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Related Concept Videos

Stomach pH Regulation01:21

Stomach pH Regulation

The human body carefully regulates the internal pH of different organs to maintain homeostasis. For example, while the blood plasma maintains a neutral pH of 7, the stomach lumen has an acidic pH of 1.5 - 3.5. The low pH of stomach lumen helps kill pathogens in the food and break down complex food molecules.
The acid-secreting gastric mucosal epithelial cells (parietal cells) lining the stomach lumen maintain the low pH in the lumen. Numerous ion transporters and channels on these parietal...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...
Gastric Phase of Digestion01:26

Gastric Phase of Digestion

The gastric phase of digestion begins as soon as food enters the stomach. The incoming food bolus triggers neural and hormonal mechanisms, which last approximately 3 to 4 hours. During this phase, the stomach undergoes significant changes to prepare the food for further digestion and absorption.
When food enters the stomach, it stretches the stomach walls and activates stretch receptors. This triggers local reflexes of the enteric nervous system, mediated through the myenteric plexus. These...
Mucosal Barrier of the Stomach01:25

Mucosal Barrier of the Stomach

The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...

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One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
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Acid activation of omeprazole in isolated gastric vesicles, oxyntic cells, and gastric glands.

M Morii1, H Takata, N Takeguchi

  • 1Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, Japan.

Gastroenterology
|June 1, 1989
PubMed
Summary
This summary is machine-generated.

Omeprazole transforms into a fluorescent molecule in acidic conditions, indicating its activation. This fluorescence decreases with the addition of sulfhydryl groups or increased pH, revealing omeprazole

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Area of Science:

  • Biochemistry
  • Pharmacology
  • Cell Biology

Background:

  • Omeprazole is a proton pump inhibitor that targets gastric hydrogen ion transporting, potassium-stimulated adenosine triphosphatase.
  • Understanding omeprazole's activation mechanism is crucial for its therapeutic application and drug development.

Purpose of the Study:

  • To investigate the transformation of omeprazole into a fluorescent molecule in acidic environments.
  • To identify the chemical nature and activation sites of this fluorescent omeprazole derivative.
  • To elucidate the interaction of omeprazole with sulfhydryl groups within the gastric proton pump.

Main Methods:

  • Utilizing fluorescence spectroscopy to detect and quantify omeprazole transformation.
  • Employing hog gastric vesicles and isolated rabbit gastric glands to study omeprazole activation in a biological context.
  • Using fluorescence imaging to visualize omeprazole activation in isolated Xenopus oxyntic cells.

Main Results:

  • Omeprazole transforms into a strong fluorescent molecule (excitation/emission 370/560 nm) in acidic media, identified as an acid-activated planar cyclic sulfenamide derivative.
  • Fluorescence intensity increased upon omeprazole addition to gastric vesicles, indicating intravesicular activation, followed by a biphasic decrease.
  • The decrease in fluorescence correlated with the reaction of the activated omeprazole with sulfhydryl groups on the gastric proton pump and was reduced by increased pH or sulfhydryl compounds.

Conclusions:

  • Omeprazole activation is pH-dependent and occurs in acidic compartments, such as the intravesicular space of gastric vesicles and the lumina of gastric glands.
  • The activated omeprazole derivative reacts with sulfhydryl groups of the gastric proton pump, providing insights into its mechanism of action.
  • Fluorescence-based methods can effectively monitor omeprazole activation and its interaction with biological targets in real-time.