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PubMed1977

Secretory surface area and phosphatase activity of frog gastric mucosa.

Gastric mucosae were isolated from the European frog, R. temporaria, and after 5-7 h, stimulated with histamine (10(-4) M) and theophylline (5 mM). Acid secretion increased about fourfold, and this was accompanied by a threefold increase in secretory surface of the oxyntic cells, as determined in electron micrographs with conventional morphometric techniques. At the same time phosphatase activity of the secretory surface increased. Other experiments showed that the latter was due to an acid phosphatase, with pH optimum near 3. It appears that the increase in surface phosphatase with stimulation can be attributed to a diminished local pH and not to the increase in surface area demonstrated in this study.

Acid Phosphatase↗

PubMed1980

Ba2+ inhibition of electrogenic Cl- secretion in vitro frog and piglet gastric mucosa.

Gastric mucosae from frogs and newborn pigs were used for in vitro investigation of the effects of Ba2+ (10 microM to 7 mM) on transepithelial potential difference (PD), resistance and conductance (G), short-circuit current (Isc), H+ secretion, and transepithelial fluxes of 36Cl-. Ba2+ in the serosal, but not the mucosal, solution of both preparations caused PD, G, Isc, and Cl- secretion (JnetCl, Isc conditions) to decrease, while H+ secretion remained constant. Because the oxyntic cells were most likely the site of action for Ba2+, these cells must have the capacity to secrete Cl- in excess of H+ ions. The inhibitory effect of Ba2+ was not due to competition in the serosal membrane by Ba2+ for surface charges, Ca2+ sites, Na+ sites, or Cl- sites. When [K+] in both the mucosal and serosal solutions or in just the serosal solution ([K+]s) alone was increased to 10 mM, the inhibitory effects of low [Ba2+] were reduced; however, at higher [Ba2+], Isc was stimulated. At least part of the Ba2+ effect seems to be due to blockage of K+ channels in the serosal membrane of oxyntic cells. High [K+]s also caused decreased PD and Isc (but increased G) with no change in H+ secretion. It is proposed that during Isc conditions, JnetCl involves a neutral Na+-dependent accumulation of Cl- within oxyntic cells and a passive, conductive efflux fromthe cells into the mucosal solution. Ba2+ and high [K+] may alter this transport by depolarizing and, under certain conditions, hyperpolarizing intracellular voltage.

Animals↗

PubMed1986

Organ culture of human gastric mucosa and gastric cancers. 1. Morphological aspects.

An organ culture system for explants of human gastric mucosa and gastric cancer from surgical resection specimens is described. Pyloric mucosa has been successfully maintained in vitro for up to 120 h, and gastric carcinoma for up to 48 h. Morphological preservation by light and electron microscopy was good, although some simplification of the glandular pattern occurred in normal mucosa with longer periods of in vitro culture. [3H]-thymidine and [3H]-leucine uptake was assessed by autoradiography, and patterns of uptake resembled those described in vivo in normal gastric mucosa and gastric intestinal metaplasia. Labelling indices with [3H]-thymidine were however low compared with in vivo estimates. Successful organ culture of human gastric tissue offers a useful method for investigating factors affecting growth control in normal and neoplastic gastric epithelium.

Adenocarcinoma↗

PubMed1999

Enhanced expression of inducible nitric oxide synthase and nitrotyrosine in gastric mucosa of gastric cancer patients.

Recent studies (K. Komoto et al., Am. J. Gastroenterol., 93: 1271-1276, 1998) have shown that Helicobacter pylori infection is associated with gastric cancer. However, the mechanism of H. pylori in carcinogenesis has not been clarified. H. pylori infection leads to a sustained production of reactive nitrogen species that may contribute to cause DNA damage. In this study, we examined the expression of inducible nitric oxide synthase (iNOS) and nitrotyrosine in gastric mucosa. The expression of iNOS and nitrotyrosine was examined by immunohistochemistry in 93 patients who initially underwent gastric biopsies between 1975 and 1992. Thirty-four individuals were later found to have gastric cancer at least 2 years after the initial biopsies (group A). The other 59 subjects have shown no evidence of gastric cancer during long-term follow-up. Fifty-one of these patients were positive for H. pylori (group B), and eight were negative for H. pylori (group C). The expression of iNOS and nitrotyrosine in the gastric mucosa was significantly higher in H. pylori-positive groups A and B than in H. pylori-negative group C. Among the H. pylori-positive patients, the expression of iNOS and nitrotyrosine was significantly higher in group A than in group B. These results suggest that high production of iNOS and nitrotyrosine in the gastric mucosa infected with H. pylori may contribute to the carcinogenesis of gastric cancer.

Adult↗

PubMed1989

Cellular energy status of the gastric mucosa and gastric mucosal prevention by vitamin A in indomethacin-treated rats.

To evaluate the cellular energy status of gastric mucosa during the development of gastric mucosal damage and its prevention by application of a cytoprotective scavenger (vitamin A) in rats treated with indomethacin, the tissue levels of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and lactate were measured enzymatically, while the concentration of cyclic adenosine monophosphate (cAMP) was measured by radioimmunoassay, 4 h after the treatment with indomethacin and vitamin A simultaneously. It was found that a) the tissue levels of ATP, cAMP, AMP and the ratio of ATP/ADP were increased dose-dependently in the gastric mucosa in connection with the development of gastric mucosal prevention produced by vitamin A, b) the tissue level of ADP was decreased dose-dependently by vitamin A in indomethacin-treated rats, and c) the value of "energy charge" and the ratio of the ATP-ADP was unchanged during the vitamin A treatment in indomethacin-treated rats. The presence of tissue hypoxia could not be proved either in the development of indomethacin-induced gastric mucosal damage nor in the prevention of gastric mucosal damage by vitamin A.

Adenosine Diphosphate↗

PubMed1979

The distribution and localization of immunoglobulin in the gastric mucosa and gastric cancer.

The distribution and localization of immunoglobulin in the gastric mucosa and gastric cancer were studied by means of immunofluorescence. In the lamina propria of the stomach, like the other parts of the gastrointestinal tract, IgA producing cells predominated, but their population density varied from case to case. The main portion of secretion of IgA in the stomach was deep foveolar epithelium. IgA containing epithelial cells in the stomach were much less than those in the intestine, but they increased with advancement of intestinal metaplasia. Some gastric cancer cells retained the ability of secretory component production and took up IgA in their cytoplasm.

Antibody-Producing Cells↗

PubMed2002

Reduced PTEN expression in gastric cancer and in the gastric mucosa of gastric cancer relatives.

OBJECTIVES: Gastric cancer is a leading cause of cancer-related deaths worldwide, and the genetic and molecular alterations underlying its pathogenesis are largely unknown. PTEN, a tyrosine phosphatase, is frequently mutated in brain and breast cancers but not in gastric cancers. In order to assess the role of PTEN in gastric carcinogenesis, we analysed the expression of PTEN in human gastric cancer and in the gastric mucosa of cancer relatives. METHODS: Gastric cancer tissues were obtained from 26 patients with gastric cancer undergoing upper-gastrointestinal endoscopy or resection for gastric cancer. Furthermore, 21 first-degree relatives of gastric cancer patients and 12 healthy individuals agreed to undergo upper-gastrointestinal endoscopy. In all cases, biopsies were taken from the antrum and corpus. PTEN expression was assessed by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) analysis and immunohistochemistry. RESULTS: PTEN expression was reduced or absent in 21/26 gastric cancers compared with the matched non-malignant gastric biopsy (P < 0.001). Furthermore, PTEN expression was reduced significantly in the antrum biopsy of first-degree relatives compared with healthy controls (P < 0.05). CONCLUSIONS: Reduced expression of PTEN in gastric cancer points to another mechanism apart from PTEN mutation that may be involved in the pathogenesis of gastric cancer. The reduction of PTEN expression was also observed in first-degree relatives.

Aged↗

PubMed1981

[Ultracytochemical study of oxidoreductases in the parietal cells of the gastric mucosa in gastric cancer].

Ultracytochemistry was used to study and compare cytochromooxidase, succinate dehydrogenase and NADH-dehydrogenase activity in gastric mucosa parietal cells in health and in gastric carcinoma associated with decreased acidity of gastric juice. The study demonstrated the reduced activity of the enzymes listed in the mucosal parietal cells in gastric carcinoma. This finding is interpreted as a consequence of disturbed energy supply of hydrochloric acid secretion in gastric carcinoma.

Electron Transport Complex IV↗

PubMed1976

[Findings in the gastric mucosa and gastric secretion in rats treated with methyl O-(4-hydroxy-3-methoxycinnamoyl)reserpate (CD-3400) and reserpine derivatives].

CD-3400 developed by Nippon Chemiphar Co. Ltd., is a new antihypertensive agent belonging to the class of rauwolfa alkaloids. Influence of the agent on gastric mucosa, healing process of acetic acid-induced gastric ulcer and gastric juice in rats was investigated and compared with effects of reserpine and rescinnamine. CD-3400-induced gastric lesions were fewer in number than those produced with reserpine and rescinnamine in fasted rats. After a three day treatment of CD-3400 to fed rats, however, there were few gastric lesions, while reserpine- and rescinnamine-induced gastric lesions were aggravated to a greater extent that when a single administration was given to fasted rats. Influence of CD-3400, reserpine and rescinnamine on the healing process of acetic acid-induced ulcer was insignificant, but treatment with high doses of reserpine and rescinnamine resulted in death. Pretreatment with CD-3400 and reserpine produced a decrease in gastric acid and K+, and an increase in Na+. Repeated administration of reserpine for 5 days resulted in a decrease of both gastric volume and acid, while such was not seen with CD-3400. Treatment with anticholinergic agents such as atropine sulfate and atropine methylbromide inhibited CD-3400- and reserpine-induced gastric lesions. From these results, it would appear that cholinergic factors play a role in the pathogenesis of CD-3400-induced gastric lesions, as in the case with reserpine, and that the responses of these lesions to reserpine and CD-3400 correlate with changes of ionic fluxes in gastric juice.

Acetates↗

PubMed1986

Hemodynamics of the gastric mucosa and gastric ulceration in rats and in patients with gastric ulcer.

The microcirculation is the fundamental nutrient supply and waste removal system of all tissues. Recent improvements in spectrophotometric technique have made possible the noninvasive assessment of oxygen supply and utilization in the gastric mucosa. The authors have utilized such methods to assess gastric mucosal hemodynamics. The technique permitted further clarification of the roles of the gastric microcirculation, mucosal oxygenation, and acid secretion in the pathogenesis of stress ulcers in the stomach of rats. Furthermore, it provided important information on the function of gastric mucosal hemodynamics in the healing of gastric ulcers in man. The technique is described along with the authors' correlation studies between spectrophotometric data and other techniques for measuring gastric blood flow (hydrogen gas clearance and aminopyrine clearance methods and direct electromagnetic flowmeter techniques) and the prevention of ulcerogenesis.

Animals↗

PubMed1976

Demethylchlortetracycline-binding proteins in uninvolved gastric mucosa of gastric carcinoma and gastric ulcer patients. Demonstration of a difference between the uninvolved mucosa of ulcer and cancer patients.

The uninvolved gastric mucosa of gastric ulcer and gastric carcinoma patients has been compared in in vitro studies as regards their capacity to bind demethylchlortetracycline (DMCT). Dialysis experiments demonstrated excessive binding of DMCT in gastric cancer. Several electrophoretic fractions were observed that bound DMCT; it was demonstrated that these fractions differed in the uninvolved mucosa of gastric ulcer and gastric cancer patients.

Adenocarcinoma↗

PubMedDate not supplied

Heterogeneous distribution of microcirculatory disturbance in the gastric mucosa during gastric hypercontraction in rats.

Gastric mucosal lesions induced by gastric hypermotility are characteristically observed along the gastric mucosal folds. To determine the role of microcirculatory disturbance in this particular condition, we measured the gastric mucosal haemodynamics after vagal stimulation and also examined histologically the transparent specimens of the transverse section of the contracted stomach in rats. Gastric mucosal haemodynamics measured with a reflectance spectrophotometer showed the repetition of ischaemia-reperfusion during gastric hypermotility. The rapidly frozen and transparent specimen of the corpus showed that gastric mucosa was stretched at the crest and compressed at the base of the mucosal folds. Characteristic distribution of red blood cells was observed; it was dense at the crest of the mucosal folds and sparse at the base. These results suggest that gastric hypermotility may induce the distinctive heterogeneous microcirculatory disturbance in the folds and may contribute to the characteristic localization of mucosal lesions.

Animals↗

PubMed1978

[Immunochemical, electrophoretic and enzymatic analysis of the pepsinogen-pepsin isoforms of human gastric mucosa and gastric tumors].

The obtained specific antiserum against the 1st isoform of pepsinogen of human gastric mucosa responds in immunodiffusion only to the 1st pepsinogen isoform but not to the IId and IIIth one. Human pepsinogen has no common antigenic determinant with pig pepsinogen. The methods of electrophoresis and immunodiffusion reveal the Ist, IId and IIIth isoforms of pepsinogen in human gastric tumors and their metastases, however, they do fail to show any enzymic activity.

Animals↗

PubMed1981

Phosphorylation of membranes from the rat gastric mucosa.

Gastric mucosal membranes derived primarily from parietal cells were found to contain endogenous protein kinase systems as well as several phosphate-accepting substrates. One specific membrane protein with a molecular weight of 88 000 was phosphorylated only in the presence of calcium, while the degree of phosphorylation of three other membrane proteins was similarly increased. The activity of the calcium-dependent protein kinase was found to be totally inhibited in the presence of trifluoperazine, a phenothiazine known to specifically inactivate calmodulin. These results suggest that a calmodulin- and calcium-dependent phosphorylation system may be a component of the parietal cell membrane. Phosphorylation of the membrane proteins was not affected by either cyclic AMP or cyclic GMP. The heat-stable inhibitor protein of cyclic AMP-dependent protein kinase did not inhibit the endogenous protein kinase activity suggesting that the membrane enzyme is not similar to the cytosolic protein kinase. However, the catalytic subunit of the soluble enzyme was capable of phosphorylating a number of membrane proteins indicating that after maximal autophosphorylation of the gastric membranes, phosphate-acceptor sites are still available to the cytosolic cyclic AMP-dependent protein kinase.

Animals↗

PubMed1988

Inhibitory antimicrobial concentrations against Campylobacter pylori in gastric mucosa.

Gastric mucosal concentrations of erythromycin, amoxycillin, ampicillin and ciprofloxacin were determined in patients at upper gastrointestinal endoscopy 38-480 min after a 500 mg dose of erythromycin ethyl succinate, erythromycin stearate, amoxycillin, pivampicillin or ciprofloxacin. All the agents attained concentrations greater than the MIC 90 for Campylobacter pylori. The macrolides attained the lowest concentrations. There was no significant difference between concentrations attained with erythromycin ethyl succinate and stearate. High concentrations were attained by amoxycillin (range 14.6-322 mg/kg) and pivampicillin (range 47.5-209 mg/kg). Ciprofloxacin attained very high concentrations (range 35-1762 mg/kg); inhibitory concentrations 35 mg/kg) were still present at 6 h after the dose. Ciprofloxacin and erythromycin are ineffective in vivo despite these high gastric mucosal concentrations. Penetration into the gastric mucus and crypts where C. pylori is found will be determined by physicochemical properties of the antimicrobials, such as pKa, stability, activity over a wide range of pH, and lipid solubility.

Adult↗

PubMed1992

Subcellular localization of prostaglandin E2 receptors in the gastric mucosa.

Gastric mucosal PG E2 receptors are the common antisecretory working point of all prostanoid types and may also be involved in "protective" effects. We investigated the subcellular localization of these receptors, as measured by displaceable 3H-PG E2 binding, and identified different organelles by monitoring the activities of specific marker enzymes. Porcine mucosal homogenates were subdivided by differential centrifugation into fractions P1 (1000 x g), P2 (20,000 x g), P3 (300,000 x g) and the supernatant S1. P3 was further fractionated over a series of sucrose step gradients. Mitochondria and lysosomes were enriched in P2 (maximum specific activities of cytochrome-c-oxidase of beta-glucosidase, beta-glucuronidase, beta-galactosidase, respectively). Plasma membranes (alkaline phosphatase, gamma-glutamyl-transpeptidase, 5-nucleotidase), tubulovesicles (H+/K(+)-ATPase) and rough endoplasmic reticulum (NADPH-cytochrome-c-reductase) were mainly found in P3, which also contained the majority of 3H-PG E2 binding sites. In contrast, prostanoid binding was barely detectable in S1. Density fractionation of P3 revealed that 3H-PG E2 binding sites shared a similar sedimentation profile with plasma membranes and tubulovesicular markers. No or negative correlation was found with lysosomes, rough endoplasmic reticulum and mitochondria. We conclude that mucosal PG E2 receptors are predominantly located at the cell surface. This supports the view that prostanoids inhibit gastric secretion through membrane receptors, but gives no clue for intracellular "protective" working points.

Animals↗

PubMed1989

[Immunochemical identification and localization of cytochrome P-45OHS; isozyme in human gastric mucosa and gastric carcinoma].

Monoclonal antibody to rat liver cytochrome P-450 j isozyme, an activating enzyme specific to nitrosamine metabolism, was used in combination with immunoblotting, densitometer scanning of SDS-PAGE gels, and immunohistochemical staining, there was a trace of P-450 isozyme (Mr. 51. 5 kd) in human gastric mucosa with or without cancer. It was similar to P-450 j in molecular weight, catalysis and immunochemistry. We named it P-450 HSj isozyme. Both in 25 gastric cancer patients and 17 non-cancer patients, the concentrations (%) of P-450 HSj in the mucosa of the lesser curvature were higher than those of the greater curvature (P less than 0.01). This might be one of the important reasons why gastric carcinoma caused by nitrosamines is most common in the lesser curvature. The P-450 HSj was localized in the cytoplasm of some epithelial cells, especially in the glands with hyperplastic and intestinal metaplastic changes adjacent to carcinoma. It was also found in some normal glands and in tumor cells of highly differentiated adenocarcinoma, but not in tumor cells of lowly differentiated adenocarcinoma.

Adenocarcinoma↗

PubMed1985

Prostaglandins and histological changes in the gastric mucosa.

Gastric 'cytoprotection' was originally defined as the prostaglandin (PG)-mediated absence of grossly visible necrotic lesions produced by any of several necrotizing agents. It was assumed that the absence of necrotic lesions was synonymous with an undamaged mucosa. Subsequent microscopic analysis showed that PG did not protect the superficial gastric epithelium against damage by a necrotizing agent and absolute ethanol. Necrotizing agents such as absolute ethanol appear to produce two major types of damage in vivo: (i) superficial damage, which is confined to the interfoveolar, gastric pit and sometimes upper gastric glands and is not accompanied by significant hemorrhage; (ii) necrotic lesions, which are focal regions of vascular stasis, hemorrhage and associated cellular necrosis extending deep within the mucosa. PG pretreatment largely prevents the formation of necrotic lesions (but does lessen the severity of) the superficial damage. Necrotic lesions heal slowly over a period of days to months whereas superficial damage in vivo heals within approximately 60 minutes by the rapid migration of mucous cells from the gastric pit and isthmus of the oxyntic gland. Exogenous PG elicits a thicker mucus gel which has been implicated in cytoprotection. Experimental evidence now suggests that mucus may have an important role in preventing further damage, after the initial insult, by forming a cap or gelatinous layer over the injured regions. In toto these studies demonstrate three additional protective mechanisms of the superficially injured gastric mucosa: (i) a shielding gelatinous layer formed of mucus and exfoliated surface epithelial cells which forms a barrier to substances in the lumen and traps an alkaline fluid next to the healing surface; (ii) a flow of alkaline mucosal fluid into the lumen which dilutes noxious agents there and helps provide an optimum healing environment at the injured surface; (iii) a rapidly healing superficial mucosal layer which quickly reinstates the physical barrier between the gastric lumen and lamina propria. It is concluded that although PGs do not protect the superficial gastric epithelium against damage by a necrotizing agent, PGs markedly lessen the severity of damage primarily by preventing hemorrhagic lesions.

Adaptation, Physiological↗