Abstract
Cholera toxin (CT) stimulated adenylate cyclase and a phospholipase which elevated levels of 3.5-cyclic adenosine monophosphate (cAMP) and arachidonic acid (AA). The AA was quickly converted to prostaglandins (PGs) via the cyclo-oxygenase pathway. Chloroquine exerted minimal inhibition of cAMP levels in CT-treated cells, although CT-induced release of [3H]AA and PGs was blocked completely when the drug was added in concentrations as low as 0.1 mM (30 μγ ml). Inhibition of [3H]AA release was complete when chloroquine was added before or within 30 min after CT. The capacity of chloroquine to inhibit either phospholipase C (PLC) or phospholipase A2 (PLA2) could explain the antisecretory activity of this drug.
Original language | English (US) |
---|---|
Pages (from-to) | 143-145 |
Number of pages | 3 |
Journal | FEBS Letters |
Volume | 275 |
Issue number | 1-2 |
DOIs | |
State | Published - Nov 26 1990 |
Externally published | Yes |
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology