Stimulatory effects of cholera toxin on arachidonic acid metabolism in Chinese hamster ovary cells.

J. C. Reitmeyer, Johnny Peterson

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Cholera toxin (CT) stimulated the release of arachidonic acid (AA) from Chinese hamster ovary cells with no apparent lag period. CT-induced release of [3H]AA or its metabolites was dose dependent during a 4-hr period of toxin exposure with a minimum effective dose of 0.1 ng/ml. CT-induced release of [3H]AA metabolites began within 15 min of toxin addition and became maximal after approximately 5 hr. Neither CT-A subunit nor CT-B subunit alone caused [3H]AA release. Furthermore, [3H]AA release was not caused by addition of dibutyryl cAMP to the culture medium, indicating that the observed effect of CT on arachidonate metabolism appeared to be independent of cAMP. The effect of CT on AA metabolism is proposed as a possible mechanism leading to the synthesis of prostaglandin E and fluid secretion during cholera.

Original languageEnglish (US)
Pages (from-to)181-184
Number of pages4
JournalProceedings of the Society for Experimental Biology and Medicine
Volume193
Issue number3
StatePublished - Mar 1990

Fingerprint

Cholera Toxin
Cricetulus
Arachidonic Acid
Metabolism
Ovary
Cells
Metabolites
Fluids and Secretions
Cholera
Prostaglandins E
Culture Media
Fluids

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

@article{3886106529e14eb3b85b4aa9b02bc6e7,
title = "Stimulatory effects of cholera toxin on arachidonic acid metabolism in Chinese hamster ovary cells.",
abstract = "Cholera toxin (CT) stimulated the release of arachidonic acid (AA) from Chinese hamster ovary cells with no apparent lag period. CT-induced release of [3H]AA or its metabolites was dose dependent during a 4-hr period of toxin exposure with a minimum effective dose of 0.1 ng/ml. CT-induced release of [3H]AA metabolites began within 15 min of toxin addition and became maximal after approximately 5 hr. Neither CT-A subunit nor CT-B subunit alone caused [3H]AA release. Furthermore, [3H]AA release was not caused by addition of dibutyryl cAMP to the culture medium, indicating that the observed effect of CT on arachidonate metabolism appeared to be independent of cAMP. The effect of CT on AA metabolism is proposed as a possible mechanism leading to the synthesis of prostaglandin E and fluid secretion during cholera.",
author = "Reitmeyer, {J. C.} and Johnny Peterson",
year = "1990",
month = "3",
language = "English (US)",
volume = "193",
pages = "181--184",
journal = "Experimental Biology and Medicine",
issn = "1535-3702",
publisher = "SAGE Publications Ltd",
number = "3",

}

TY - JOUR

T1 - Stimulatory effects of cholera toxin on arachidonic acid metabolism in Chinese hamster ovary cells.

AU - Reitmeyer, J. C.

AU - Peterson, Johnny

PY - 1990/3

Y1 - 1990/3

N2 - Cholera toxin (CT) stimulated the release of arachidonic acid (AA) from Chinese hamster ovary cells with no apparent lag period. CT-induced release of [3H]AA or its metabolites was dose dependent during a 4-hr period of toxin exposure with a minimum effective dose of 0.1 ng/ml. CT-induced release of [3H]AA metabolites began within 15 min of toxin addition and became maximal after approximately 5 hr. Neither CT-A subunit nor CT-B subunit alone caused [3H]AA release. Furthermore, [3H]AA release was not caused by addition of dibutyryl cAMP to the culture medium, indicating that the observed effect of CT on arachidonate metabolism appeared to be independent of cAMP. The effect of CT on AA metabolism is proposed as a possible mechanism leading to the synthesis of prostaglandin E and fluid secretion during cholera.

AB - Cholera toxin (CT) stimulated the release of arachidonic acid (AA) from Chinese hamster ovary cells with no apparent lag period. CT-induced release of [3H]AA or its metabolites was dose dependent during a 4-hr period of toxin exposure with a minimum effective dose of 0.1 ng/ml. CT-induced release of [3H]AA metabolites began within 15 min of toxin addition and became maximal after approximately 5 hr. Neither CT-A subunit nor CT-B subunit alone caused [3H]AA release. Furthermore, [3H]AA release was not caused by addition of dibutyryl cAMP to the culture medium, indicating that the observed effect of CT on arachidonate metabolism appeared to be independent of cAMP. The effect of CT on AA metabolism is proposed as a possible mechanism leading to the synthesis of prostaglandin E and fluid secretion during cholera.

UR - http://www.scopus.com/inward/record.url?scp=0025395557&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025395557&partnerID=8YFLogxK

M3 - Article

VL - 193

SP - 181

EP - 184

JO - Experimental Biology and Medicine

JF - Experimental Biology and Medicine

SN - 1535-3702

IS - 3

ER -