Inhibitory effect of aspirin on cholera toxin-induced phospholipase and cyclo-oxygenase activity

Yi fan Liang, Johnny Peterson, James C. Reitmeyer

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Cholera toxin (CT) stimulated phospholipase activity and caused [3H]arachidonic acid (3H-AA) release in a murine macrophage/monocyte cell line. Pretreatment of cells with dexamethasone, a phospholipase A2 (PLA2) inhibitor, did not affect CT-induced 3H-AA release. In contrast, aspirin, which is an inhibitor of phospholipase C (PLC), blocked CT-induced 3H-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 3H-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.

Original languageEnglish (US)
Pages (from-to)137-141
Number of pages5
JournalFEMS Microbiology Letters
Volume72
Issue number1-2
DOIs
StatePublished - 1990

Fingerprint

Phospholipases
Cholera Toxin
Prostaglandin-Endoperoxide Synthases
Aspirin
Arachidonic Acid
Type C Phospholipases
Dexamethasone
Prostaglandins
Culture Media
Monocytes
Macrophages
Cell Line
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Genetics
  • Molecular Biology
  • Applied Microbiology and Biotechnology
  • Microbiology

Cite this

Inhibitory effect of aspirin on cholera toxin-induced phospholipase and cyclo-oxygenase activity. / Liang, Yi fan; Peterson, Johnny; Reitmeyer, James C.

In: FEMS Microbiology Letters, Vol. 72, No. 1-2, 1990, p. 137-141.

Research output: Contribution to journalArticle

@article{b614cbc4164a499e9684567bd12bfa81,
title = "Inhibitory effect of aspirin on cholera toxin-induced phospholipase and cyclo-oxygenase activity",
abstract = "Cholera toxin (CT) stimulated phospholipase activity and caused [3H]arachidonic acid (3H-AA) release in a murine macrophage/monocyte cell line. Pretreatment of cells with dexamethasone, a phospholipase A2 (PLA2) inhibitor, did not affect CT-induced 3H-AA release. In contrast, aspirin, which is an inhibitor of phospholipase C (PLC), blocked CT-induced 3H-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 3H-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.",
author = "Liang, {Yi fan} and Johnny Peterson and Reitmeyer, {James C.}",
year = "1990",
doi = "10.1016/0378-1097(90)90360-3",
language = "English (US)",
volume = "72",
pages = "137--141",
journal = "FEMS Microbiology Letters",
issn = "0378-1097",
publisher = "Wiley-Blackwell",
number = "1-2",

}

TY - JOUR

T1 - Inhibitory effect of aspirin on cholera toxin-induced phospholipase and cyclo-oxygenase activity

AU - Liang, Yi fan

AU - Peterson, Johnny

AU - Reitmeyer, James C.

PY - 1990

Y1 - 1990

N2 - Cholera toxin (CT) stimulated phospholipase activity and caused [3H]arachidonic acid (3H-AA) release in a murine macrophage/monocyte cell line. Pretreatment of cells with dexamethasone, a phospholipase A2 (PLA2) inhibitor, did not affect CT-induced 3H-AA release. In contrast, aspirin, which is an inhibitor of phospholipase C (PLC), blocked CT-induced 3H-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 3H-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.

AB - Cholera toxin (CT) stimulated phospholipase activity and caused [3H]arachidonic acid (3H-AA) release in a murine macrophage/monocyte cell line. Pretreatment of cells with dexamethasone, a phospholipase A2 (PLA2) inhibitor, did not affect CT-induced 3H-AA release. In contrast, aspirin, which is an inhibitor of phospholipase C (PLC), blocked CT-induced 3H-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 3H-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.

UR - http://www.scopus.com/inward/record.url?scp=0025133117&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025133117&partnerID=8YFLogxK

U2 - 10.1016/0378-1097(90)90360-3

DO - 10.1016/0378-1097(90)90360-3

M3 - Article

VL - 72

SP - 137

EP - 141

JO - FEMS Microbiology Letters

JF - FEMS Microbiology Letters

SN - 0378-1097

IS - 1-2

ER -