Somatostatin depletion by cysteamine: mechanism and implication for duodenal ulceration
Cysteamine (CSH) and its close derivatives deplete immunoreactive somatostatin (SS) in rat organs. The effect of CSH is dose and time dependent and reversible. Structural requirements of the analogs are the presence of either -SH or -NH2 on a two- or three-carbon alkyl molecule; both radicals together increase, whereas insertion of carboxyl abolishes potency. The duodenal ulcerogenic potency of CSH derivatives is correlated significantly with their SS-depleting activity in the gastric mucosa. The mechanism of this action of CSH is poorly understood, but it is not caused by increased release, enhanced degradation of the peptide, or selective necrosis of SS cells. It is likely that in the intracellular environment CSH causes a conformational change in the peptide that affects the antigenic and functional properties of SS.
- OSTI ID:
- 5118955
- Journal Information:
- Fed. Proc.; (United States), Vol. 9
- Country of Publication:
- United States
- Language:
- English
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CYSTAMINE
BIOLOGICAL EFFECTS
MUCOUS MEMBRANES
PATHOLOGICAL CHANGES
CEREBRAL CORTEX
DOSE-RESPONSE RELATIONSHIPS
RATS
SMALL INTESTINE
SOMATOSTATIN
ULCERS
AMINES
ANIMALS
BODY
BRAIN
CENTRAL NERVOUS SYSTEM
CEREBRUM
DIGESTIVE SYSTEM
DRUGS
GASTROINTESTINAL TRACT
INTESTINES
MAMMALS
MEMBRANES
NERVOUS SYSTEM
ORGANIC COMPOUNDS
ORGANIC SULFUR COMPOUNDS
ORGANS
RADIOPROTECTIVE SUBSTANCES
RODENTS
VERTEBRATES
560305* - Chemicals Metabolism & Toxicology- Vertebrates- (-1987)