Microcystin-induced activation of prostaglandin synthesis and phospholipid metabolism in rat hepatocytes
Autor: | K.A. Mereish, Harry B. Hines, Syed M. Naseem, R. Solow |
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Rok vydání: | 1991 |
Předmět: |
medicine.medical_specialty
Phospholipid Prostaglandin Prostacyclin General Medicine Lipid signaling Metabolism Biology Toxicology Thromboxane B2 chemistry.chemical_compound Endocrinology chemistry Biochemistry Internal medicine polycyclic compounds medicine lipids (amino acids peptides and proteins) Arachidonic acid Phosphatidylinositol medicine.drug |
Zdroj: | Toxicology in Vitro. 5:341-345 |
ISSN: | 0887-2333 |
DOI: | 10.1016/0887-2333(91)90011-2 |
Popis: | The effects of microcystin-LR, a trichothecene, T-2 and saxitoxin on membrane lipid mediators of inflammatory processes were evaluated in cultured rat hepatocytes using [(14)C]arachidonic acid. Microcystin-LR significantly stimulated the release of prostacyclin, measured as 6-keto PGF(1)alpha, by 38%, and thromboxane B(2) by 50%, in a concentration-dependent manner. The trichothecene toxin T-2 enhanced the release of prostaglandin F(2)alpha by 24% and arachidonic acid by 29%; while saxitoxin did not affect the release prostaglandins or arachidonic acid. Incorporation of arachidonic acid into the lipid pool was reduced by 47% by 1 mum microcystin-LR. Changes in the distribution of radioactivity derived from [(14)C]arachidonic acid within phospholipid classes indicated that prostaglandin formation induced by microcystin-LR was also due to the release of arachidonic acid from the phosphatidylinositol pool. No statistically significant effect of toxin was observed on the contribution of [(14)C]arachidonic acid release by other classes of phospholipids or neutral lipids. These effects may be important in the mechanism of microcystin-LR-induced toxicity in the liver. |
Databáze: | OpenAIRE |
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