Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.17.3.2 (xanthine oxidase)
 8,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxidative stress is believed to be involved in cataract development. The protective effect of the xanthomatine derivative, pirenoxine, and the 21-aminosteroid U74389F on oxidative insult in mammalian lenses was evaluated in vitro, ex vivo and in vivo. In vitro pirenoxine and U74389F inhibited lipid peroxidation induced by iron or haemoglobin in guinea-pig homogenate lens or whole lenses. Both compounds produced the same effect when lens oxidation was induced by superoxide producing system such as xanthine/xanthine oxidase or fMLP stimulated macrophages. In all the in vitro experiments, the values of biochemical lipid peroxidation markers, such as lipid hydroperoxides or thiobarbituric reactant substances, fell to the basal values with the addition of either pirenoxine (10(-5) M) or U74389F (10(-5) M). When two drops (60 microl) of the above molecular solutions (0.005 and 0.012% in saline respectively) were instilled in rabbit eyes (every hour for 8 hours over 2 days), the extracted lenses appeared to have better defences against an in vitro iron-induced lipid peroxidation, as shown by the values of conjugated dienes and lipid soluble fluorescent substances. These values also proved to be significantly lower when the same parameters were assayed in lenses from eyes where a lipid peroxidation was induced in vivo by haemoglobin or Diquat intravitreal injection followed by instillations of pirenoxine sodium salt or U74389F solutions (2 drops of about 60 microl every hour for 8 hours over 4 days) administered topically. Polarographic and chronocoulometric measurements were also performed in order to investigate the action mechanisms of both compounds. Experimental data indicate that the pirenoxine sodium salt and U74389F may be considered effective tools for rejecting an oxidative attack on the lenses, which can finally lead to cataract formation.
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PMID:Protective effect of pirenoxine and U74389F on induced lipid peroxidation in mammalian lenses. An in vitro, ex vivo and in vivo study. 1007 43

Chronic gut inflammation is associated with radical oxygen species (ROS) genesis. ROS may activate certain transcription factors such as nuclear factor kappa beta (NF-kappaB), which regulates cyclooxygenase-2 (COX-2). Diquat, a food contaminant, is responsible for oxidative stress. This work aimed to establish the involvement of ROS and prostanoids on diquat-induced gastrointestinal inflammation and mast cell hyperplasia. Diquat increased gastrointestinal MPO activity and mast cell number. Its effect on gastric MPO activity was reversed by PD 138,387 (a COX-2 selective inhibitor) and PDTC (an inhibitor of NF-kappaB activation) but not by DMSO (a hydroxyl radical scavenger) and allopurinol (a xanthine oxidase inhibitor). In contrast, increased jejunal MPO activity was blocked by both DMSO, PD 138,387, and PDTC, while allopurinol enhanced it. PD 138,387 and PDTC reduced gastrointestinal mast cell number while DMSO and allopurinol did not Diquat-induced inflammation involves a gastrointestinal NF-kappaB activation and COX-2 dependent proinflammatory prostanoid synthesis. Furthermore, the hydroxyl radical is involved in intestinal but not gastric inflammation.
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PMID:Pathways involved in mild gastrointestinal inflammation induced by a low level exposure to a food contaminant. 1206 6