SRIF-14. Plasma glucose, lactate, and NEFA concentrations increased (P = .001) after CSH administration and reached peak at 2 h after treatment and declined to Pre-trt concentrations by 24 h. Insulin increased (P = .001) to a maximum at h 4 and returned to Pre-trt by 24 h. Mean and baseline GH were higher (P < .07) on day of CSH administration, and pulse amplitude was lower (P < .10) on d 0 and 1. These data show that CSH rapidly reduces SRIF in abomasal tissue in a reversible manner; suggesting that CSH-treated sheep may provide a SRIF-deficient model for studying the physiological role of SRIF in ruminants.

Animals↗
PubMed1988

Effect of furazolidone on gut catecholamine in cysteamine-induced duodenal ulcer in the rat.

The effect of furazolidone, a monoamine oxidase (MAO) inhibitor, on cysteamine-induced duodenal ulcer and gut catecholamines was studied in rats, since previous reports have suggested protective effects of MAO inhibitors against other forms of experimental mucosal injury. Furazolidone (100 mg kg-1, orally) pretreatment significantly reduced the frequency and severity of cysteamine-induced duodenal ulcer. By means of a spectrofluorometric technique, gastric and duodenal norepinephrine concentrations and duodenal dopamine concentrations were measured and found to be increased in animals treated with the MAO inhibitor. It is concluded that the protective effect of furazolidone against cysteamine-induced duodenal ulcer may in part be related to modulation of gut norepinephrine and dopamine concentrations.

Animals↗
PubMed1989

Metabolism of a new radioprotector; S-acetyl-N-glycyl cysteamine. II. Main tissue metabolites in mice bearing EMT6 tumours.

1. The major tissue metabolites of the radioprotector S-acetyl-N-glycl cysteamine (I) labelled with 14C on the cysteamine group, were quantified and identified in normal tissues and EMT6 tumours implanted in mice, by chromatographic comparison with authentic reference compounds. 2. In all tissues the radioprotector undergoes rapid deacetylation and hydrolysis leading to the formation of cysteamine, which is the main metabolite involved in radioprotection. A major part of this metabolite is reversibly inactivated by binding to endogenous SH. 3. The differential radioprotection of healthy tissues versus EMT6 tumour is explained both by a lower uptake of radioprotector, and a weaker deacetylation and hydrolysis rate, in the tumour cells.

Animals↗
PubMed2002

Negligible urinary cysteamine loss in cystinosis patients with Fanconi syndrome.

Cystinosis is an inborn error of lysosomal cystine transporter, resulting in cystine accumulation in lysosomes of all cells. Renal Fanconi syndrome is an early sign of kidney involvement in cystinosis patients. Cysteamine, a small amino-thiol, depletes intralysosomal cystine content and reduces organ damage. However, it does not reverse renal Fanconi syndrome and only postpones the progression to renal failure. We examined whether cysteamine could be lost in the urine of cystinosis patients with Fanconi syndrome, which may explain the inefficiency of treatment. Urinary cysteamine loss was studied in 6 cystinosis patients with and without Fanconi syndrome and was less than I% of ingested dose in all patients.

Adolescent↗
PubMed1978

The treatment of paracetamol overdose with charcoal haemoperfusion and cysteamine.

A 53-year-old female was admitted to hospital one hour after taking an overdose of 60 g of paracetamol and 960 mg of codeine. Two hours after ingestion of the drug, the plasma concentration of paracetamol was 3040 mumol/l. In view of the enormous, and potentially fatal, plasma concentration of the drug, charcoal haemoperfusion was undertaken as well as cysteamine therapy. Charcoal haemoperfusion and cysteamine therapy led to the rapid removal of the paracetamol from the body and consequently prevented the development of severe hepatic necrosis. It is suggested that charcoal haemoperfusion as well as cysteamine has a role in the management of severe overdosage with paracetamol. This is the first report on the use of charcoal haemoperfusion for acute poisoning in Australia.

Acetaminophen↗
PubMedDate not supplied

Determination by liquid chromatography with electrochemical detection of cysteamine and cysteine, possible precursors of N-nitrosothiazolidine.

A method is described that is selective, sensitive, rapid, and accurate for the quantitative measurement in meat products of both cysteamine and cysteine, potential precursors for N-nitrosothiazolidine (NTHZ) and N-nitrosothiazolidine-4-carboxylic acid (NTHZC), respectively. In general, a ground meat sample is homogenized with acetonitrile-formate buffer in the presence of dithiothreitol, and then is centrifuged, filtered, and recentrifuged in a disposable microfilter. The thiols are quantitated by liquid chromatography using an amperometric detector equipped with a gold/mercury electrode, operated in the oxidative mode. Cysteamine was found in 6 of 20 samples of raw pork belly in concentrations ranging from 150 to 450 ppb, and cysteine was found in all samples in concentrations ranging from 2.4 to 36.5 ppm. Analysis for the thiols and their corresponding nitrosamines--NTHZ and NTHZC--of bacon before and after processing showed no correlation between cysteamine and cysteine levels before processing nor with nitrosamine levels after processing. Liquid chromatography with electrochemical detection was found to be an extremely selective technique to measure the 2 free sulfhydryl compounds in a complex food substrate.

Animals↗
PubMed1987

Effect of dopamine-related drugs on duodenal ulcer induced by cysteamine or propionitrile: prevention and aggravation may not be mediated by gastrointestinal secretory changes in the rat.

Dose- and time-response studies have been performed with dopamine agonists and antagonists using the cysteamine and propionitrile duodenal ulcer models in the rat. The experiments demonstrate that the chemically induced duodenal ulcer is prevented by bromocriptine, lergotrile and reduced by apomorphine or L-dopa. Aggravation of cysteamine-induced duodenal ulcer was seen especially after (-)-butaclamol, (-)-sulpiride, haloperidol and, less effectively, after other dopaminergic antagonists. The duodenal antiulcerogenic action of dopamine agonists was more prominent after chronic administration than after a single dose, whereas the opposite was found concerning the proulcerogenic effect of dopamine antagonists. In the chronic gastric fistula rat, both the antiulcerogens bromocriptine or lergotrile and the proulcerogens haloperidol, pimozide or (-)-N-(2-chlorethyl)-norapomorphine decreased the cysteamine- or propionitrile-induced gastric secretion. No correlation was apparent between the influence of these drugs on duodenal ulcer development and gastric and duodenal (pancreatic/biliary) secretions. In the chronic duodenal fistula rat, decreased acid content was measured in the proximal duodenum after haloperidol, and diminished duodenal pepsin exposure was recorded after bromocriptine. Furthermore, the aggravation by dopamine antagonists of experimental duodenal ulcer probably involves a peripheral component. The site of dopamine receptors and physiologic effects which modulate experimental duodenal ulcer remain to be identified, but their elucidation may prove to be an important element in the pathogenesis and treatment of duodenal ulcer.

Animals↗
PubMedDate not supplied

[Mechanism of the radioprotective effect of cysteamine].

The radioprotective effect of cysteamine combined with the modification of the chromatin state by sodium butyrate has been studied using V-79 and CHEL lines of Chinese hamster cells and HeLa cells. Sodium butyrate enhances the chromatin sensitivity to nucleases and removes the radioprotective effect of cysteamine as measured by the yield of cells with chromosome aberrations. As is indicated by changes in the intensity of fluorescence of the DNA-ethidium bromide complex, measured by laser flow cytometry, the protective agent decreases the binding of the dye with both irradiated and nonirradiated DNA whereas ionizing radiation and sodium butyrate increase thereof. It is concluded that the radioprotective effect of cysteamine depends in its ability to reduce the susceptibility of DNA to nucleases.

Animals↗
PubMed1985

Selective decrease of hypothalamic noradrenaline by cysteamine.

In dose studies, cysteamine pretreatment in a dose of 200 mg/kg or 300 mg/kg (subcutaneously, s.c.) markedly decreased the hypothalamic noradenaline content, but did not influence the dopamine and serotonin contents. In time studies, pretreatment with cysteamine in a dose of 300 mg/kg (s.c.) led to markedly decreased hypothalamic noradrenaline contents 4 hr, 8 hr and 12 hr after treatment. These results suggest that cysteamine treatment selectively decreases the hypothalamic noradrenaline content in dose- and time-related manners.

Animals↗
PubMed1982

Depletion of somatostatin-like immunoreactivity in the rat central nervous system by cysteamine.

Selective neurotoxins have been of value in providing a means for specifically interfering with the actions of endogenous neurotransmitter candidates. Others have shown cysteamine (CSH) to deplete the gastrointestinal tract and hypothalamus of rats of immunoreactive somatostatin, suggesting a toxic action of that compound directed against somatostatin-containing cells. The present study further defines the actions of cysteamine on somatostatin in the central nervous system. (CNS). Cysteamine hydrochloride administered subcutaneously results in a depletion of somatostatin-like immunoreactivity (SLI) in the retina, brain, and cervical spinal cord of rats. The effect is demonstrable at doses of 30 mg/kg of body weight and above, occurs within 2 to 4 hr of a single injection of the drug, and is largely reversible within 1 week. The mean depletion of SLI observed within the CNS varies from 38% in cerebral cortex to 65% in cervical spinal cord 24 hr following administration of CSH, 300 mg/kg of body weight, s.c. By gel permeation chromatography, all molecular weight forms of SLI are affected, with the largest reductions in those forms that co-chromatograph with synthetic somatostatin-14 and somatostatin-28. These results indicate that CSH has a generalized, rapid, and largely reversible effect in depleting SLI from the rat CNS.

Animals↗
PubMed1984

[Interrelation between the analgesic and ulcerogenic action of cysteamine].

Interrelationship was studied between the influence of cysteamine on pain threshold and ulcerogenic effect on the duodenum. Cysteamine (350 mg/kg) induced analgesia in mice which was prevented by naloxone (1.5 mg/kg). In rats, cysteamine produced duodenal ulcers with concomitant analgesia. The intensity of ulceration was higher in animals with lower basal pain threshold. The correlation between central and peripheral effects of endogenous opioids in the development of experimental duodenal ulcers is discussed.

Analgesics↗
PubMed1984

[Cysteamine in the treatment of cystinosis in children. In vitro and in vivo studies].

The effect of cysteamine was studied in 6 children with nephropathic cystinosis. In 3 of them an in vitro study on fibroblasts was performed. The cystine content of fibroblasts was immediately diminished (about 90% of total cystine content) as soon as the concentration of cysteamine in the medium was greater than or equal to 0,1 mmole/l. In vivo, 50 to 89 mg/kg/day of cysteamine was administered for 9 to 37 months (mean 21,3). There was no adverse reaction. In all cases a dramatic decline in leukocyte cystine level was observed (in 5 cases the level was within the range seen in clinically unaffected heterozygotes). Growth was not improved. The renal function was stabilised in 3 cases. Photophobia which was present in 4 children decreased in 2 cases or disappeared in 2 cases.

Cells, Cultured↗
PubMedDate not supplied

[Molecular mechanisms of radiation death of lymphoid cells. Radioprotective effect of cysteamine on a subpopulation of thymocytes differing in radiation sensitivity].

The radioprotective effect of cysteamine, incubated with thymocytes for 20 min prior to gamma-irradiation, was much more manifest with regard to subpopulations of radiosensitive small cortical cells (DMF = 1.8) than large thymocytes (DMF = 1.2). Radioprotective concentrations of cysteamine relaxed completely superhelical DNA of thymocytes. The relaxation was not due to the formation of single-strand breaks. A partial recovery of superhelical conformation of DNA of small thymocytes before irradiation reduced the radioprotective effect of cysteamine.

Animals↗
PubMed1983

[The effect of cysteamine on the duodenal defense mechanism in the vagotomized rats--with special reference to the parietal cell vagotomy with CO2-laser].

The parietal cell vagotomy with CO2-Laser defocused beam has been developed and its efficacy was confirmed in cysteamine induced duodenal ulcer in rat. Rats were classified into the truncal, parietal cell and Laser vagotomy groups and control. After cysteamine was administered, the change of the Brunner's gland were examined histologically for each group. Duodenal ulcer was seen and the depletion of the Brunner's glands was observed in all control rats. Duodenal ulcer formation was prevented in all vagotomized rats regardless of the type of vagotomy and the preservation of synthetic activity of the Brunner's gland was noted. However, multiple gastric ulcer was seen in truncal vagotomy group. Laser vagotomy was done very easily and safely. It consumed much less time and prevented duodenal ulcer formation. It prevented the cysteamine induced duodenal ulcer formation in rats by preservation of the Brunner's gland activity.

Animals↗
PubMed1983

Effects of the metabolites of the branched-chain amino acids and cysteamine on the glycine cleavage system.

The effects of ten metabolites of the branched-chain amino acids, CoA and cysteamine (beta-mercaptoethylamine), on the glycine cleavage system were investigated with the liver extracts. It was found that CoA derivatives including tiglyl CoA, isobutyryl CoA, succinyl CoA, methylmalonyl CoA, isovaleryl CoA, propionyl CoA and CoA itself and cysteamine significantly inhibited the glycine cleavage system of the liver extracts. Further studies on the glycine-14CO2 exchange catalyzed by p-protein and H-protein purified from chicken liver indicated that tiglyl CoA inhibited the activity of P-protein in an apparently competitive manner with respect to H-protein, and that cysteamine inhibited the activity of P-protein in two ways, by increasing the Km value for glycine and changing Vmax.

Adult↗
PubMed1981

Treatment of cystinosis with cysteamine. A pilot study determining dose and form of application.

A pilot study with cysteamine treatment was performed in three children with the nephropathic form of cystinosis. Two children underwent renal transplantation shortly before treatment. The aim of the study was to find a practicable form of application and a corresponding effective dose. Cysteamine in gelatine capsules together with 0.2% silicic acid as a dessicator turned out to be the most acceptable galenic form, compared to sirup or suppositories. Among three dosage regimens, the dosage of 50 mg/kg/day is effective as judged by the leucocyte cystine content, even if given in only three doses per day. No side effects of the cysteamine treatment (even at a dose of 90 mg/kg/day) were noted. Whether this treatment is preventing progression of disease will have to be examined either in transplanted patients by measuring non-renal parameters or in very young infants with cystinosis whose kidneys are not damaged yet.

Child, Preschool↗
PubMed1981

[Patterns in the x-ray induction of mutations in resistance to 5-thioguanine in Chinese hamster cell cultures studied using cysteamine].

X-ray induction of 5-thioguanine resistance mutations and the protective effect of cysteamine were studied in cultured cells of chinese hamster clone 431. Expression of mutations was studied for 8--10 days of post-irradiated growth, when cells surviving radiation at doses 200, 400, 600, 800 R were passing from 3 to 12 generations. The maximum frequency of induced mutations was found after 3-5 generations. After reaching the maximum, the number of registered mutations decreased with the number of cell generations. Pre-irradiated treatment with 5mM cysteamine decreased induction of mutations 2--4 times when using doses 200--800 R. The frequency of mutations induced by mere radiation increased non-linearly with increasing doses, while in the presence of cysteamine the linear dose dependence was observed.

Animals↗
PubMed1994

Differential repair of radiation-induced DNA damage in cells of human squamous cell carcinoma and the effect of caffeine and cysteamine on induction and repair of DNA double-strand breaks.

The goal of these experiments was to investigate further the relationship between DNA double-strand breaks and cell killing in human tumor cells, first by comparing different cell lines, and second by radiomodification studies. Field-inversion gel electrophoresis was used to quantify double-strand breaks. Two subclones of the radioresistant human squamous cell carcinoma line SQ20B (SQD9 and SQG6) were compared. These subclones differed in DNA index by a factor of 1.7 but showed the same resistance to radiation as cells of the parental cell line. It was found that, although induction of DSBs was not significantly different in the two cell lines, the t1/2 of the fast component of repair was significantly shorter for SQD9 cells, leading to greater overall repair which was not reflected in increased survival. Caffeine and cysteamine were tested as modifiers of radiosensitivity, using the radioresistant SQ20B line and the radiosensitive SCC61 cell line. No effect of caffeine was seen when the drug was present only during irradiation. Postirradiation incubations with caffeine, however, resulted in a dose reduction factor greater than 2.0 in cell survival for both cell lines. In contrast, induction of DSBs was reduced by caffeine, and no effect on DSB repair was observed. Cysteamine led to a dose protection factor greater than 1.8 in cell survival in both cell lines. A reduction in induced DSBs was found at high doses corresponding approximately with the increase in cell survival. Over the same (low) dose range, however, the correlation between DSB induction and cell killing was poor. These data indicate that DSB induction does not correlate well with cell killing either for different cell lines, for radiochemical modification (cysteamine) or for some other types of modification (caffeine).

Caffeine↗