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At least 1,405 records · Page 78Linked to original sources
PubMed1978

Mechanism of the radioprotecting action of chemical compounds on Escherichia coli cells.

The effect of radioprotection of indolylalkylamines (5-methoxytryptamine) and aminothiols (cysteamine) on E. coli cells is practically absent if the cells have genetic defects in the repair systems. This means that the explanation of radioprotection by scavenging of free radicals is invalid and that specific repair mechanisms may be involved. In order to explain the radioprotective mechanism it was suggested that the radioprotectors interact with the damaged sites in DNA so that they become partly screened from repairing endonucleases. Under these conditions the reduction of incision rate results in diminished enzymatic induction of lethal double-strand breaks in DNA, this being important only in wild type cells. To prove this hypothesis an experimental procedure was developed using bacterial cells carrying plasmids (ColE1). This procedure enabled to determine the in vivo rate of enzymatic incision of gamma-sites. It was found that the protectors did not change the total amount of gamma-damages in DNA but reduced the rate of enzymatic incision.

5-Methoxytryptamine↗
PubMed1975

Pathogenic mechanisms not operating in Eimeria necatrix infections.

Having investigated certain aspects of Eimeria necatrix coccidiosis in chickens, workers of the Hannover Veterinary School postulated "that death following a single inoculation of a large number of oocysts is due to an alarm reaction and not a specific pathogenic action of the parasites". Because this hypothesis is somewhat revolutionary in its consept, several pieces of evidence on which it is based and several logical deductions which can be made from it have been examined. It has been confirmed that injection of chichens with cysteamine or 5-hydroxytryptamine 30 min before inoculation of the birds with a lethal dose of E. necatrix oocysts reduces subsequent mortality; the reason for this, however, appears not to be the neutralisation of the proposed shock reaction, but rather an inhibition of the excystation process, brought about indirectly through the host. Inoculation of chickens with a non-lethal dose of E. necatrix oocysts 30 min before inoculation with a lethal dose of oocysts was followed by increased mortality rather than the decreased mortality which the hypothesis would predict. Treatment of chickens with sulphadimidine starting 48 h after inoculation resulted in survival of the birds rather than death which would ensue if in fact mortality was due to a shock reaction irreversibly initiated at the time of inoculation. A direct effect of sulphadimidine on the parasite has been shown both in vivo and in vitro.

Adrenocorticotropic Hormone↗
PubMed1982

Induction of c-mutations in extracellular phage lambda by gamma-rays.

Mutagenic action of 60Co gamma-rays on extracellular phages lambda red1 and lambda red113 after irradiation in 4% nutrient broth in the absence or in the presence of 0.1 M cysteamine or in dried samples was studied. The yield of c mutations was almost independent of the repair genotype of the host cells (uvrA6, polA1, recA13, lexA102, uvrE502, uvrD3 or xthA9), of the phage Red function and of the conditions of gamma-irradiation and was 1 . 10(-12) per base pair and 1 rad. When the SOS-repair system of the host cells was induced by moderate UV irradiation, the yield of c-mutations was drastically enhanced in phage irradiated in broth, but not in phage irradiated in the dried state. These data allow us to suppose that the direct action of gamma-rays induces, in phage DNA, premutational lesions that are fixed into mutations by replication. On the other hand after gamma-irradiation in broth, when indirect radiation effects are only partially suppressed, about 85% of premutational lesions are converted into mutations by means of the inducible, errorprone SOS-repair system.

Bacteriophage lambda↗
PubMed1987

Synthesis of cysteinylphenol, cysteaminylphenol, and related compounds, and in vivo evaluation of antimelanoma effect.

Phenolic and catecholic compounds were synthesized, by combination with cysteine or cysteamine through thioether bond, and their antimelanoma and melanocytotoxic effects were evaluated. Among nine compounds tested, 4-S-cysteaminylphenol (CAP) resulted in an increase in the life span (% ILS) of melanoma-bearing mice and in the growth inhibition (% GI) of melanoma tissue. 4-S-Cysteinylphenol (CP) and its methyl ester form also showed some increase in % GI. The 2-S-isomers of CP and CAP and diphenolic derivatives of CP did not show any significant antimelanoma effect. In addition, the s.c. injection of 4-S-CAP and 4-S-CP, in particular 4-S-CAP, caused the depigmentation of black hair which was manifested by loss of functioning melanocytes, as seen under light microscopy. The 4-S-CAP appears to provide a basis for development of a new class of antimelanoma and melanocytotoxic agents that are more stable than catecholic compounds, which have been most widely utilized as a source of rational chemotherapy for malignant melanoma.

Animals↗
PubMed1986

Electrophysiological actions of somatostatin (SRIF) in hippocampus: an in vitro study.

The electrophysiological actions of somatostatin (somatotropin release inhibiting factor; SRIF) were investigated in the in vitro hippocampal slice preparation. Intracellular recordings were obtained from pyramidal neurons in area CA1 in slices of hippocampus from guinea pigs and rabbits. Somatostatin, applied via micropressure ejection to CA1 pyramidal-cell somata, was primarily excitatory. The effects, however, were quite variable, with nearly all cells displaying pronounced tachyphylaxis. A majority of cells was depolarized by SRIF, but hyperpolarizations or biphasic depolarization/hyperpolarization responses were also recorded. Only minimal conductance changes were associated with the SRIF-induced voltage changes. Depletion of SRIF, by injection of the intact animal with cysteamine several hours before preparing slices, resulted in no obvious abnormalities in hippocampal slice electrophysiology. Our results obtained with application of exogenous SRIF are consistent with the concept that SRIF acts as an excitatory neurotransmitter/neuromodulator in hippocampus. However, our attempts to demonstrate endogenous SRIF action have thus far been unsuccessful.

Animals↗
PubMed1994

Progression of chronic renal failure in a historical group of patients with nephropathic cystinosis. European Collaborative Study on Cystinosis.

In a historical group of 205 patients with infantile or adolescent cystinosis treated without cysteamine, the rate of deterioration of renal function was analysed retrospectively. Patient survival curves and renal survival data are presented. Longitudinal data of serum creatinine values (n = 3280) in 157 patients were plotted for each patient, smoothed by the method of the running medians and grouped into 12 serum creatinine classes. In every patient the age at the last smoothed serum creatinine value observed in each serum creatinine class was determined. These virtual age values were then summarized per serum creatinine class, expressed as median and centiles and plotted, thus describing the "natural" course of the disease. In 9 pairs of affected siblings the rate of progression showed a median difference of about 12 months. Our data describe the "natural" course of nephropathic cystinosis and can be used as a prognostic aid for recently detected patients. The data can also be applied for the assessment of the influence of new therapeutic strategies on the rate of progression of renal failure in cystinotic patients.

Child, Preschool↗
PubMed1990

Different effects of cytoprotective drugs on ethanol- and aspirin-induced gastric mucosal injury in pylorus-ligated rats.

In anesthetized rats oral administration (2 ml) of both ethanol (50% in 150 mM HCl) and aspirin (80 mM in 150 mM HCl) produced bandlike lesions in the stomach, while more generalized lesions occurred in the pylorus-ligated stomach when the irritant was given intragastrically through the fistula prepared in the rumen and the mucosal folds were removed by stomach distension. The bandlike lesions induced in the intact stomach by both irritants were significantly and dose-dependently prevented by 16,16-dimethyl PGE2 (dmPGE2: 3 and 10 micrograms/kg, subcutaneously), cysteamine (30 and 100 mg/kg, subcutaneously) or timoprazole (10 and 30 mg/kg, per os) at the doses which significantly inhibited gastric motility. In the pylorus-ligated stomach, however, neither of these agents showed any protection against the generalized lesions induced by ethanol, but such lesions caused by aspirin were significantly prevented only by dmPGE2. These agents also showed similar effects against the reduction of transmucosal PD in the pylorus-ligated stomach exposed to ethanol and aspirin. These results suggest that (1) the formation of bandlike lesions caused by ethanol and aspirin depends on the presence of mucosal folds and may be prevented by the agents that inhibit gastric motility, (2) the pathogenesis of the lesions induced by aspirin and ethanol may be different in the pylorus-ligated stomach, and (3) dmPGE2 has a unique protective ability that is not shared by usual cytoprotective agents.

16,16-Dimethylprostaglandin E2↗
PubMed1989

The hypothalamic somatostatinergic pathways mediate feeding behavior in the rat.

The level of somatostatin in the hypothalamus was higher in satiated rats than in hungry rats. Elevating hypothalamic somatostatin levels by administering somatostatin into the hypothalamus produced a decrease in food intake, whereas lowering hypothalamic somatostatin levels by administering cysteamine into the peritoneal cavity produced an increase in food intake in rats.

Animals↗
PubMed1983

Indication of reduced doxorubicin-induced cardiac toxicity by additional treatment with antioxidative substances.

The influence of antioxidative substances on doxorubicin-induced cardiac toxicity was studied in C 57 BL mice. Tocopherol (500 mg/kg), glutathione (1000 mg/kg), cysteamine (15 mg/kg) and L-cysteine (1000 mg/kg), injected i.p. 24 h before doxorubicin treatment (15 mg/kg i.p.) were able to reduce malonaldehyde production in cardiac tissues significantly. SH-containing substances with high reducing activity, such as vitamin E, could be a useful tool in clinical trials to prevent doxorubicin induced cardiac damage.

Animals↗
PubMed1990

On the possible role of different endogenous opiate receptors in gastroduodenal ulceration of the rat.

In Wistar rats of both sexes stress(restraint)- and drug (indomethacin)-induced gastric, as well, as cysteamine-induced duodenal ulceration was treated by morphine and nalorphine, given either alone or in combination. Neither morphine nor nalorphine had a significant anti-ulcerogenic effect. In contrast, the combined morphine + nalorphine treatment showed a highly significant anti-ulcerogenic action in the case of gastric ulceration but it was ineffective on duodenal ulcer formation. It seems that the chi and sigma endogenous opiate receptors play a significant role in the anti-ulcerogenic effect, while the mu receptors are involved to a considerably lesser degree. Moreover, the experimental results strengthen the view that gastric and duodenal ulceration are two different pathological entities and that ulcer formation is only a common consequence.

Animals↗
PubMed1984

Renal cell culture using autopsy material from children with cystinosis.

Renal cell cultures were initiated using fresh autopsy material from two individuals with cystinosis, ages 5 and 8 yr. Cells obtained from collagenase treated autopsy material were grown in a selective kidney medium containing Coon's modified F12, 2.5% fetal bovine serum, transferrin, insulin, selenium, hydrocortisone, PGE1, and fibronectin. These cells had an epithelial appearance, formed domes, and were periodic acid-Schiff positive. Both tight junctions and microvilli were seen by electron microscopy. Fibroblasts had a cloning efficiency of zero in the selective medium and grew poorly compared to their growth in Coon's F12 with 10% fetal bovine serum. The lysosomal cystine content of the renal cells was greatly elevated and comparable to that of fibroblasts from cystinotic patients. Renal cell lysosomal cystine levels were only partially reduced by exposure to either pantethine or the aminothiol, cysteamine. However, exposure to either compound effectively depleted cystinotic cultured fibroblasts of their lysosomal cystine. Study of cultured renal material may have practical significance in pharmacologic considerations.

Autopsy↗
PubMed2001

Voltammetric behavior of L-cysteine in the presence of CPB at a silver electrode.

The voltammetric behavior of L-cysteine at a silver electrode is described. L-Cysteine can be anodically accumulated at a silver electrode surface as a sparingly soluble silver salt; at more negative potentials, the insoluble compound is stripped cathodically yielding a small current peak at about -1.10 V (vs. SCE). In the presence of cetyl pyridine bromide (CPB), the stripping peak shifts slightly to a more negative potential, and the peak height increases significantly. Thus, the peak becomes more useful for the determination of L-cysteine. In contrast to other surfactants, CPB can improve the accumulation and stripping of L-cysteine obviously. The voltammetric behavior of cysteamine, 3-mercaptopropionic acid and homocysteine is discussed as well.

3-Mercaptopropionic Acid↗
PubMed1999

Effects of intrapancreatic neuronal activation on cholecystokinin-induced exocrine secretion of isolated perfused rat pancreas.

The role of intrapancreatic neurons in the action of cholecystokinin (CCK) on pancreatic exocrine secretion of the totally isolated, perfused rat pancreas was investigated. Intrapancreatic neurons were activated by applying electrical field stimulation (EFS) to the isolated pancreas for 45 min. When applying EFS, spontaneous pancreatic secretions of fluid and amylase increased until the second 15-min period of EFS and then decreased during the third 15-min period. Atropine (2 microM) notably reduced the EFS-evoked pancreatic secretions of fluid and amylase. The CCK-induced (10 pM) pancreatic secretions of fluid and amylase elevated further in the first 15-min period of EFS and then gradually resumed to the levels observed during application of CCK alone in the third 15-min period of EFS. However, the CCK-induced pancreatic secretions remained elevated even in the third 15-min period of EFS when an action of endogenous somatostatin was inhibited by cyclo-(7-aminoheptanonyl-Phe-d-Trp-Lys-Thr[BZL]) (10 nM) or pertussis toxin (200 ng/ml). EFS further elevated spontaneous exocrine secretion by the cysteamine-treated (300 mg/kg) pancreas, but this was markedly reduced, to normal levels, by infusing somatostatin (100 pM). EFS increased the numbers of immunoreactive somatostatin cells in the Langerhans' islets. The results indicate that intrapancreatic neuronal activation influences CCK-induced pancreatic secretions in a dual-phase pattern in the rat: an increase during the early phase and a decrease during the late phase. Endogenous somatostatin released from the islets appears to inhibit the enhancing effect of neuronal activation on CCK-induced pancreatic secretion. Of the intrapancreatic neurons, the cholinergic ones appear to predominate in EFS's effects on CCK-induced pancreatic secretion.

Amylases↗
PubMed2000

Distal myopathy in nephropathic cystinosis.

In long-standing nephropathic cystinosis complications are observed in various organs. Distal myopathy was first described in detail in 1994. The prevalence was calculated to be 24%. We studied seven patients with nephropathic cystinosis with neurophysiological techniques. Only two patients complained of a distal muscle weakness but all showed signs of myopathy on electromyography, which was more pronounced in the distal muscles. Motor and sensory nerve conduction parameters were within normal ranges. One patient with the juvenile form of nephropathic cystinosis also had myopathy. We conclude that distal myopathy can be detected in nephropathic cystinosis even in the absence of clinically overt muscle weakness. Cystine-depleting therapy with cysteamine is recommended for all patients with cystinosis, even after renal transplantation, and the effect on the myopathy should be studied.

Adolescent↗
PubMed2005

Cystinosis as a cause of noncirrhotic portal hypertension.

Cystinosis is a rare autosomal recessive storage disorder, characterized by the abnormal accumulation of cystine in cellular lysosomes. This accumulation, which can occur in any organ system, leads to crystallization of trapped cystine and ultimately cellular death. Hepatic manifestations of Cystinosis although rare, have been described in the literature. However, to our knowledge, only one other case of non-cirrhotic portal hypertension secondary to cystine accumulation in Kupffer cells has been reported. In this case and ours, portal hypertension was found in the absence of bridging fibrosis. Furthermore, in our case, for the majority of the patient's course, hepatic synthetic function remained normal. Cysteamine is therapeutic in this disorder, and can lead to significant removal of cystine, and thus to reversibility of disease, however, it requires high doses and must be taken regularly. Porto-systemic shunting in combination with aggressive medical therapy could potentially benefit patients who develop non-cirrhotic portal hypertension in this clinical setting.

Adult↗
PubMed1991

In vivo voltammetric detection of neuropeptides with micro carbon fiber biosensors: possible selective detection of somatostatin.

The electrochemical activity of catechol- and indoleamines, measured by differential pulse voltammetry (DPV) with specifically electrically pretreated carbon fiber microelectrodes, has been utilized to develop sensitive assays for amine neurotransmitters and metabolites. So far, four oxidation peaks have been recorded in vivo between -200 and +500 mV and are well identified. We now report that by increasing the potential sweep range to +950 mV, a further peak, called Peak 5, was detected at +800 mV in vivo in the striatum of anesthetized rats. Neuropeptides containing tyrosine, tryptophan and/or cysteine appear to be electrochemically active between +600 and +900 mV in vitro in a buffered solution at pH 7.4. The present study investigates the chemical nature of Peak 5 and the possible contribution of electroactive neuropeptides to this in vivo voltammetric signal. Experiments performed in vitro and in vivo with amino acids, neuropeptides, or bacitracin (a potent peptidase inhibitor) support the view that Peak 5 is peptidergic. Furthermore, peripheral administration of cysteamine and intrastriatal injection of specific somatostatin antisera both cause the eventual disappearance of Peak 5, suggesting that somatostatin (which oxidases in vitro at approx +800 mV), or a structurally related peptide, could be the principal component of striatal Peak 5.

Animals↗
PubMed1991

Determination of oxalyl thiolesters, N-oxalylcysteine and N-oxalylcysteamine in biological materials.

A convenient method is described for the quantitative analysis of oxalyl thiolesters (OTEs), a newly discovered class of mammalian metabolites, in biological samples. By this particular technique the total concentration of all OTEs in the sample is determined. The method involves first reacting the biological material with cysteamine (2-aminoethanethiol) or cysteine under conditions that convert OTEs quantitatively to N-oxalylcysteamine (or N-oxalylcysteine), followed by reaction with monobromobimane to give a highly fluorescent derivative that is analyzed by reversed-phase ion-pair chromatography, with tetrabutylammonium ion as the counterion and N-(2-mercaptopropionyl)glycine as an internal standard. The method is capable of detecting as little as 0.6 pmol of the bimane derivative of the N-oxalyl compound in a single HPLC injection. The application of this method has led to the discovery that not only OTEs but also N-oxalylcysteine and N-oxalylcysteamine are normal mammalian metabolites. In various rat tissues the OTE concentration ranges up to 65 nmol/g (wet wt), the N-oxalylcysteine concentration is approximately 10 nmol/g, and the N-oxalylcysteamine concentration is 0-3 nmol/g.

Animals↗
PubMed1990

Cellular recovery of glyceraldehyde-3-phosphate dehydrogenase activity and thiol status after exposure to hydroperoxides.

The activity of the thiol-dependent enzyme glyceraldehyde-3-phosphate dehydrogenase (GPD), in vertebrate cells, was modulated by a change in the intracellular thiol:disulfide redox status. Human lung carcinoma cells (A549) were incubated with 1-120 mM H2O2, 1-120 mM t-butyl hydroperoxide, 1-6 mM ethacrynic acid, or 0.1-10 mM N-ethylmaleimide for 5 min. Loss of reduced protein thiols, as measured by binding of the thiol reagent iodoacetic acid to GPD, and loss of GPD enzymatic activity occurred in a dose-dependent manner. Incubation of the cells, following oxidative treatment, in saline for 30 min or with 20 mM dithiothreitol (DTT) partially reversed both changes in GPD. The enzymatic recovery of GPD activity was observed either without addition of thiols to the medium or by incubation of a sonicated cell mixture with 2 mM cysteine, cystine, cysteamine, or glutathione (GSH); GSSG had no effect. Treatment of cells with buthionine sulfoximine (BSO) to decrease cellular GSH by varying amounts caused a dose-related increase in sensitivity of GPD activity to inactivation by H2O2 and decreased cellular ability for subsequent recovery. GPD responded in a similar fashion with oxidative treatment of another lung carcinoma cell line (A427) as well as normal lung tissue from human and rat. These findings indicate that the cellular thiol redox status can be important in determining GPD enzymatic activity.

Cell Line↗