Branched blood group A-active fucolipids of hog gastric mucosa.

New complex glycolipids have been extracted from hog gastric mucosa with the mixture of 0.4 M sodium acetate in methanol/chloroform/water. Three A-active fucolipids having branched carbohydrate chains have been purified from this extract. The postulated structures of these glycolipids are based on the results of partial acid hydrolysis, oxidation with periodate and chromium trioxide, and permethylation studies.     

Characterization of three new fucolipids from hog gastric mucosa.

Three new fucolioids have been isolated from the water-soluble glycolipid fraction of hog gastric mucosa. Fucolipid A and C exhibited blood-group-A activity, whereas Fucolipid B was not active in A-anti-A, B-anti-B and H-anti-H systems. The structures of these glycolipids were identified by partial acid hydrolysis and methylation analysis, as: (see article)     

Structure of the ceramide octadekahexoside isolated from gastric mucosa

A fucose-containingceramide octadekahexoside exhibiting blood-group (A+H) activity has been isolated from hog gastric mucosa. Based on the results of partial acid hydrolysis, sequential degradation with specific glycosidases, oxidation with periodate and chromium trioxide, and permethylation analysis, we propose that the carbohydrate chain of this fucolipid contains four branches. Two of the branches are terminated by βGall→4βGlcNAc, one by $\text{αFucl→2βGall→}\text{3}\text{4}\text{βGlcNAc}$ and one by $\text{αGalNAcl→3(αFucl→2)βGall→}\text{3}\text{4}\text{βGlcNAc}$.     

Partial characterization of the highly complex fucolipids from gastric mucosa.

Six highly complex fucolipids containing 18, 20–21, 24, 28, 32, and 35–36 sugar residues, respectively, have been isolated from hog gastric mucosa. All six compounds exhibited blood-group (A+H) activities, and were different from each other with respect to the number of fucose, galactose, N-acetylglucosamine and N-acetylgalactosamine residues. Based on the results of chemical, immunological and enzymatic analyses, we suggest that the carbohydrate chains of these glycolipids are highly branched. The branches, number of which is proportional to the degree of molecular complexity, are terminated by GalNAcα1→3(Fucα1→2)Gal, Fucα1→2Gal, Galβ→GlcNAc and βGlcNAc.     

Forssman glycolipid variants of dog gastric mucosa. Structure of a branched ceramide octasaccharide.

A fucose-containing ceramide octasaccharide exhibiting Forssman antigenic activity, and reacting in human H anti-H and anti-A systems, was isolated from water-soluble glycolipids of dog gastric mucosa. Defucosylation of the glycolipid resulted in the loss of H-activity, but had no effect on its Forssman nor blood-group A antigenic activity. The branched structure of glycolipid was identified by partial acid hydrolysis, sequential degradation with specific glycosidases and comparison of the permethylation products of the native and enzyme-degraded compound. The structure of this glycolipid is proposed to be: formula.     

Structural studies on branched fucosphingolipids of hog gastric mucosa

A structural studies have been performed on new complex glycolipids extracted from hog gastric mucosa by 0.4 M sodium acetate in methanol-chloroform-water, and which were purified to homogeneity by DEAE-Sephadex and Florisil column chromatography and by preparative thin-layer chromatography in three solvent systems. Five branched fucolipids have been purified from this extract, three of which have been characterized previously [1] and remaining two were subject of this investigations. Based on the results of partial acid hydrolases, oxidation with periodate and chromium trioxide, permethylation and serological activities following structures were proposed:Fucolipid IVa

     

Phosphorylation and dephosphorylation kinetics of potassium-stimulated ATP phosphohydrolase from hog gastric mucosa.

Partial reactions of potassium-stimulated ATP phosphohydrolase from hog gastric mucosa were studied by means of a rapid-mixing apparatus. At 21 degrees C, in the presence of 2 mM MgCl2 and 5 microM [gamma-32P]ATP there was a rapid phosphorylation of the enzyme with a pseudofirst order rate constant of 1400 min-1. Addition of the ATP about 120 ms before the MgCl2 increased this rate constant to 4400 min-1. In the absence of MgCl2 there was no phosphorylation. Addition of 4 or 10 mM KCl to the phosphoenzyme which had been formed in the absence of KCl produced a rapid initial rate of dephosphorylation (k = 2600 and 3200 min-1 respectively). An additional slow component of dephosphorylation was observed when unlabeled ATP was added together with the KCl (k = 700 to 900 min-1). At a 4 mM concentration, KCl stimulated the ATPase activity about 9-fold. At higher concentrations, the activity was reduced in parallel with a reduction of the steady state level of phosphoenzyme. Addition of KCl to the enzyme before the addition of ATP plus MgCl2 resulted in a low rate and extent of phosphorylation. KCl appeared to inhibit the phosphorylation at a level preceeding the E.ATP complex.     

Location of the carbohydrates present in the HK-ATPase vesicles isolated from hog gastric mucosa

The glycosylation of H+K(+)-ATPase vesicles isolated from hog gastric mucosa was investigated by various methods. Following protein separation on sodium dodecyl sulfate reducing gels and transfer to poly(vinyl difluoride) membranes, binding of concanavalin A was confined to the 94-kDa band which corresponds to the catalytic subunit. In contrast, wheat germ agglutinin binding occurred in a region below the 94-kDa subunit, corresponding to the 60-85-kDa region, and also to protein just above the catalytic subunit. Treatment with glycopeptidase F removed most of the concanavalin A staining and also the wheat germ agglutinin staining found below the 94-kDa region, but spared the higher molecular weight wheat germ agglutinin reactive material. During the deglycosylation experiments a protein of 35-kDa was produced. Sequencing analysis of V8 protease generated peptide fragments of the 35-kDa protein show at least 30% homology with the Na+K(+)-ATPase beta-subunits. Labeling of the carbohydrates by galactosyltransferase and [3H]uridine diphosphate-galactose showed that the sites of labeling were extracellular and were confined to the wheat germ agglutinin staining regions. Two molecular weight regions, below the 94-kDa region, of 60 and 85 kDa were identified. Electron microscopy using postembedding staining techniques showed that both concanavalin A and wheat germ agglutinin staining occurred on the extracellular face of the gastric vesicles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Structure of the gastric mucosa following experimental antrectomy]

The important role of the antral part of the stomach in sustaining the gastric mucosa tissue homeostasis has been shown in chronic experiment in dogs. In 5-13 months after antrectomy the thickness of the gastric mucosa diminishes by 21% at an average, the height of the fundal glands-by 29%, the amount of the parietal cells-by 54%, the amount of basic cells-by 34%. Hypoplastic lesions of the gastric mucous membrane develop and complete within the first months after antrectomy. After the 5th month the degree of hypoplasia fails to markedly increase, i. e. the shifts found are not of constantly progressing character.     

Homeostasis of the gastric mucosa and blood circulation. 2. Role of ischemia in disruption of the gastric mucosa

To date there is a lot of data of literature indicating that microcirculatory disorders play the main role in the development of gastric mucosal damages induced by stress, ethanol, nonsteroidal antiinflammatory drugs and tobacco smoke. Under stress gastric mucosal blood flow disorders may be caused by the actication of sympathetic nervous system. Ulcer healing is accompanied by the angiogenesis and by the increase of blood flow in the ulcer border and tissues surrounding the ulcer. Therefore now the main studies are concentrated on the search of defence-enhancing agent rather than drugs for antisecretory therapy. Therapeutic strategy suggests the use of some potential vasodilators such as NO donors, prostaglandin analogues, oxygen radical scavengers, endothelin, leukotrienes, platelet-activating factor antagonists and/or their synthesis inhibitors. At present, the therapeutic possibilities seem to be restricted and nothing indicates that stimulation of the defensive factor only, is more effective in the treatment of peptic ulcer than inhibition of aggressive factors. However we suggest that blood flow correction may be very important for the treatment of refractory ulcers or for prophylaxis of stress ulceration and peptic ulcer recurrence.