Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We tested the preventive effects of catalase, an enzymatic scavenger of hydrogen peroxide, or dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, on intravenous alloxan-induced lung edema in four groups of pentobarbital sodium-anesthetized, ventilated dogs for 3 h: saline (20 ml.kg-1.h-1) infusion alone (n = 5), alloxan (75 mg/kg) + saline infusion (n = 5), catalase (150,000 U/kg) + alloxan + saline infusion (n = 5), or DMSO (4 mg/kg) + alloxan + saline infusion (n = 5). Catalase or DMSO significantly prevented the increase in plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha over 3 h after alloxan and the accumulation of extravascular lung water after 3 h [3.95 +/- 0.52 (SE) g/g with catalase, 3.06 +/- 0.42 g/g with DMSO] but not early pulmonary arterial pressor response. An electron microscopic study indicated that catalase or DMSO significantly reduced the endothelial cellular damages after alloxan. These findings strongly suggest that hydrogen peroxide and hydroxyl radical are major mediators responsible for intravenous alloxan-induced edematous lung injury in anesthetized ventilated dogs.
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PMID:Pretreatment with catalase or dimethyl sulfoxide protects alloxan-induced acute lung edema in dogs. 144 76

We determined the effect of H2O2 on both the physiological and biochemical lung changes seen in the adult sheep after endotoxin. Fourteen unanesthetized adult sheep with chronic lung lymph fistula were given Escherichia coli endotoxin (1 microgram/kg) over 30 min. Seven sheep were given catalase (32,500 U/kg body wt) as an intravenous bolus 30 min before endotoxin. Four sheep were given catalase alone. Oxidant lung changes were measured using arterial plasma conjugated dienes and lung tissue malondialdehyde (MDA) content, both reflecting the lipid peroxidation process. Animals were killed 5 h after endotoxin. We found that endotoxin alone caused an early increase in pulmonary arterial pressure lung lymph flow (QL), plasma thromboxane B2, 6-keto-prostaglandin F1 alpha, and plasma conjugated dienes. A decrease in cardiac output and arterial PO2 was also seen. A three- to four-fold increase in protein-rich QL was noted at 3-4 h as well as a continued increase in arterial conjugated dienes. Lung MDA and water content were also significantly increased from base line. Catalase pretreatment significantly attenuated both the physiological changes and the prostanoid and conjugated diene release. Lung MDA and water content also remained at base line. We conclude that H2O2 plays a major role in endotoxin-induced lung injury as well as the resulting lipid peroxidation process.
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PMID:Catalase prevents prostanoid release and lung lipid peroxidation after endotoxemia in sheep. 318 91

We have examined the effect of activated neutrophils on the release of prostacyclin (PGI2) from cultured endothelial cells by radioimmunoassay and thin layer chromatography of its stable metabolite, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). Phorbol myristate acetate-activated neutrophils induced a time- and dose-dependent release of 6-keto-PGF1 alpha from human and bovine endothelial cell monolayers, whereas phorbol myristate acetate alone and neutrophils alone did not. Pretreatment of the endothelial cells with aspirin prevented neutrophil-mediated 6-keto-PGF1 alpha release, indicating that it did not depend upon neutrophil-generated endoperoxides. Phorbol myristate acetate-activated neutrophils from a patient with chronic granulomatous disease failed to induce endothelial 6-keto-PGF1 alpha release. Addition of catalase but not of superoxide dismutase significantly reduced human and bovine endothelial 6-keto-PGF1 alpha release by phorbol myristate acetate-activated neutrophils. Catalase-inhibitable endothelial 6-keto-PGF1 alpha release was also observed after the addition of the hydrogen peroxide-generating system, glucose-glucose oxidase, to bovine and human endothelial cell monolayers. Bovine endothelial 6-keto-PGF1 alpha release induced by exogenously generated hydrogen peroxide was attenuated by the phospholipase inhibitor mepacrine, suggesting that hydrogen peroxide may act by triggering endothelial membrane phospholipase activation. The release of 6-keto-PGF1 alpha by enzymatically or neutrophil-generated hydrogen peroxide was not associated with endothelial cell lysis as assessed by 51Cr release. We conclude that exogenously generated hydrogen peroxide or a hydrogen peroxide-derived product mediates rapid nonlytic release of PGI2 from cultured endothelial cells.
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PMID:Role of hydrogen peroxide in the neutrophil-mediated release of prostacyclin from cultured endothelial cells. 637 74

Hydrogen peroxide (H2O2) is known to cause transient pulmonary vasoconstriction in isolated lungs perfused with a solution containing no blood components, by inducing vasoactive arachidonate metabolites such as thromboxane A2 (TXA2). However, the exact site of production of the vasoactive arachidonates in the lung tissue is unclear. Using isolated main pulmonary arterial rings obtained from male Sprague-Dawley rats (B.W. 300-350 g), we attempted to examine the arachidonate metabolism, especially that mediated by cyclooxygenase, in the vascular wall of pulmonary artery without endothelium. Changes in isometric tension were used to measure contraction or dilatation of the ring preparation. H2O2 caused transient contraction of the ring, which was treated previously with a solution containing a high concentration of potassium (20 mM). The contractile response was enhanced in parallel with the concentration of H2O2 in the presence or absence of endothelium. Catalase (1000 U/ml), a H2O2 scavenger, completely inhibited the response of the isolated ring (without endothelium) to H2O2. OKY-046 (10(-5) and 10(-4) M), a TXA2 synthetase blocker, partially attenuated the contractile response induced by H2O2. ONO-3708 (10(-5) M), a TXA2 and prostaglandin H2 receptor blocker, fully inhibited the vasoconstriction and caused relaxation of the ring without endothelium after addition of H2O2. Indomethacin (5 microM), a cyclooxygenase inactivator, completely inhibited both vasoconstriction and vasodilation of the denuded ring. H2O2 also induced the release of 6-keto-prostaglandin F1 alpha, a stable metabolite of the vasodilator, prostacyclin, from the pulmonary artery without endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mechanism of constriction and dilatation of pulmonary artery induced by hydrogen peroxide]. 836 17