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)

We examined the effects of FK506, an immunosuppressive agent, on the genesis of water immersion stress-induced gastric lesions in rats. Using high-performance liquid chromatography, four kinds of prostaglandins, ie, 6-keto-prostaglandin F1 alpha, prostaglandin F2 alpha, prostaglandin E2, and prostaglandin D2, were detected, and no leukotrienes were detected in gastric mucosa in rats without stress. After 6 hr of stress, gastric lesions developed with decreases in all prostaglandin contents, and the emergence of peptide leukotrienes was observed. Intramuscular administration of FK506 (0.1, 0.25, 0.5, 1.0, and 2.0 mg/kg) reduced lesion index dose-dependently. Administration of FK506 at doses over 0.25 mg/kg decreased all prostaglandin contents, but did not affect the increase in leukotriene contents. Pretreatment with famotidine or omeprazole reduced lesion index, and the protective effects were equivalent to those of 1.0 mg/kg of FK506, although FK506 did not affect gastric secretion during water-immersion stress. Water-immersion stress did not change the activities of xanthine oxidase in either stomach or serum. Polyoxyethylene-modified superoxide dismutase did not prevent gastric lesions. Water-immersion stress significantly increased myeloperoxidase activity in gastric mucosa, and FK506 reduced the increase in myeloperoxidase activity induced by stress. From our results, other factors besides gastric acid secretion and tissue eicosanoid contents, such as chemoattractant factor, might also be involved in the genesis of water-immersion stress-induced gastric lesions in rats.
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PMID:Effects of FK506, an immunosuppressive agent, on genesis of water-immersion stress-induced gastric lesions in rats. 751 15

To determine the mechanism of hemolysis following organ transplantation, we studied the effect of immunosuppressants and/or superoxide (SO) on the in vitro destruction of red cells. The immunosuppressants tested included cyclosporin A (CyA), deoxyspagarine (DSG), and FK506. SO was obtained from the hypoxanthine-xanthine oxidase reaction. Of the three immunosuppressants studied, only CyA affected the size of red cells and directly produced hemolysis in an isotonic buffer without the involvement of an immune mechanism. In addition, SO and CyA showed a synergistic effect on hemolysis during prolonged incubation. Catalase and allopurinol prevented hemolysis by counteracting the activity of SO. In that SO is produced in excess during the recovery of blood flow after organ transplantation, the prolonged contact of red cells with CyA and SO may be involved in the development and reinforcement of hemolysis in vivo.
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PMID:Reinforcement of cyclosporin A-induced red cell destruction by superoxide. 753 79

Mitochondrial permeability transition (MPT) is a phenomenon which occurs under adverse conditions such as an increase in mitochondrial calcium content and oxidative stress. The MPT causes the opening of mitochondrial megachannels, loss of mitochondrial membrane potential, and uncoupling of mitochondrial respiration, leading to cellular energy failure. Recent experiments have suggested that the MPT also releases specific proteins from mitochondria and activates the cascades of programmed cell death. Although many investigators have reported that ischemia-reperfusion leads to apoptosis in the brain tissue, there are only a few studies on the roles of MPT in ischemia-reperfusion injury in the brain. The present study was aimed to assess the effects of calcium, pH, temperature and free radicals on permeability transition of brain mitochondria in vitro, by the use of spectrophotometry. The effect of cyclosporin A (CsA), which is known to be a potent suppressor of MPT in other organs such as liver and heart, was also evaluated. The author also studied the protective effects of CsA on delayed neuronal death in CA1 sector, using transient forebrain ischemia model of the gerbil. Non-synaptosomal (free) mitochondria isolated from the forebrain of the rat had well-coupled respiration. MPT was induced by more than 10 microM of calcium. However, oxygen free radicals derived from t-butyl hydroperoxide and xanthine/xanthine oxidase could not induce MPT. Acidosis and low temperature significantly suppressed calcium-induced MPT. CsA (0.1-10 microM) but not FK506 (0.1-1 microM) inhibited MPT. CsA (50 mg/kg, i.p.) dramatically protected CA1 neurons in the hippocampus for 7 days after 5-min forebrain ischemia in the gerbil. These results suggest that calcium is the major inducer of MPT of the brain mitochondria, and that CsA can potentially inhibit MPT and ameliorate the ischemic tissue injury of the brain.
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PMID:[The roles of mitochondrial permeability transition in brain ischemia]. 1097 4