Open AccessInhibitory effect of aspirin on cholera toxin‐induced phospholipase and cyclo‐oxygenase activity
Author(s) -
Liang Yifan,
Peterson Johnny W.,
Reitmeyer James C.
Publication year - 1990
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.1990.tb03877.x
Subject(s) - arachidonic acid , cholera toxin , aspirin , phospholipase a2 , phospholipase , pharmacology , prostaglandin , chemistry , phospholipase a , toxin , enzyme inhibitor , biochemistry , biology , endocrinology , enzyme
Cholera toxin (CT) stimulated phospholipase activity and caused [ 3 H]arachidonic acid ( 3 H‐AA) release in a murine macrophage/monocyte cell line. Pretreatment of cells with dexamethasone, a phospholipase A 2 (PLA 2 ) inhibitor, did not affect CT‐induced 3 H‐AA release. In contrast, aspirin, which is an inhibitor of phospholipase C (PLC), blocked CT‐induced 3 H‐AA release and subsequent prostaglandin (PC) synthesis. The inhibitory effect of aspirin was dose dependent, with 4 mM reducing the CT response by approximately 50%. Similarly, inhibition was time dependent, occurring when the drug was added to the culture medium as late as 30 min after CT. Brief exposure (30 min) of the cells to aspirin did not alter their subsequent response to CT, but 3 H‐AA release from cells exposed to aspirin for 2.5 h was irreversibly inhibited. The data suggested that CT stimulation of AA metabolism may involved increased PLC activity.