Chloroquine inhibition of cholera toxin

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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.