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PubMedDate not supplied

Somatostatin and Alzheimer's disease.

One of the most consistent neurochemical deficits in Alzheimer's disease is a reduction in cortical somatostatin concentrations. The probability of a predominant regulatory change is heightened by the finding that 90% of somatostatin positive nonpyramidal neurons are also positive for NADPH, and NADPH neurons are 'protected' in Alzheimer's disease and do not appear to be lost. The first evidence that somatostatin influences learning and memory processes in experimental animals was published more than a decade ago. These reports of somatostatin effects on cognitive functions in rats were later confirmed by several other studies. The somatostatin depleting substance cysteamine inhibited the learning and memory performance of rats in active and passive avoidance behavior tests. Post-mortem human studies suggest that although somatostatin concentration is reduced, the somatostatin receptors are less affected in the brain in Alzheimer's disease. These findings may be of importance for possible therapeutic approaches using somatostatin-receptor-influencing compounds.

Journal Article↗
PubMed1994

Amylin given by central and peripheral routes inhibits acid gastric secretion.

The effect of rat amylin on acid gastric secretion in the pylorus-ligated, unanesthetized rat system (Shay test) was examined. Amylin administered peripherally (2.5, 5, 10, 40, 100, or 160 micrograms/kg, SC) or intracerebroventricularly (1.5, 2.7, or 5 micrograms/rat, ICV) decreased acid gastric secretion in a dose-dependent manner. Central administration of amylin gave a stronger suppression of gastric secretion than peripheral injection. In addition, ICV-injected amylin inhibited insulin-stimulated acid gastric secretion and was effective in suppressing acid gastric secretion in rats depleted of somatostatin by pretreatment with cysteamine. This study suggests that amylin may participate in the central regulation of acid gastric secretion and indicates a possible biological function of amylin as a gastrointestinal peptide.

Amyloid↗
PubMed1984

Paradoxical effects of perturbation of intracellular levels of glutathione on halothane-induced hepatotoxicity in hyperthyroid rats.

Exposure of hyperthyroid rats to halothane results in a centrilobular necrosis of the liver and an 11-fold increase in serum glutamate-pyruvate transaminase (SGPT) levels. These effects are not seen in euthyroid animals. Paradoxically, administration of diethylmaleate to hyperthyroid rats significantly decreased the levels of hepatic glutathione and blocked the halothane-induced hepatic necrosis as well as decreased the elevation of SGPT. In contrast, pretreatment of animals with N-acetylcysteine, an intracellular sulfhydryl repletor , significantly increased the severity of the halothane-induced hepatic necrosis and increased the elevation of SGPT. Similarly, cysteamine, another intracellular sulfhydryl repletor , also exacerbated halothane-induced liver injury. Halothane-induced hepatotoxicity is at least in part apparently regulated by cellular glutathione levels. Paradoxically, glutathione seems to be involved in the bioactivation rather than the detoxification of halothane.

Acetylcysteine↗
PubMed1992

Central dopamine involvement in experimental gastrointestinal injury.

1. Rats were prepared with intracerebral cannulas for microinjection of test compounds into various brain regions. 2. Selective dopamine D1 agonists (SKF38393, SKF75670C) and a D1 antagonist (SCH23390) were injected into the cell body regions of the nigrostriatal, mesolimbic and mesocortical dopamine tracts or into a terminal field of these tracts (caudate nucleus, central nucleus of the amygdala and medial prefrontal cortex) prior to gastric ulcer induction by cold-restraint stress or duodenal ulcer induction by cysteamine. 3. The dopamine D1 agonists reduced both stress gastric ulcers and duodenal lesions most significantly when given into either the cell body region or a terminal field of the mesolimbic DA tract with much less effects seen for the nigrostriatal tract. 4. No effects were seen upon infusion of the agonists into the mesocortical cell body or terminal field regions. 5. The D1 antagonist worsened both stress-induced gastric lesions and duodenal lesions if given into mesolimbic regions and, to a much lesser extent when injected into the nigrostriatal tract. 6. No effect of the D1 antagonist was seen upon administration into the mesocortical tract. 7. Central dopamine D1 receptors, particularly in the mesolimbic DA tract, appear to be involved in mediating the gastrointestinal consequences of exposure to stress.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1982

Studies on paracetamol-induced lipid peroxidation.

Post-mitochondrial supernatants isolated from livers of rats given a single large oral dose of paracetamol (800 mg/kg) showed rapid rates of lipid peroxidation when incubated in vitro. As a result of paracetamol administration the level of reduced glutathione (GSH) declined to approx. 20-25% of the peak physiological value. Addition of reduced GSH to the supernatant inhibited the peroxidation. Paracetamol-induced lipid peroxidation was inhibited in vitro by antioxidants (e.g. vitamin E) but was unaffected by superoxide dismutase and mannitol. N-acetyl cysteine and cysteamine inhibited lipid peroxidation in vitro in a cytosol-dependent manner in the absence of glutathione. Lipid peroxidation probably occurs simultaneously with the proposed covalent binding of the active metabolite of paracetamol. Since the former process is known to cause severe and extensive membrane damage, it may be a very important factor in paracetamol-induced liver necrosis.

Acetaminophen↗
PubMed1990

Interactions between paraquat, endogenous lung amines' antioxidants and isolated mouse Clara cells.

The ability of paraquat to damage mouse lung Clara cells in the presence and absence of herbicide inhibitors is investigated using a cell culture system. Clara cell damage is assessed on the loss of nitroblue tetrazolium reductase activity and the inability to attach and spread on an extracellular matrix. Endogenous amines such as putrescine and spermidine reduce paraquat-induced damage at low concentrations indicating that they compete for the same cell surface receptor as paraquat and thus potentially block the accumulation of the herbicide. The efficacy of 10 microM exogenous putrescine as a protectant is reduced the longer the time before it is added to the cultures. Clara cells contain high levels of NADPH-dependent P-450 reductase which is required to redox cycle the paraquat and generate reactive oxygen radicals. Compounds with antioxidant properties are examined for their ability to reduce the Clara cell damage. Cystamine, the disulphide form of the naturally occurring thiol, cysteamine, and taurine, a metabolite of cystamine, both of which are accumulated in the lung, do not reduce paraquat-induced Clara cell damage. Another antioxidant, alpha-tocopherol is also ineffective but reduced glutathione (GSH), present in high quantities (3.2 mM) in clara cells, could reduce damage to the cultured cells. Cysteine, a precursor of GSH, can also prevent Clara cell damage when the concentration of paraquat is low.

Animals↗
PubMed1990

Protein synthesis stimulated in sonicated sugar beet cells and protoplasts.

Sugar beet suspension cells and protoplasts were exposed to 20 kHz ultrasound and the amount of 35S-methionine incorporated into cellular protein was determined after 2 days of culture. The incorporation of 35S-methionine in cells was enhanced up to 90% after sonication for 220-770 ms at 1.2-3.5 W/cm2 which reduced viability 5-11% and decreased the average size of cell aggregates. In protoplasts, the 35S-methionine incorporation was increased up to 31% after sonication for 220-550 ms at 0.3-1.0 W/cm2 with a concomitant reduction in viability of 10-16%. At higher ultrasonic energies, 35S-methionine incorporation declined proportionally to the reduction in protoplast viability. At concentrations up to 30 mM, cystamine and cysteamine did not affect 35S-methionine incorporation or viability of the sonicated protoplasts. These results show that mild ultrasonic irradiation can stimulate protein synthesis in plant cells and protoplasts significantly.

Plant Cells↗
PubMed1989

Production and secretion of the 21-23.5 kDa prolactin-like molecules.

We recently described the presence of a series of prolactin (PRL)-like molecules (PLMs) in the rat pituitary gland and showed that their formation was not due to artifactual proteolysis of 24 kDa PRL during extraction or to degradation of PRL in lysosomes. In this study we have found (1) in vitro translation of pituitary cell RNA to result in the production of only 24 kDa monomer isoform 2 and no PLMs, (2) that secretion of newly synthesized PLMs is differently regulated than at least a proportion of newly synthesized monomers, (3) that secretion of newly synthesized PLMs occurs after at least a 6 h delay, (4) that cysteamine (a) inhibits the release of the PLMs, (b) causes an increase in their amount versus isoform 2, and (c) causes an intracellular accumulation of pleiomorphic, immature secretory granules, and (5) that cells grown under degranulating culture conditions do not contain PLMs. These results, using normal anterior pituitary cells in primary culture, demonstrate the potential for differential release of the PLMs versus monomer PRL in vivo and are consistent with the production of the PLMs from 24 kDa monomer isoform 2 during secretory granule condensation.

Animals↗
PubMed1984

Enhancement by phenothiazine and 2,5-di-O-acetyl-D-glucosaccharo-(1,4)(6,3)-dilactone of bladder carcinogenicity of N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide in rats.

Rats concomitantly fed N-[4-(5-nitro-2-furyl)-2-thiazolyl] formamide (FANFT) and phenothiazine, or concomitantly fed FANFT and Glucaron then fed Glucaron alone had significantly greater incidences of transitional cell carcinomas of the bladder than rats fed FANFT alone. Caffeine and cysteamine did not affect FANFT bladder carcinogenesis. Phenothiazine induced nitroreductase activity of hepatic microsomes.

Animals↗
PubMed1987

Anti-ulcer activity of calcitonin gene-related peptide in rats.

Calcitonin gene-related peptide (CGRP, 5-10 micrograms/kg s.c.). reduced both incidence and degree of indomethacin- or acetylsalicylic acid (ASA) plus HCl-induced gastric as well as cysteamine-induced duodenal ulcers in rats. CGRP had no effect on ethanol-induced gastric lesions. The anti-ulcer activity of CGRP is most likely ascribable to its potent antisecretory properties.

Animals↗
PubMedDate not supplied

Misonidazole-induced biochemical alterations of mammalian cells: effects on glycolysis.

Incubation of Ehrlich ascites tumor cells with misonidazole under aerobic conditions causes a stimulation of glucose consumption which is probably related to stimulation of hexose monophosphate shunt activity. Incubation of Ehrlich cells with 5 mM misonidazole under hypoxic conditions results in a time-dependent inhibition of glycolysis, seen when treated cells are washed and resuspended in fresh buffered saline or media. This inhibition does not appear to be related to breakdown and loss of pyridine nucleotides from the cells during misonidazole treatment, nor is it a consequence of cell death. Post-incubation in buffer containing cysteine or cysteamine restores cellular glycolytic activity to near control levels. Partial inhibition of glucose consumption after incubation with misonidazole also occurs with V79-379A, V79-171B, EMT6 and A549 cell lines. The extent of inhibition varies among the lines, but is accompanied by approximately a 50% reduction in intracellular non-protein thiol levels in all cases. Ehrlich cells incubated anaerobically with misonidazole lose their response to the uncoupler 2,4-dinitrophenol, which normally increases glucose consumption, and exhibit less ability to metabolize pyruvate. Cells incubated under anaerobic conditions but in the absence of misonidazole do not show these effects.

Aerobiosis↗
PubMedDate not supplied

Misonidazole: inter-related factors affecting cytotoxicity.

A detailed investigation was undertaken of reported modifiers of the toxicity towards hypoxic cells of misonidazole. The modifiers tested were medium type, cell type, cell density, concentration of misonidazole, addition of serum, addition of sulfhydryl, addition of oxygen and pH. The latter 5 modifiers were found to be most important and were studied in many of the possible combinations. Serum has its greatest protective effect at low concentration (e.g. 0.5 mM) of misonidazole. In the absence of serum, the (log10) survival curve for misonidazole toxicity can be described mathematically as a function of time by a shoulder (DQ) inversely related to misonidazole concentration, and a slope (1/D0) related directly to log10 misonidazole concentration. Sulfhydryl's (cysteamine) protective effect dominates at high concentrations of misonidazole. The protective action of SH can change to potentiative in the absence of serum or at high pH. Addition of oxygen results in overall protection but no relative changes in the effect of the other modifiers. Drugs like ascorbate and disulfide may only potentiate toxicity to the level found in the absence of serum.

Animals↗
PubMed1986

Potentiation of nitrogen mustard cytotoxicity to leukemia cells by sulfur-containing compounds administered in vivo.

Fifteen sulfur-containing compounds were examined for their ability to both protect normal hematopoietic stem cells (NCFU) from the cytotoxic effect of nitrogen mustard (HN2), and potentiate the cytotoxicity of HN2 to AKR leukemia cells (LCFU). All except four agents demonstrated some protection of NCFU with WR-2721 being most active. Five of the agents were also protective for LCFU with cysteine and glutathione being most active. However, a number of agents potentiated the cytotoxicity of HN2 to LCFU, the most active being disulfiram and AET followed by cysteamine, DMSO, WR-638, and WR-3689. The dose-response relationship for the potentiation was defined for DMSO. A second leukemia model, L1210, was also studied for potentiation of HN2 cytotoxicity by four of the most active agents--WR-2721, AET, DMSO, and disulfiram. The first two agents showed no effect (either protection or potentiation) when given either 15 min or 6 hr before HN2 administration. The last two agents, however, potentiated the cytotoxicity to a level similar to that found with the AKR leukemia.

Amino Acids↗
PubMed1986

Modulatory role for prolactin in the elevation of striatal dopamine receptor density induced by chronic treatment with dopamine receptor antagonists.

The chronic administration of haloperidol (HAL), domperidone (DOM), or sulpiride (SUL) increased the density of striatal dopamine (DA) receptors in intact but not in hypophysectomized (Hypox) male rats. This effect was independent of changes in body weight of the rats and of the drugs' abilities to produce cataleptic behavior. All treatments of intact rats increased serum rat prolactin (rPRL) concentrations, while Hypox rats had rPRL levels equivalent to zero. At the doses used in these studies, the striatal DA receptor densities were increased only if the rPRL levels were also increased. Chronic cysteamine (CYS) treatment decreased body weight gain, acutely decreased cataleptic behavior to HAL, decreased serum rPRL levels, and prevented the increase in serum rPRL levels due to HAL administration. While CYS itself did not alter striatal DA receptor density, it prevented the increase in density associated with the chronic administration of HAL (1 mg/kg). Since CYS decreased rPRL levels, these results lend further support to the hypothesis that rPRL (and prolactin in general) is a pituitary hormone with modulatory action on the increase in striatal DA receptor density.

Animals↗
PubMed1987

High-performance liquid chromatography-fluorometry for the determination of thiols in biological samples using N-[4-(6-dimethylamino-2-benzofuranyl) phenyl]-maleimide.

The selective determination of thiols in biological samples was investigated by high-performance liquid chromatography using N-[4-(6-dimethylamino-2-benzofuranyl)phenyl] maleimide, which was found to give fluorescent products when treated with certain thiols. Six kinds of thiol (reduced glutathione, cysteine, N-acetylcysteine, cysteamine, homocysteine and coenzyme A) could be separated simultaneously within ca. 12 min and determined at final level of sensitivity. The method was successfully applied to the determination of thiols in rat tissues and plasma and in human normal serum.

Animals↗
PubMed1986

Anti-ulcerogenic effect of banana powder (Musa sapientum var. paradisiaca) and its effect on mucosal resistance.

Orally administered banana pulp powder (Musa sapientum var. paradisiaca) was shown to have significant anti-ulcerogenic activity in rats subjected to aspirin, indomethacin, phenylbutazone, prednisolone and cysteamine and in guinea-pigs subjected to histamine. Banana powder not only increased mucosal thickness but also significantly increased [3H]thymidine incorporation into mucosal DNA. Relative to untreated control sections, histological studies showed that banana treatment increased staining by alcian blue in the apical cells with staining noted in the deeper layers of the mucosal glands. Banana-treated and control sections were also stained for DNA by the Feulgen reaction. The banana-treated sections showed a greater aggregation and intensity of pink spots when compared to controls. The present study suggests that banana powder treatment not only strengthens mucosal resistance against ulcerogens but also promotes healing by inducing cellular proliferation.

Animals↗
PubMed1986

Evaluation of mastic, a crude drug obtained from Pistacia lentiscus for gastric and duodenal anti-ulcer activity.

The effect of mastic, a concrete resinous exudate obtained from the stem of the tree Pistacia lentiscus, has been studied on experimentally-induced gastric and duodenal ulcers in rats. Mastic at an oral dose of 500 mg/kg produced a significant reduction in the intensity of gastric mucosal damage induced by pyloric ligation, aspirin, phenylbutazone, reserpine and restraint + cold stress. It produced a significant decrease of free acidity in 6-h pylorus-ligated rats and a marked cytoprotective effect against 50% ethanol in rats which could be reversed by prior treatment with indomethacin. The protective effect was not seen when it was given intraperitoneally in phenylbutazone and restraint + cold stress models. The reduction in the intensity of ulceration in cysteamine-induced duodenal ulcers was not found to be statistically significant in mastic-pretreated rats. The results suggest that mild antisecretory and a localized adaptive cytoprotectant action may be responsible for its anti-ulcer activity. These observations support the results of an earlier study on the clinical effectiveness of mastic in the therapy of duodenal ulcer.

Animals↗
PubMed1996

Protective effect of UL-409, a herbal formulation against physical and chemical factor induced gastric and duodenal ulcers in experimental animals.

UL-409, a herbal formulation, was investigated for its possible ulcero-protective activity in Wistar rats of either sex and male guinea pigs. Oral administration of UL-409 at a dose of 600 mg/kg significantly prevented the occurrence of cold-restraint stress induced ulcerations. It significantly inhibited gastric ulceration induced by alcohol and aspirin, as well as cysteamine and histamine induced duodenal ulcers in rats and guinea pigs, respectively. The volume and acidity of gastric juice in pyloric ligated rats was reduced by UL-409. It also significantly, and dose dependently, promoted gastric mucus secretion in normal as well as in stress, drug and alcohol induced ulceration in animals. On the basis of these observations, we conclude that UL-409 possesses antiulcer activity and that the observed activity may be due to the modulation of defensive factors by improvement in gastric cytoprotection.

Animals↗