Inhibition of Microcystin-Induced Release of Cyclooxygenase Products from Rat Hepatocytes by Anti-Inflammatory Steriods

We showed previously that exposure to microcystin causes eicosanoid release from rat hepatocytes. That study was extended further to test the effect of glucocorticoids on microcystin-induced release of (Carbon 14) arachidonic acid and its metabolites. Treatment of hepatocyte cultures with either mic...

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Bibliographic Details
Main Authors: Naseem, Syed M, Hines, Harry B, Creasia, Donald A
Format: Report
Language:English
Subjects:
ALGAE
Biochemistry
CELLS
CELLS(BIOLOGY)
CORTISOL
CYCLOOXYGENASE
DOSAGE
FATTY ACIDS
HEPATOCYTES
HUMANS
INCUBATION
INHIBITION
LIVER
METABOLISM
METABOLITES
MICROCYSTIS
Pharmacology
PHYTOTOXINS
POTENCY
PROSTAGLANDIN
PROTEINS
PSEUDOMONAS AERUGINOSA
RADIOACTIVITY
RANK ORDER STATISTICS
RATS
RELEASE
RESPONSE(BIOLOGY)
STEROIDS
Toxicology
TOXINS AND ANTITOXINS
VIABILITY
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Summary:We showed previously that exposure to microcystin causes eicosanoid release from rat hepatocytes. That study was extended further to test the effect of glucocorticoids on microcystin-induced release of (Carbon 14) arachidonic acid and its metabolites. Treatment of hepatocyte cultures with either microcystin (1 micromole) or steroids had no effect on cell viability or total cell protein. Total radioactivity released into the incubation medium was not affected by glucocorticoid alone. Release of total radioactivity increased four- fold after 2-hr of incubation with microcystin, Fluocinolone pretreatment decreased the microcystin-induced synthesis and release of prostacyclin (6-keto F1 alpha) by 24 + or - 2.6% (p 0.05) and thromboxane B2 (TxB2) by 39 + or - 3% (p 0.025). Under these experimental conditions, the quantities of prostaglandin F2 alpha and PGE2 released were not significantly different when control and microcystin-treated cultures were compared. The half maximal inhibition (IC50) values obtained from the dose-response data for the inhibition of arachidonic acid release were comparable to normal cortisol levels in humans. Dose-response curves gave the following rank order of potency: fluocinolone dexamethasone hydrocortisone. These results suggest that glucocorticoid therapy might be beneficial in microcystin toxicosis. Keywords: Metabolism, Prostaglandin, Microcystin, Toxin, Phytotoxins, Algae microcystis aeruginosa.