Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cysteamine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources
PubMed1986

Augmentation of cysteamine and mepirizole-induced lesions in the rat duodenum and stomach by histamine or indomethacin.

Repeated administration of histamine X 2HCl (40 mg/kg X 4) significantly augmented mepirizole (200 mg/kg) or cysteamine (300 mg/kg)-induced duodenal and gastric lesions in rats within 6 hr. Most of the duodenal lesions were penetrating ulcers and were located over the entire duodenum. Gastric lesions were mainly located in the antrum adjacent to the duodenum. Indomethacin pretreatment did not significantly augment the duodenal lesions induced by mepirizole or cysteamine, but did augment the gastric lesions induced by these compounds.

Animals↗
PubMed1989

Pathogenesis of the earliest epithelial cell damage induced by mepirizole and cysteamine in the rat duodenum.

Mepirizole (200 mg/kg) and cysteamine (100 mg/kg) induced epithelial cell damage in the proximal duodenum of rats within 30 min after s.c. administration. The injury induced was severe 60 min later. Gastric acid secretion determined in intact animals was stimulated by these agents 30 and 60 min later when the intraluminal pH of the duodenum was significantly decreased. Duodenal blood flow was significantly decreased beginning 5 min after administration up to 60 min. Oral treatment with sodium bicarbonate (300 mg/kg), cimetidine (100 mg/kg), omeprazole or NC-1300 (gastric proton pump inhibitors, 30 mg/kg) and 16,16-dimethyl prostaglandin E2 (10 micrograms/kg) protected the epithelium from damage induced by the two duodenal ulcerogens. Epithelial cell damage in the duodenum in response to mepirizole and cysteamine appears to be related to the increased gastric acid secretion followed by lowered intraduodenal pH of the duodenum having decreased blood flow.

Animals↗
PubMed1997

Effects of exogenous somatostatin and cysteamine on net nutrient flux across the portal-drained viscera and liver of sheep during intraduodenal infusion of starch hydrolysate and casein.

We used eight Polypay wethers (36 +/- .6 kg BW) fitted with hepatic portal, hepatic venous, mesenteric arterial and venous, and duodenal catheters in a crossover design experiment to determine the influence of somatostatin (SRIF) on splanchnic metabolism. Each crossover period consisted of 14 d, with net flux of nutrients and hormones (venoarterial differences x blood flow) measured on d 14. Before flux measurements, wethers received an i.v. dose (0 h) of either 0 (vehicle) or 50 mg x kg BW(-1) x 10 min(-1) cysteamine (CSH, SRIF-depleting agent) followed by a continuous duodenal infusion (h 10 to 22) of a starch hydrolysate-casein solution. Six sets of arterial, portal, and hepatic blood samples were obtained (h 12 to 16), after which a primed (10 microg), continuous jugular infusion of SRIF-14 (5.0 microg x kg BW(-1) x h(-1)) was initiated and sampling protocol repeated (h 18 to 22). Cysteamine administration increased (P < .01, vs control) portal and hepatic blood flow in the absence of exogenous SRIF (CSH x SRIF, P < .01). Net portal-drained viscera (PDV) release of glucose, alpha-amino N, ammonia N, beta-hydroxybutyrate, and oxygen consumption were decreased (P < or = .10) and lactate release increased (P = .005) during SRIF infusion. The CSH increased (P < .05) PDV release of beta-hydroxybutyrate and insulin and increased (P = .09, CSH alone vs control) net release of glucose in the absence of exogenous SRIF. Exogenous SRIF increased (P = .10) and CSH decreased (P = .09) net hepatic glucose output, whereas liver oxygen consumption was decreased (P = .04) with exogenous SRIF and increased (P = .01) with CSH. Net total splanchnic alpha-amino N release and oxygen consumption were decreased (P < .10) with exogenous SRIF, but CSH increased (P < .05) insulin release and oxygen consumption. These data provide initial evidence for a regulatory involvement of SRIF in visceral metabolism in ruminants.

3-Hydroxybutyric Acid↗
PubMed1989

Changes in levels of mucosal glycoprotein on cysteamine-induced duodenal ulcers in rats.

Duodenal ulcers were induced in rats by cysteamine administration. Time-course changes in duodenal hexosamine, blood flow and intragastric pH were measured, as well as changes in the susceptibility of Brunner's glands to concanavalin A (Con A) staining. Hexosamine contents in the duodenum decreased significantly at 5 and 24 h. In the control group, Brunner's glands were stained brown using Con A staining. One day after cysteamine administration, the extent of Con A staining markedly decreased. At 3 and 7 days, gland susceptibility to staining was essentially the same as that of the control group.

Animals↗
PubMed1989

The role of the sympathetic nervous system in cysteamine-induced gastric lesions in rats.

Cysteamine.HCl, when administered subcutaneously at 350 mg/kg, consistently induced severe gastric lesions in Wistar Kyoto rats (WKY), but not in spontaneously hypertensive rats (SHR). In both WKY and SHR, visible ulcers could not be induced in the duodenum in response to cysteamine. It appears that the stomach and duodenum of SHR are resistant to cysteamine due to hyperfunctioning of the sympathetic nervous system.

Animals↗
PubMedDate not supplied

The effect of topical cysteamine drops on reducing crystal formation within the cornea of patients affected by nephropathic cystinosis.

We studied the usefulness of topical cysteamine ophthalmic drops in reducing crystal formation within the corneas of patients affected by nephropathic cystinosis. A dosage of 0.3% cysteamine given four times daily was chosen as a more manageable method than a previously reported protocol of hourly administration of 0.11% drops. No reduction in crystal formation was observed in our patients; they were followed for seven months.

Administration, Topical↗
PubMed1975

[Simultaneous effect of 5-bromodeoxyuridine and cysteamine on x-irradiated diploid cells of Chinese hamster, Cricetulus griseus, in vitro].

Cells of the Chinese hamster line B 14 FAF 28 were treated with BUdR and irradiated with X-rays under the presence of cysteamine. The dose-dependent inactivation rates could be determined rather precisely by marking single cells. Daily cell counts in the growing colonies made it possible to establish individual colony growth curves. The results of both analyses show for untreated and treated cells a nearly equal factor with respect to the protecting effect of cysteamine. Also in the "macrocolonies" this effect is clearly measurable even five days after irradiation indicating a still existing very different vitality of the cells at that time. The results are discussed with concern to following irradiations.

Animals↗
PubMed1992

Oxalate production from glyoxylate by lactate dehydrogenase in vitro: inhibition by reduced glutathione, cysteine, cysteamine.

Lactate dehydrogenase is known to act as a dismutase converting glyoxylate to oxalate and glycolate. LDH (sources: human erythrocytes, human plasma; rabbit muscle; rat liver) activity was assayed at 340 nm using glyoxylate (5.0 mmol/l) and NADH. The LDH activity (approx. % of control) in all the cases decreased respectively in the presence of 5.0 and 10.0 mmol/l of cysteine (45 and 20), cysteamine (45 and 20), and GSH (55 and 30). This decrease in LDH activity resulted in decreased oxalate production from glyoxylate (0.5 mmol/l). A 50% inhibition in oxalate production was observed in presence of 0.3 mmol/l cysteine, 0.35 mmol/l cysteamine, and 2.0 mmol/l GSH. The results suggest that the net LDH activity towards oxalate production may be regulated by the free SH-groups in the cell. This possibility needs evaluation as a tool to lower endogenous oxalate production and the associated risk of stone formation.

Animals↗
PubMed1991

A fall in duodenal PGE2 synthesis precedes histological changes and ulceration in the cysteamine model of duodenal ulceration.

The temporal association of histological damage and mucosal prostaglandin E2 (PGE2) synthesis was examined in the cysteamine model of duodenal ulceration in the rat. Four groups of 10 animals were used; a control group (which had a light ether anaesthetic, an i.m. injection of vehicle and were killed 18 h later) and three treatment groups (which were similarly treated but injected with cysteamine (0.3 mg/g body weight) and killed at 6, 18 or 24 h). Estimates of duodenal PGE2 synthesis and histological assessment of mucosal damage were performed. There were four early deaths in the 24-h group due to intra-thoracic haemorrhage. The 6-h group appeared normal macroscopically. There were seven established and three early ulcers in the 18-h group and two established and four early ulcers in the survivors of the 24-h group. Microscopically, the 6-h group did not differ from controls, but the 18 and 24-h groups showed evidence of mucosal damage compared to the control group (P less than 0.001). All three treatment groups synthesized less PGE2 than did the control group (P less than 0.001). Thus at 6-h post-injection, a decrease in PGE2 synthesis was evident but mucosal damage occurred later. Histological features correlated negatively with PGE2 synthesis (P less than 0.001).

Animals↗
PubMedDate not supplied

[The modifying effect of glycerine and cysteamine on prophage lambda induction in E. coli cells under gamma irradiation].

In studying the modifying influence of glycerol and cysteamine of gamma radiation induction of lambda prophage it was shown that dose curves for lambda prophage induced upon irradiation in normal conditions and in the presence of glycerol are those with a maximum. In the presence of cysteamine, the prophage induction is inhibited significantly.

Bacteriophage lambda↗
PubMed1988

23Na NMR study of DNA thermal transconformation in presence of cysteamine radioprotector.

DNA thermal transconformation is studied in absence and in presence of the cysteamine radioprotector, by observing the delta nu 1/2 variation of 23Na NMR peaks. The sodium state (Free or Bound) is discussed with the help of a two states model with RF and RB relaxation rates. The delta nu 1/2 behaviour during the DNA transconformation shows clearly the electrostatic interaction with cysteamine which is accompanied by an Na+ ejection out of phosphate sites. The temperature dependence of delta nu 1/2 in all cases leads to the conclusion that RBc (the average relaxation rate of sodium nuclei that remain bound in the coil state of DNA) tends to zero.

Cysteamine↗
PubMedDate not supplied

[Protective effects of cysteamine and anoxia in Escherichia coli mutants].

The values of the oxygen effect (m) and maximum radioprotective effect of cysteamine (DMF*) have been determined for the following Escherichia coli strains: AB1157 (the wild type), AB1886 (uvrA), AB2463 (recA), and p3478 (polA). Three mechanisms are shown to be responsible for the protective effect of cysteamine, they are: (1) anoxia, (2) diminution of the indirect effect, (3) an increased efficiency of enzyme repair. Anoxia is the main contributor to the protective effect in all the strains under study while mechanism (3) is only effective in the wild type strain.

Cysteamine↗
PubMed1988

Cysteamine protects against diarrhoea induced by castor oil. This protective effect can be potentiated by SH-alkylator treatment.

Cysteamine given orally or subcutaneously protects against diarrhoea induced by castor oil. Pretreatment with N-EM, an SH-alkylator, does not influence the occurrence of diarrhoea. Furthermore, N-EM pretreatment does not influence the protective effect of loperamide or difenoxilate. However, N-EM pretreatment potentiates the protective effects of cysteamine or indomethacin against diarrhoea. These findings indicate that sulfhydryl-sensitive processes may also be involved in the mechanisms of diarrhoea.

Alkylating Agents↗
PubMed1987

[Effect of the ulcerogenic agent cysteamine on the content of glutathione and glutathione-dependent enzymes in the mucous membrane of the gastroduodenal region in the rat].

A comparative study of reduced and oxidized glutathione forms and the activity of glutathione-dependent enzymes (glutathione peroxidase, glutathione-S-transferase, and glutathione reductase) has been performed in the rat mucous membranes of different gastroduodenal areas 24 hours after the injection of cysteamine--a specific ulcerogenic agent. It has been shown that cysteamine causes a decrease in the concentration of reduced and an increase in the concentration of oxidized glutathione forms in all gastroduodenal areas. The fall in reduced glutathione form concentration is the greatest in the duodenal mucosa. A considerable decrease in glutathione-dependent enzyme activity, especially glutathione-S-transferase, was observed in duodenal mucosa. It is concluded that glutathione and glutathione-dependent enzyme system may be directly related to pathogenetic mechanisms of gastroduodenal ulcer formation.

Animals↗
PubMedDate not supplied

[Effect of hyperthermia on the radioprotective action of cysteamine and isoproterenol].

Heating of mouse bone marrow cells up to 42 degrees C was shown to increase their radiosensitivity (DMF = 0.80 +/- 0.12). At this temperature, the radioprotective efficiency of cysteamine was lost completely (DMF = 0.78 +/- 0.09), and radioprotective activity of d,l-isoproterenol significantly decreased (DMF declined from 2.41 +/- 0.23 to 1.67 +/- 0.16). It is assumed that the radioprotective effect of cysteamine on mammalian cells is associated with the processes of the postirradiation DNA repair for just these processes are inhibited by heating. The mechanism of action of a beta-agonist of isoproterenol is perhaps only partially associated with DNA repair.

Animals↗
PubMed1982

Thiazolidine-2-carboxylic acid, an adduct of cysteamine and glyoxylate, as a substrate for D-amino acid oxidase.

A mixture of cysteamine and glyoxylate, proposed by Hamilton et al. to form the physiological substrate of hog kidney D-amino acid oxidase (Hamilton, G. A., Buckthal, D. J., Mortensen, R. M., and Zerby, K. W. (1979) Proc. Natl. Acad. Sci. U. S. A. 76, 2625-2629), was confirmed to act as a good substrate for the pure enzyme. As proposed by those workers, it was shown that the actual substrate is thiazolidine-2-carboxylic acid, formed from cysteamine and glyoxylate with a second order rate constant of 84 min-1 M-1 at 37 degrees C, pH 7.5. Steady state kinetic analyses reveal that thiazolidine-2-carboxylic acid is a better substrate at pH 8.5 than at pH 7.5. At both pH values, the catalytic turnover number is similar to that obtained with D-proline. D-Amino acid oxidase is rapidly reduced by thiazolidine-2-carboxylic acid to form a reduced enzyme-imino acid complex, as is typical with D-amino acid oxidase substrates. The product of oxidation was shown by NMR to be delta 2-thiazoline-2-carboxylic acid. Racemic thiazolidine-2-carboxylic acid is completely oxidized by the enzyme. The directly measured rate of isomerization of L-thiazolidine-2-carboxylic acid to the D-isomer was compared to the rate of oxidation of the L-isomer by D-amino acid oxidase. Their identity over the range of temperature from 2-30 degrees C established that the apparent activity with the L-amino acid can be explained quantitatively by the rapid, prior isomerization to D-thiazolidine-2-carboxylic acid.

Amino Acids, Sulfur↗
PubMed1984

Effect of pentobarbital anesthesia and bile acids on cysteamine-induced duodenal and gastric ulcers in rats.

Cysteamine given three times within 8 h produced severe duodenal and gastric ulcers in female SIV rats. A pentobarbital anesthesia during the first 10 h prevented gastric ulcer formation without affecting duodenal ulcer. An additional 10 h lasting intragastric infusion with 0.6 ml/h Ringer containing 5 mmol/l of a mixture 3: 1 pure taurocholic and glycocholic acid or 20 and 50 mmol/l pure taurocholic acid in 0.2 N HCl did not reverse the protective effect of pentobarbital, e.g. incidence and intensity of gastric ulcer did not change. Treatment with somatostatin significantly reduced the intensity of duodenal ulcer. The inhibition of cysteamine-induced gastric ulcer formation by pentobarbital does not seem to be due to a possible inhibition of duodenogastric reflux but more likely to an inhibition of central nervous stress reactions by anesthesia.

Anesthesia, General↗
PubMed1983

[Gene mutations, chromosome aberrations and survival after the x-ray irradiation of a Chinese hamster cell culture protected by cysteamine].

The protective effect of cysteamine against 6-thioguanine-resistance (TCr) mutations, chromosome aberrations and inactivation caused by X-ray in cultured cells of Chinese hamster (clone 431) has been studied. The dose-effect curves have been obtained under irradiation condition without protector and with it. Dose-modifying factor of 2 was calculated for chromosome aberrations and cells inactivation and 2,8 for TCr mutations. It is supposed that the cysteamine acts on the general mechanisms involved in damages realization which results in gene mutations, chromosome aberrations and cell inactivation.

Animals↗