Action of cholera toxin in the intestinal epithelial cells
The primary event in the action of cholera toxin on the isolated chick intestinal epithelial cell is its interaction with the cell membrane. This involves a large number (17 million per cell) of high affinity binding sites which belong to a single class. Binding of biologically active /sup 125/I-labeled toxin is rapid, temperature-dependent, reversible, and saturable over a wide range of concentrations and includes only a small contribution from nonspecific sites. A characteristic lag phase of 10 min occurs following the complete binding of toxin before any increase in cellular cAMP levels can be detected in the isolated cells. The response (elevation of cellular cAMP) of the enterocytes to cholera toxin is linear with time for 40-50 min and causes a six- to eight-fold increase over control levels at steady stae. cAMP and agents that increase cAMP production inhibit Cl/sup -/-independent Na/sup +/ influx into the isolated enterocytes whereas chlorporomazine (CPZ) which completely abolishes toxin-induced elevation of cAMP both reverses and prevents the cAMP-mediated inhibition of Na/sup +/ entry. Correlation between cellular cAMP levels and the magnitude of Na/sup +/ influx into the enterocytes provides evidence for a cAMP-mediated control of intestinal Na/sup +/ uptake, which may represent the mechanistic basis for the antiabsorptive effect of CT and Na/sup +/ during induction of intestinal secretion. The effect of cAMP on Na/sup +/ but no Cl/sup -/ influx in our villus cell preparation can be partially explained in terms of a cAMP-regulated Na/sup +//H/sup +/ neutral exchange system.
- OSTI ID:
- 6072255
- Resource Relation:
- Other Information: Thesis
- Country of Publication:
- United States
- Language:
- English
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ALKALI METAL COMPOUNDS
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550301* - Cytology- Tracer Techniques