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  • Title: Formation of 6,15-diketoprostaglandin F1 alpha from prostaglandin G2 by bovine aortic endothelial cells.
    Author: Mayer B, Gleispach H, Kukovetz WR.
    Journal: Biochim Biophys Acta; 1987 Apr 24; 918(3):209-16. PubMed ID: 3032265.
    Abstract:
    Besides 6-ketoprostaglandin F1 alpha, bovine aortic endothelial cells also produced considerable amounts of 6,15-diketoprostaglandin F1 alpha from arachidonic acid, either exogenously added or released from cellular phospholipids. Incubations of particulate fractions of endothelial cells with the cyclic endoperoxides prostaglandin G2 and prostaglandin H2 showed that 6,15-diketoprostaglandin F1 alpha is formed by the action of prostaglandin I2 synthetase on prostaglandin G2. The labile metabolite 15-hydroperoxyprostaglandin I2 is then converted nonenzymatically to the 15-keto derivative. In the presence of reduced glutathione, quantitative analysis of both metabolites by gas chromatography-mass spectrometry showed a significant decrease of 6,15-diketoprostaglandin F1 alpha formation, whereas prostaglandin I2 synthesis was markedly increased. This shift seems to be due to a stimulation of peroxidase by GSH, a well known cofactor of this enzyme. Thus, it seems that a decreased endothelial prostaglandin I2 formation may occur when cellular glutathione levels are reduced as a consequence of oxidant injury and lipid peroxidation. Additionally, ferrous ions seems to be involved in the regulation of endothelial prostaglandin I2 synthesis, since Desferal, a specific ferrous ion chelator that might have antimetastatic properties, produced a pronounced shift from 6,15-diketoprostaglandin F1 alpha to the 6-keto derivative, i.e., prostaglandin I2.
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