Biomedical subjects

J Piotrowski

Publications and source records attributed to J Piotrowski.

At least 109 records · Page 6Linked to original sources

PubMed1993

Control of mucin molecular forms expression by salivary protease: differences with caries.

1. A protease activity capable of degradation of the high mol. wt salivary mucus glycoprotein to a low mol. wt glycoprotein form was identified in human submandibular gland secretion. 2. The protease exhibited optimum activity at pH 7.0-7.4, and gave on SDS-PAGE under reducing conditions two major protein bands of 48 and 53 kDa. The enzyme showed susceptibility to PMSF, alpha 1antitrypsin, and egg white and soybean inhibitors, a characteristic typical to serine proteases. 3. The activity of the protease towards the high mol. wt mucus glycoprotein was found to be 3.8-fold higher in submandibular gland secretion of caries-resistant individuals than that of caries-susceptible. Furthermore, the enzyme from both groups displayed greater activity against the mucus glycoprotein of caries-resistant subjects. 4. Since the low mol. wt salivary mucus glycoprotein form is more efficient in bacterial clearance than the high mol. wt mucin, the enhanced expression of this indigenous salivary protease activity towards mucin may be the determining factor in the resistance to caries.

Animals↗

PubMed1993

Inhibition of Helicobacter pylori glycosulfatase activity towards human gastric sulfomucin by a gastroprotective agent, sulglycotide.

1. A glycosulfatase activity towards human gastric sulfomucin was identified in the extracellular material elaborated by Helicobacter pylori, a pathogen implicated in the etiology of gastric disease. 2. The purified enzyme displayed an apparent molecular weight of 30 kDa, and exhibited maximum activity at pH 5.7 in the presence of 0.3% Triton X-100 and 100 mM CaCl2. 3. The H. pylori glycosulfatase activity towards human gastric sulfomucin was inhibited by a gastroprotective agent, sulglycotide. The inhibitory effect was proportional to the concentration of sulglycotide up to 20 micrograms/ml, at which a 98% decrease in mucin desulfation occurred. However, the drug lost the inhibitory effect following its chemical desulfation. 4. The results demonstrate that sulglycotide is a potent inhibitor of H. pylori glycosulfatase and, hence, may be of value in the treatment of gastric disease associated with this bacterial infection.

Anti-Ulcer Agents↗

PubMed1993

Helicobacter pylori lipopolysaccharide inhibition of gastric mucosal laminin receptor: effect of sulglycotide.

1. The effect of cell-wall lipopolysaccharide from Helicobacter pylori, a bacterium implicated in the etiology of gastric disease, on the gastric mucosal laminin-receptor was investigated. 2. The receptor, isolated from gastric epithelial cell membrane by affinity chromatography on laminin-coupled Sepharose, was radioiodinated and incorporated into liposomes which exhibited specific affinity towards laminin-coated surface. 3. The binding of liposomal receptor to laminin-coated surface was inhibited by H. pylori lipopolysaccharide, which at 50 micrograms/ml caused a nearly complete (97%) inhibition in binding. 4. The inhibitory effect of the lipopolysaccharide was prevented by a cytoprotective agent, sulglycotide, that evoked a 92% restoration in binding at 40 micrograms/ml. 5. The results demonstrate that through its lipopolysaccharide H. pylori is capable of disrupting the gastric mucosal integrity and that this detrimental effect could be successfully countered by sulglycotide.

Animals↗

PubMed1993

Inhibition of gastric mucosal mucin receptor by Helicobacter pylori lipopolysaccharide.

A gastric mucosal mucin receptor has been isolated from the epithelial cell membrane by affinity chromatography on wheat germ agglutinin. The receptor protein displayed an apparent molecular weight of 97kDa and exhibited binding specific to gastric mucin in a concentration-dependent manner. The binding of mucin to the mucosal receptor was inhibited by lipopolysaccharide from H. pylori. The inhibitory effect was proportional to the concentration of lipopolysaccharide up to 30 micrograms/ml, at which concentration a 91% decrease in binding occurred. The results suggest that H. pylori lipopolysaccharide is capable of disrupting the integrity of mucus perimeter of gastric mucosal defense by interfering with epithelial cell-mucin binding.

Animals↗

PubMed1993

Effect of ebrotidine on gastric mucosal EGF and PDGF receptor expression.

The effect of ebrotidine, a new H2-blocker with gastroprotective properties, on the expression of gastric mucosal epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) receptors, was investigated. Mucosal cell membranes were isolated from rats receiving twice daily for 5 days a dose of 100mg/kg ebrotidine or 100mg/kg ranitidine or vehicle only. Assays for EGF and PDGF revealed the presence of both types of receptors, activation of which led to enhanced tyrosine kinase activity. The receptor binding values in the control group were 2.4 fmol for EGF and 1.45 fmol/mg protein for PDGF, whereas the values in the ebrotidine group increased for EGF by 65.7% and 38.6% for PDGF, but no such effect was observed with ranitidine. The results suggest that the gastroprotective properties of ebrotidine stem from its ability to stimulate the epithelial proliferative activities through the enhancement of EGF and PDGF receptors expression.

Animals↗

PubMed1993

Identification of buccal mucosal mucin receptor.

A receptor for salivary mucin was isolated from epithelial cell membrane of buccal mucosa by a procedure involving membrane solubilization with octylglucoside followed by affinity chromatography on Sepharose-bound wheat germ agglutinin. The receptor protein displayed an apparent molecular weight of 97kDa and exhibited binding specific to mucin in a concentration-dependent manner. The receptor, furthermore, showed a requirement for carbohydrate chains in mucin for binding, as their removal caused a marked (89%) reduction in binding capacity. Scatchard analysis revealed a linear plot with a single class of high affinity binding (Kd = 1.1 microM; Bmax = 7.68nmol/mg protein. The results provide for the first time evidence for the existence in buccal mucosa of a specific receptor for salivary mucin.

Animals↗

PubMed1993

[Evaluation of microsomal enzyme function in the liver in patients with duodenal ulcer treated with famotidine].

The studies of microsomal liver enzyme activity by means of a respiratory test with 14C-aminopyrine (ABT) were carried out in 20 patients with duodenal ulcer treated for eight weeks with famotidine. The respiratory test was performed before the introduction of treatment (group I), after four weeks of treatment (group II), and after eight weeks of treatment (group III). The mean value of the respiratory test before treatment was 5.32% of the dose/h. After four weeks of treatment with famotidine a significant decrease was found of the test value (x = 4.79% of the dose/h). An even stronger inhibitory action of famotidine on the microsomal system was shown after eight weeks of the treatment (x = 4.46% of the dose/h). These results evidence a depressive effect of famotidine on the activity of liver monooxygenases. In patients taking this drug, other drugs metabolised in the hepatocyte microsomal system should be used with high caution, as well as those which are known to be inhibitors of this system.

Adult↗

PubMed1993

[Transforming growth factors and their role in chronic liver diseases].

The transforming growth factors are endogenous polypeptide substances having own cell receptors. Among them two main factors have been isolated--transforming growth factor alpha (TGF alpha) and beta (TGF beta). TGF alpha is secreted by activated proliferating hepatocytes and by certain neoplastic cells. It stimulates the synthesis of DNA and migration of hepatic epithelial cells. In chronic liver diseases it is produced in increased amounts and stimulates then proliferation and regeneration. TGF beta is released by non-parenchymal liver cells, thrombocytes, and neoplastic cells. It inhibits the synthesis of DNA in many cells, inhibits the synthesis of albumins and fibrinogen and regulates the production of acute phase proteins. In chronic liver diseases it increases the production of fibronectin and collagen, inhibiting at the same time their enzymatic breakdown. TGF beta participates in the development and progression of hepatic fibrosis.

Animals↗

PubMed1993

[Liver microsomal enzyme function in patients with duodenal ulcer treated with cimetidine].

The functional status of hepatocytes was evaluated using the breathing test with 14C-aminopyrine in a group of patients with duodenal ulcer treated with cimetidine, and the reversibility of liver microsomal system activity changes was assessed at various time intervals after the completion of treatment with the above mentioned drug. Thirty patients with duodenal ulcer treated with cimetidine were examined: before the treatment (Ia), after one day of treatment (Ib), after four weeks of treatment (Ic), after eight weeks of treatment (Id), one week after completion of treatment (Ie), and four weeks after completion of treatment. A significant decrease was found of the value of the breathing test already after one day of treatment with cimetidine which was more pronounced after four and eight weeks of treatment. An impaired microsomal system activity was shown even one week after completion of the treatment with cimetidine. The obtained results indicate the necessity of caution when other drugs are administered to patients treated with cimetidine, and this refers particularly to drugs impairing liver function, or metabolized in this organ.

Adult↗

PubMed1993

Enhancement in gastric mucosal laminin receptor expression with ulcer healing.

The expression of gastric mucosal laminin receptor with chronic ulcer healing was investigated. The receptor protein was isolated from gastric epithelial cell membrane of rats at various stages of ulcer healing and following radioiodination incorporated into vesicles which exhibited specific affinity towards laminin-coated surface. The binding assays revealed that the ulcer healing was accompanied by an increase in laminin receptor expression. A significant increase (2.5-fold) in the receptor expression occurred by the third day following the development of ulcer, reached a maximum of 8.6-fold increase by the 14th day when the ulcer was virtually healed, and its high level remained for at least 20 days. The results demonstrate the importance of laminin receptor as an indice of gastric mucosal repair in ulcer healing.

Acetates↗

PubMed1993

Characterization of gastric mucosal mucin receptor.

Mucin receptor was isolated from gastric epithelial cell membrane by a procedure involving membrane solubilization with octylglucoside followed by affinity chromatography on Sepharose-bound wheat germ agglutinin. The receptor protein yielded on SDS-PAGE a single 97kDa band and displayed specific affinity, in a concentration-dependent manner, towards the mucin-coated surface. The receptor showed requirement for carbohydrate chains in mucin for binding, as their removal caused a marked (87%) reduction in binding capacity. Scatchard analysis revealed a linear plot with a single class of high affinity binding (Kd = 43.8 nM; Bmax = 140 pmol/mg protein) sites. The results demonstrate for the first time the presence in gastric mucosa of a specific receptor for mucin.

Animals↗

PubMed1993

[Assessment of microsomal enzyme function in liver of patients with duodenal ulcer treated with famotidine].

The liver microsomal enzymes activity was measured by aminopyrine breath test in 20 subjects with duodenal ulcer disease treated with famotidine for 8 weeks. Aminopyrine breath test was performed, before treatment (group I), after 4 weeks of therapy (group II) and after 8 weeks of treatment with famotidine (group III). The mean aminopyrine breath test value before treatment was 5.32% dose/h. After 4 weeks of treatment with famotidine statistically significant decrease of breath test values (x = 4.79% dose/h) was found. More strong microsomal enzymes inhibition was found after 8 weeks of famotidine therapy (x = 4.46% dose/h). These data indicate an inhibitory effect of famotidine on liver monooxygenases activity. In patients taking this drug, treatment with other drugs metabolised in liver and with drugs inhibiting the microsomal system must be very cautions.

Adult↗

PubMed1993

[Assessment of the functional state of microsomal enzymes in the liver in patients with small cell lung cancer treated with cytostatic drugs].

Assessment of the functional state of the liver microsomal enzymes with 14C-aminopyrine breath test (ABT) was performed in 42 patients with small cell lung cancer before treatment (group I), in 30 patients with small cell lung cancer treated with cytostatic drug after remission induction of Houston program (group II) and in 30 healthy volunteers of control group (group III). The classic liver tests were determined. Statistically low values of aminopyrine breath test in patients with advanced cancer (stadium III) were found. Values of ABT decreased further after the cytostatic drugs treatment. Abnormal results were found in 83% of patients in the group II. Values of classic liver tests in whole population (group I, II, III) were within normal limits. Abnormal values of ABT that indicate inhibition of aminopyrine demethylation may indicate early functional hepatocytes lesion after cytostatic treatment. This test should be done previously in patients needing treatment with other metabolised in liver or with microsomal system inhibitors.

Adult↗

PubMed1993

Salivary mucin modulation of buccal mucosal calcium channel activity.

The effect of the low and high molecular weight salivary mucins on the activity of calcium channel isolated from buccal epithelial cell membranes was investigated. The 45Ca2+ uptake into the vesicle-reconstituted channels, while only moderately (15%) affected by the intact mucin forms, was significantly inhibited (60%) by the acidic mucin fractions. This effect was associated with the sialic acid and sulfate ester groups of the glycoproteins. The channel complex in the presence of epidermal growth factor (EGF) and ATP responded by an increase in protein tyrosine phosphorylation, and the vesicles containing the phosphorylated channels showed a 46% increase in 45Ca2+ uptake. The phosphorylation process was inhibited by the acidic mucins, which also interfered with the binding of EGF to the channel protein. The inhibitory effect was dependent upon the presence of sulfate ester and sialic acid groups, and the loss of the inhibitory capacity occurred following their removal. The results demonstrate the salivary mucins actively participate in the modulation of buccal mucosal calcium channel activity.

Adenosine Triphosphate↗

PubMed1993

Glycosulfatase activity of Porphyromonas gingivalis a bacterium associated with periodontal disease.

Porphyromonas gingivalis, a bacterium implicated in the pathogenesis of periodontal disease, was found to elaborate an extracellular glycosulfatase enzyme. Upon purification by low temperature acetone fractionation, an active enzyme at 60% acetone was obtained which on SDS-PAGE gave a protein band of 37kDa. The glycosulfatase effectively caused desulfation of galactosyl- and lactosylceramide sulfates (pH 5.0) which contain the sulfate ester groups at C-3 of galactose, a well as proteoglycans (pH 5.7-6.2) of gingival tissue which are rich in N-acetylgalactosamine-4-sulfate, but not the sulfated salivary mucin with the sulfate groups at C-6 of galactose and C-6 of N-acetylglucosamine. The results demonstrate for the first time that P. gingivalis displays glycosulfatase activity and that the disruptive action of this enzyme may be a major factor in the etiology of periodontal disease.

Culture Media↗

PubMed1993

Salivary and plasma insulin levels in man.

Changes in plasma and salivary immunoreactive insulin were studied in saliva and blood of 9 healthy subjects following either oral glucose or a test meal ingestion at 30 min intervals for up to 3h. The levels of plasma immunoreactive insulin reached maximum at 60 min with a value of 62.77 +/- 6.52 microU/ml after the glucose load and 62.62 +/- 6.52 microU/ml after the test meal. In the case of salivary immunoreactive insulin levels, the maximum was attained at 90 min with a value of 18.47 +/- 2.68 microU/min after the glucose load and 22.40 +/- 2.01 microU/min after the test meal. Positive linear correlation (r = 0.74) was found between the salivary and plasma immunoreactive insulin levels.

Administration, Oral↗

PubMed1993

Inhibition of Helicobacter pylori colonization by an antiulcer agent, sulglycotide.

Sulglycotide, a potent antiulcer agent derived from duodenal mucus glycopeptide through sulfation of the carbohydrate moieties, was evaluated with respect to its ability to interfere with H. pylori mucosal attachment. H. pylori cells were incubated with sulglycotide or human gastric mucin and then examined for their inhibitory capacity of H. pylori attachment to erythrocytes. Titration data revealed that the mucin inhibitory activity was confined to its sulfomucin fraction, the titer of which was found to be 16-fold higher than that of intact mucin. The data with sulglycotide showed that the inhibitory titer of this agent against H. pylori attachment was at least 30-fold higher than that of the sulfated gastric mucin fraction. The results point towards the involvement of sulfomucins in the protection of gastric mucosa from H. pylori colonization and demonstrate that sulglycotide, because of structural similarities, is ideally suited to augment the inherent mucosal defenses against this pathogen.

Anti-Ulcer Agents↗

PubMed1993

Glycosulfatase activity of Helicobacter pylori towards gastric sulfomucin: effect of nitecapone.

A glycosulfatase activity towards human gastric sulfomucin was identified in the extracellular material elaborated by H. pylori, a pathogen implicated in the etiology of gastric disease. The purified enzyme exhibited maximum activity at pH 5.7 in the presence of 0.3% Triton X-100 and 100mM CaCl2, and displayed on SDS-PAGE an apparent molecular weight of 30kDa. The H. pylori glycosulfatase effectively caused desulfation of N-acetylglucosamine-6-sulfate and galactose-6-sulfate of the carbohydrate chains of mucins, as well as that of glucose-6-sulfate of glyceroglucolipids, but was ineffective towards galactosyl -and lactosylceramide sulfates which contain galactose-3-sulfate. The glycosulfatase activity towards human gastric sulfomucin was inhibited by an antiulcer agent, nitecapone, which at its optimal concentration (100 micrograms/ml) caused a 61% decrease in mucin desulfation. The results show that H. pylori through its glycosulfatase activity causes desulfation of sulfated mucins and glyceroglucolipids of the protective mucus layer, and that nitecapone is able to interfere with this detrimental action.

Anti-Ulcer Agents↗