Effects of endotoxin and anti-inflammatory agents on superoxide dismutase in the rabbit iris.
Superoxide dismutase activity (SOD) was measured in the irides of control animals and 24 h after the intravitreal administration of Escherichia coli endotoxin. A 3-fold increase in SOD was noted (p less than 0.001). To protect against the inflammatory process, either topical dexamethasone (Dex) or medrysone (Med) was administered t.i.d. for 2 days before and 1 day after endotoxin. Although Dex prevented the iritis seen with endotoxin alone, a 2-fold increase in SOD was measured (p less than 0.001). The Med regimen failed to prevent the signs of endotoxin-induced ocular inflammation yet also reduced the induction of SOD (p less than 0.02). The phospholipase A2 inhibitor, quinacrine, and the lipoxygenase inhibitor, nordihydroguaiaretic acid, blocked the induction of SOD, while the cyclooxygenase inhibitor, indomethacin, did not. Thus, it appears that the induction SOD may be mediated by a product of the lipoxygenase pathway.
Recasens
J F
JF
Department of Ophthalmology, Medical College of Georgia, Augusta.
Green
K
K
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D003513:Cycloheximide / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004731:Endotoxins / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D004790:Enzyme Induction / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology; D007498:Iris / Q000187:drug effects / Q000201:enzymology*; D009637:Masoprocol / Q000494:pharmacology; D011282:Pregnenediones / Q000494:pharmacology; D011796:Quinacrine / Q000494:pharmacology; D011817:Rabbits; D013482:Superoxide Dismutase / Q000096:biosynthesis / Q000378:metabolism*
D000893:Anti-Inflammatory Agents; D004731:Endotoxins; D011282:Pregnenediones; C044101:endotoxin, Escherichia coli; D009637:Masoprocol; D003907:Dexamethasone; D003513:Cycloheximide; C100283:medrysone; D013482:Superoxide Dismutase; D011796:Quinacrine; D007213:Indomethacin