Pepsin In Gastric Juice Research Articles

A thin layer of sucrose octasulfate protects the oesophageal mucosal epithelium in reflux oesophagitis

Sucralfate is effective for the treatment of gastric and duodenal ulcers owing to its protective gel-forming ability. However, the mechanism by which sucralfate protects the oesophageal mucosa against reflux oesophagitis has not been clarified. We aimed to investigate the mechanisms of action of sucralfate and sucrose octasulfate (SOS), a component of sucralfate. SOS and sucralfate were administered to oesophagitis-induced rats, and the ulcer lesion size was macroscopically examined and scored. Effective pepsin activity in the gastric juices obtained from the animal model was evaluated by a casein digestion test. Sucralfate and SOS improved the pathology scores in a dose-dependent manner, whereas gastric juice pepsin activity was not impaired by therapeutic doses of SOS. As SOS lacks the ability to form a thick gel layer by polymerisation, we examined the distribution of SOS in the mucosal lumen by imaging mass spectrometry (IMS) to determine whether SOS directly adheres to the mucosal surface. A clear homogeneous thin-layer SOS film (>100 μm thick) was visualized on the oesophageal mucosal surface. Moreover, this SOS film formation was enhanced at ulcer lesion sites. Taken together, SOS appears to protect oesophageal mucosa against reflux oesophagitis via thin-layer formation on the mucosal surface.

Probing the influence of food colorant on digestive ability: sunset yellow-pepsin system

The binding mechanism of sunset yellow on pepsin was studied by fluorescence quenching method, synchronous fluorescence method, and molecular docking technique. The results showed that sunset yellow can effectively quench the endogenous fluorescence of pepsin, which was accompanied by non-radiative energy transfer. A 1:1 stable complex with a binding constant of 104 was formed by sunset yellow and pepsin. The binding site of sunset yellow located in the active center of the pepsin and the binding was driven by electrostatic attraction and hydrogen bonding, thereby changed the conformation of pepsin. The binding rate of sunset yellow was 2.45–1.35% at 310 K, and the binding rate model was W(Q) = 5.538 × 10−6R2−5.188 × 10−4R + 0.02494. The binding rate of the pepsin was 2.45–47.11%; the binding rate model was W(B) = 2.271 × 10−4R2 + 0.02103 R + 0.009030. Through estimation, it can be seen that when sunset yellow was set at the maximum intake of 0.0025 g at every time, it would reduce the pepsin in gastric juice by 58.79% and seriously affect the body’s digestive function. It was theoretically proved that sunset yellow has serious side effects on human digestive ability.

The diagnostic value of indicators of acid-forming and pepsinoguena functions of the stomach in the detection of precancerous changes of the gastric mucosa in patients with chronic gastritis

It was found that in patients with chronic atrophic gastritis, low gastric secretory functions are present in the localization of atrophy in the mucous membrane of the body of the stomach with a tendency to decrease in indices as the degree of atrophy increases and are not associated with the presence of disregenerative changes in the gastric mucosa (intestinal metaplasia and dysplasia). Reduced levels of pepsin in gastric juice and reduced levels of pepsinogen in the mucous membrane of the body of the stomach reliably reflect the presence of severe atrophy of the mucous membrane of the body of the stomach. However, neither the concentration of pepsinogen in the tissues of the mucous membrane of the body of the stomach nor the level of pepsin in the gastric juice make it possible to differentiate the degree of atrophy of the gastric mucosa. The most profound disregenerative changes in gastric mucosa such as colonic metaplasia or dysplasia were detected, accordingly in 18,4 and 10,5% of patients. The presence of intestinal metaplasia or dysplasia causes a low activity of pepsinogen-pepsin. It worth noting that in case of the presence of intestinal metaplasia and dysplasia there is a significant difference between indicators of the concentration of pepsinogen-pepsin and those at patients with chronic gastritis, but without disregenerative changes of the mucous membrane. Also was found an association between the severity of disregenerative changes in the gastric mucosa and the degree of the reduction of pepsin-forming function.

Cytoprotective and antioxidant effects of the methanol extract of Eremomastax speciosa in rats.

Ethno-botanical information shows that Eremomastax speciosa is used in the traditional management of various stomach complaints including gastro-duodenal ulcers. In this study, we tested the cytoprotective potential of the whole plant methanol extract (100-200 mg/kg, p.o), against HCl/ethanol, absolute ethanol, cold/restraint stress rats, and pylorus legated rats pre-treated with indomethacin. The effects of the extract on gastric lesion inhibition, the volume of gastric juice, gastric pH, gastric acid output, mucus production and gastric peptic activity were recorded. Oxidative stress parameters were measured in blood and gastric tissue samples obtained from the animals in all the models tested. The extract significantly (p<0.05), reduced the formation of cold/restraint ulcers by (31-60%, inhibition), completely inhibited (100%) the formation of lesions induced by HCl/ethanol at the highest dose, but was less effective against absolute ethanol (22-46% inhibition). The extract (200 mg/kg), significantly reduced lesion formation (P<0.01), gastric acidity (P<0.01), and volume of gastric secretions (P<0.05), in the indomethacin/pylorus ligation model, and did not affect the activity of pepsin in gastric juice. Blood concentrations of antioxidant enzymes (catalase, SOD and GSH), increased significantly and MDA concentrations decreased in all models tested. Cytoprotection by E. speciosa methanol extract was attributed to its ability to reduce acid secretion, and to enhance mucosal defence and in vivo antioxidant status.

178: Does Pepsin in Gastric Juice Aspirated into the Lung Allograft Stimulate Mucus Hypersecretion?

178: Does Pepsin in Gastric Juice Aspirated into the Lung Allograft Stimulate Mucus Hypersecretion?

Sucralfate Protects Blood Clots from Peptic Digestion by Gastric Juice in vitro

Objective: To test in vitro the ability of sucralfate to protect a blood clot from peptic digestion by gastric juice. Material and Methods: Blood clots adhering to the bottom of plastic tubes were exposed to native acidic gastric juice or gastric juice to which Al-Mg antacids, sucralfate or alkali had been added. The tubes were tilted regularly at room temperature and clot digestion monitored by measuring the diameters of the clots. After 15 h, the liquids, but not the adherent clots, were poured out and the tubes refilled with native acidic gastric juice. Further clot digestion was measured, as before. Results: Native gastric juice digested the clots completely during approximately 7 h, while in neutralized gastric juice or in gastric juice containing antacids or sucralfate no digestion was seen. In the second experiment, native gastric juice completely digested all remaining clots, except those previously exposed to sucralfate. A dose-response study indicated that gastric juice containing 3% or more of sucralfate had this long-lasting, clot-protective effect. Conclusions: In vitro, sucralfate adheres to and protects blood clots from digestion by gastric juice pepsin. This unique effect of sucralfate may be of clinical relevance in the treatment of bleeding peptic ulcers.

Pepsin concentration in gastroduodenal biopsy homogenates in chronic ulcer disease.

A modification of Berstad's spectrophotometric method was tested and proved capable of detecting pepsin concentrations in mucosal perendoscopic biopsy homogenates. The relationship between this parameter and pepsin in gastric juice and pepsinogen group I in serum and in biopsy homogenates was analyzed. From the biochemical point of view, the assay was found sufficiently accurate. Mucosal pepsinogen group I, but not mucosal pepsin, concentration was found higher in gastric and duodenal ulcer patients than in controls. Patients with corpus-fundic gastric ulcer showed significantly lower mucosal pepsin and mucosal pepsinogen group (PG) I. Aging and smoking did not influence either parameter but male duodenal ulcer subjects presented higher mucosal pepsinogen group I concentration. The lack of any relationship between serum and mucosal PG I and between pepsin in gastric juice and in mucosa raises a question, at least in methodological terms, about the validity of using serum pepsinogen group I and pepsin as indicators of peptic output.

Adherent and soluble mucus in the stomach and duodenum.

Gastroduodenal mucus is present as a water insoluble gel adherent to the mucosal surface and as a viscous mobile solution in the lumen. The protective properties of the mucus against acid (with bicarbonate), pepsin (diffusion barrier) and mechanical damage depend on the quality (structure) and quantity (thickness) of the adherent mucus gel layer. Adherent mucus is a viscoelastic gel which is 95% (v/v) water. It is permeable to ions and smaller molecules (Mr c. 1000), but is impermeable to large proteins (Mr c. 17,000) including pepsins. However, mucus is solubilized rapidly by pepsin, more slowly (greater than or equal to 1 h) by thiol agents, and is unchanged following exposure to bile, acid and ethanol (less than 40%). Glycoprotein macromolecules (Mr greater than or equal to 2 X 10(6] are the structural components of the mucus gel and have a polymeric structure of glycoprotein subunits (Mr c. 5 X 10(5), for gastric mucus) joined by disulphide bridges between their protein cores. This glycoprotein polymerization, which is essential for gel formation and hence function, is the site of action of proteolytic enzymes and thiol agents. The glycoprotein polymeric structure is deficient in antral mucus from patients with peptic ulcer disease. In vivo, adherent mucus forms a thin but continuous cover of variable thickness (50-450 micron in man, about two-fold less in rat) over the gastroduodenal mucosa. Pepsin in gastric juice will rapidly dissolve this mucus cover and can be active up to luminal pH values of 5.(ABSTRACT TRUNCATED AT 250 WORDS)

Stability of gastric-juice pepsin, and a method for its preservation.

Stability of gastric-juice pepsin, and a method for its preservation.

Effect of cimetidine on histamine-stimulated gastric acid and electrolytes in dogs.

Intravenous administration of cimetidine (0.25-2.0 mg X kg-1 X h-1) inhibited histamine-stimulated gastric acid secretion in both intact (Ki = 1.0 mg X kg-1 X h-1) and vagotomized (Ki = 1.75 mg X kg-1 X h-1) dogs. During histamine infusion, all doses of cimetidine reduced gastric volume output; high doses increased gastric juice pepsin and [Na+] and reduced [H+] and [Cl-]. Gastric juice [K+] was not affected during cimetidine infusion. The cimetidine-induced changes in electrolyte concentrations were qualitatively comparable with those observed on withdrawal of histamine stimulation. On termination of cimetidine infusion with continued histamine administration, gastric [K+] and volume output increased immediately, followed 30 min later by an increase in [H+] and a reciprocal decrease in [Na+]; [Cl-] did not recover. The changes in gastric juice electrolytes after termination of cimetidine, with the exception of [Cl-], mimicked the changes observed on initiation of histamine stimulation. These data indicate that the effects of cimetidine may be totally explained by its antagonism of histamine binding to the parietal cell H2-receptor, that vagotomy reduces cimetidine binding to the H2-receptor, and that cimetidine antagonism of histamine is rapidly reversed on removal of the antagonist.

Kinetic assay of human pepsin with albumin-bromphenol blue as substrate.

A novel substrate, albumin complexed with bromphenol blue, has been developed for the assay of human gastric juice pepsin by a kinetic method in the Cobas centrifugal analyzer. The action of pepsin on the complex degrades the albumin and releases the dye. The change in the color of the substrate is a zero-order reaction. Human and porcine pepsin have different Km's with the new substrate. This kinetic method has a throughput of 28 tests in approximately 10 min and good precision (CV = 2.0%). Other advantages are analysis in homogeneous solution (thereby eliminating the need to separate substrate and products), lack of interference from bilirubin or phenol red, and the expression of pepsin activity in IUB enzyme units.

Effects of cimetidine upon gastric secretion and mucosal blood flow in the rat stressed by restraint. A dose-response and prophylaxis trial.

The effect of the histamine-H2-receptor blocking agent cimetidine (CT) on gastric secretion, mucosal blood flow (MBF), and gastric mucosal stress ulcer index was studied in rats (n = 96) during control conditions (3.9, 15.6, 62.4 microMol/kg/h CT i.p. over 8 h) with calculation of kinetic constants (Vmax; Km) for gastric secretion, MBF and ulcer index, it is shown that CT actions become considerably modified by severe stress. Under mild stress the reduction of MBF and acid secretion by increasing CT doses is parallel. Severe stress alone reduces MBF more than gastric acid (65 vs. 30%). This phenomenon is partly reversed by a dose of 62.4 microMol/kg/h (= 16 mg/kg/h), which is associated with the lowest ulcer index observed. There is no significant correlation between the latter and either acid concentration, acid output, or MBF. The concentrations of pepsin in gastric juice or of serum gastrin neither change with severe stress alone or with additional CT. It is concluded that CT has anti-stress ulcer properties coinciding with reduced acidity in the gastric lumen, but that in addition this beneficial effect may be mediated by factors other than acid reduction.

Role of gastric mucosal pepsin in the pathogenesis of acute stress ulceration

AbstractMeasurements of acid and pepsin in gastric juice and the pepsin concentration in the fundic mucosa were performed in 4 patients who underwent partial gastrectomy for bleeding from acute gastric mucosal erosions (“stress ulcers”) and in 30 patients who underwent partial gastrectomy for chronic gastric or duodenal ulcers. The most striking finding was a significantly higher level of fundic mucosal pepsin in the patients with acute gastric erosions than the chronic ulcer patients. This finding was associated with a significantly lower concentration of pepsin in gastric juice, a low level of acid secretion, and the expected high plasma level of corticosteroids associated with stress. As a result, the ratio of gastric mucosal pepsin to gastric juice pepsin was significantly higher in patients with acute gastric erosions than in those with chronic ulcers. It is possible that a rapid increase in endogenous corticosteroid levels induces an increase in intracellular pepsin in the fundic mucosa, and that this sequence of events plays a role in the pathogenesis of stress ulcer.

Inhibitory effect of cycloheximide on gastric secretion in rats

Cycloheximide administered to rats in non-toxic doses immediately after pyloric ligation results in a lower incidence of experimental gastric ulcers. The effect is paralleled by an impaired secretion of hydrochloric acid (more than 90 per cent inhibition). Simultaneously the activity of pepsin in gastric juice and in homogenates of gastric mucosa was reduced by 60 per cent and mucoproteins were lowered by 30 per cent. The basal and pentagastrin-stimulated secretion were inhibited by cycloheximide to the same extent.

Effect of urogastrone in the Zollinger-Ellison syndrome.

The effects of human urogastrone (0-25 mug. per kg. per hour intravenously) in four male patients with proven Zollinger-Ellison syndrome (z.e.s.) and in four healthy control subjects have been studied. After urogastrone in z.e.s. patients gastric acid volume and concentration decreased and basal acid output was reduced by 50-82%; the concentrations of intrinsic factor and pepsin in gastric juice increased by 60-300%; and peak plasma-gastrin concentration increased by 127-164% of basal concentration. A significant negative correlation between increase in plasma-gastrin concentration and decrease in acid output was observed (r=-0-72, P less than 0-01). Ulcer pain was relieved 30-60 minutes after the beginning of urogastrone infusion. These results suggest that urogastrone can inhibit the endogenously stimulated acid hypersecretion in z.e.s.

Effect of Acid in the Duodenal Bulb on Acid and Pepsin Responses to Test Meal in Dogs

Dogs were provided with innervated pouches of the fundic stomach and of the duodenal bulb. Gastric secretion was stimulated by a test meal. Bulbar perfusion with 0.1 N HCl profoundly ibhibited the secretion of acid. Also pepsin output and concentration of pepsin in gastric juice were reduced by bulbar acidification. The results may mean that reduction of the intrabulbar pH also plays a role in regulation of the secretion of pepsin from the stomach.

A Modified Hemoglobin Substrate Method for the Estimation of Pepsin in Gastric Juice

Berstad, A. 1970. A Modified Hemoglobin Substrate Method for the Estimation of Pepsin in Gastric Juice. Scand. J. Gastroent. 5, 343-348.Human hemoglobin was used as substrate for the estimation of pepsin, instead of bovine hemoglobin as used by Anson (1), becausc it is easily prepared and the sensitivity of the method encreased. In order to evaluate the method the influence of variation in substrate and enzyme concentration, time, temperature, and pH of incubation, trichloracetic acid concentration, and type of filter paper were investigated. The standard error of the method was ± 2.7%.

Cause of pepsin in gastric juice for gastroduodenal diseases (by Ogawa’s colloid reaction)

Cause of pepsin in gastric juice for gastroduodenal diseases (by Ogawa’s colloid reaction)

Electrolytes in human gastric secretion. Observations and a theory.

1. The values of volume, acid, sodium, potassium, chloride, and pepsin in gastric juice in the basal state and following stimulation with histamine given subcutaneously or infused intravenously are reported. Nearly 160 studies were done in five groups consisting of control subjects and patients with duodenal ulcer, gastric ulcer, gastritis, and cancer.

Effects of atropine on synthesis and secretion of pepsinogen in the rat.

Simultaneous measurements of gastric juice pepsin and stomach mucosal pepsinogen were made in groups of pylorus-ligated rats at intervals from 2 to 24 hours to examine the effects of atropine sulfate (20 mg/100 gm/8 hrs.) on pepsinogen secretion and synthesis. Animals given subcutaneous injections of water served as controls. Atropine caused a marked reduction in pepsinogen secretion and a concomitant accumulation of pepsinogen in the mucosa which increased with time to a plateau; pylorus ligation had the opposite effect, indicating that atropine effected the reduction in secretion of pepsinogen by blocking the release of pepsinogen from peptic cells. In untreated rats the hematocrit increased proportionately to presumed body water loss, but in the atropine-treated rats the hematocrit failed to increase to the same degree for equivalent body water loss. Indirect evidence is presented to suggest that the rate of water secretion may be one of the rate-limiting factors in pepsinogen secretion. Although synthesis of pepsinogen can proceed without secretion, correlation of the rates of synthesis with those of secretion suggested that the rate of synthesis could be increased by an increased rate of secretion.