Activation of polyamine biosynthetic decarboxylases during the acute phase response of rat liver.
The activities of ornithine decarboxylase and S-adenosylmethionine decarboxylase increase in the livers of rats during the acute-phase response to inflammation. The increase reaches its maximum at 2.5 hr from injection of turpentine, and is maintained at the same level for the following 2 days. Pretreatment in vivo with an inhibitor of cyclooxygenase prevents the inflammation-associated increases of both polyamine biosynthetic decarboxylases: an inhibitor of the lipoxygenase pathway seems to counteract only the increase of ornithine decarboxylase. The administration of diaminopropane, an inhibitor of ornithine decarboxylase, has only limited effects on the activation of RNA synthesis by liver nuclei, which occurs 10 hr after turpentine treatment. The results suggest that stimulation of the polyamine biosynthetic decarboxylases is surely part of the acute-phase response and depends on the previous activation of arachidonate metabolism: however its role in supporting later events of the acute-phase response will need further investigations.
D000210:Acute-Phase Reaction / Q000201:enzymology*; D012437:Adenosylmethionine Decarboxylase / Q000378:metabolism*; D000818:Animals; D002262:Carboxy-Lyases / Q000378:metabolism*; D004789:Enzyme Activation / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology; D007249:Inflammation / Q000201:enzymology*; D008099:Liver / Q000201:enzymology*; D008297:Male; D009637:Masoprocol / Q000494:pharmacology; D009955:Ornithine Decarboxylase / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D009637:Masoprocol; D002262:Carboxy-Lyases; D009955:Ornithine Decarboxylase; D012437:Adenosylmethionine Decarboxylase; D007213:Indomethacin