title: Effects of eicosanoids on lipopolysaccharide-induced ornithine decarboxylase activity and polyamine metabolism in the mouse liver.
abstract: OBJECTIVE
  During endotoxic shock, arachidonic acid is released from the inflammatory cell membranes and is metabolized to form eicosanoids, which modify the deleterious effects of lipopolysaccharide (LPS) on liver function. However, it is not known which prostaglandins (PGs) or leukotrienes (LTs) are produced or how they affect the LPS-treated liver. As LPS treatment elevates hepatic ornithine decarboxylase (ODC) activity and affects the polyamine levels of the mouse liver, this study was carried out to examine the effects of eicosanoids and their inhibitors on the induction of ODC activity and polyamine levels in the LPS-treated mouse liver.
  
  
  METHODS
  LPS in the presence or absence of other drugs was intraperitoneally administered to 6-week-old mice and the livers were then removed. The hepatic ODC activity, polyamine levels, and level of ODC mRNA were determined.
  
  
  RESULTS
  The levels of LPS-induced ODC activity, the putrescine (PUT) and N1-acetylspermidine (A-SPD) were reduced by the administration of PGE1. ODC activity was enhanced by the administration of corticosterone, AA-2414 (an antagonist of thromboxane (TX) A2) and TXB2, whereas the A-SPD level was reduced by corticosterone and AA-2414 treatment. The level of ODC mRNA changed in parallel with the change in ODC activity.
  
  
  CONCLUSIONS
  PGE1 may reduce the LPS-induced production of inflammation-accelerating cytokines and reduce the level of ODC activation. Corticosterone and AA-2414 treatment may attenuate the LPS-induced production of eicosanoids, and enhance the LPS-induced ODC activation. It is possible that the eicosanoids produced by LPS treatment inhibit ODC activation during endotoxic shock.
authors.affiliation: First Department of Internal Medicine, School of Medicine, Gunma University, Maebashi, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Matsuzaki
authors.forename: H
authors.initials: H
authors.lastname: Sugimoto
authors.forename: K
authors.initials: K
authors.lastname: Hamana
authors.forename: T
authors.initials: T
authors.lastname: Nagamine
authors.forename: S
authors.initials: S
authors.lastname: Matsuzaki
authors.forename: M
authors.initials: M
authors.lastname: Mori
mesh_terms: D000527:Alprostadil / Q000494:pharmacology; D000818:Animals; D016227:Benzoquinones / Q000494:pharmacology; D015152:Blotting, Northern; D003345:Corticosterone / Q000494:pharmacology; D015777:Eicosanoids / Q000378:metabolism*; D004790:Enzyme Induction / Q000187:drug effects; D004926:Escherichia coli; D006538:Heptanoic Acids / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000097:blood / Q000633:toxicity*; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009955:Ornithine Decarboxylase / Q000096:biosynthesis*; D011073:Polyamines / Q000378:metabolism*; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D011700:Putrescine / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D012772:Shock, Septic / Q000201:enzymology / Q000209:etiology / Q000378:metabolism*; D013095:Spermidine / Q000031:analogs & derivatives / Q000378:metabolism; D013928:Thromboxane A2 / Q000037:antagonists & inhibitors
chemical_list: D016227:Benzoquinones; D015777:Eicosanoids; D006538:Heptanoic Acids; D008070:Lipopolysaccharides; D011073:Polyamines; D011448:Prostaglandin Antagonists; D012333:RNA, Messenger; C017988:N(1)-acetylspermidine; C060230:seratrodast; D013928:Thromboxane A2; D009955:Ornithine Decarboxylase; D000527:Alprostadil; D013095:Spermidine; D011700:Putrescine; D003345:Corticosterone