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Acid activation of omeprazole in isolated gastric vesicles, oxyntic cells, and gastric glands.
Omeprazole, a potent inhibitor of gastric hydrogen ion transporting, potassium-stimulated adenosine triphosphatase, was found to be transformed into an SH-reactive strong fluorescent molecule (excitation and emission wavelengths of 370 and 560 nm, respectively) in an acidic medium. The addition of glutathione- or protein-containing sulfhydryl groups such as pepsin to the medium decreased the fluorescence. Also, the increase in the pH of the medium decreased the fluorescence. The fluorescent molecule was identified to be an acid-activated planar cyclic sulfenamide derivative of omeprazole. The transformation was studied in H+-preaccumulated hog gastric vesicles, which contain the hydrogen ion transporting, potassium-stimulated adenosine triphosphatase. The addition of omeprazole to the vesicle suspension induced a rapid increase in the fluorescence intensity, indicating that omeprazole was activated in the intravesicular space. Then, the intensity biphasically decreased with time. The slower small decrease was due to the reaction of the sulfenamide with sulfhydryl group(s) located on the acid secretory side of the hydrogen ion transporting, potassium-stimulated adenosine triphosphatase. Omeprazole was also activated in the acidic lumina of isolated rabbit gastric glands that were stimulated with histamine. Furthermore, direct evidence was obtained from the imaging of the fluorescence that omeprazole was activated in the acidic compartments of the isolated Xenopus oxyntic cell.[1]References
- Acid activation of omeprazole in isolated gastric vesicles, oxyntic cells, and gastric glands. Morii, M., Takata, H., Takeguchi, N. Gastroenterology (1989) [Pubmed]
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