Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While free radical-mediated reperfusion injury is clearly important in a variety of disparate organs, the particular cellular source of these radicals is unclear. To address this question, we subjected relatively pure (92% +/- 3% by factor VIII immunoassay) cultures of rat pulmonary artery endothelial cells to 0 to 45 minutes of anoxia (95% N2, 5% CO2), followed by reoxygenation (95% air, 5% CO2), to simulate ischemia/reperfusion. Cell injury was assayed after reoxygenation by the release of previously incorporated 51chromium and/or lactate dehydrogenase, and viability was determined by means of trypan blue exclusion. These three end points correlated closely. Without anoxia, the cells remained viable, with minimal evidence of injury for the entire experimental period, while 45 minutes of hypoxia followed by 30 minutes of reoxygenation produced substantial evidence of cell injury in 71% +/- 6% of the cells. This injury was reduced to 21% +/- 2% by treatment with the highly specific free radical scavengers superoxide dismutase and catalase together, either before anoxia or after anoxia, but just before reoxygenation. Similar protection was provided by xanthine oxidase inhibition with allopurinol. The injury was mimicked (without anoxia) by the exogenous generation of superoxide radicals with xanthine and xanthine oxidase. These experiments establish the essential components of free radical generation at reperfusion to be localized within the isolated endothelial cell in the absence of neutrophils or parenchymal cells.
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PMID:The primary localization of free radical generation after anoxia/reoxygenation in isolated endothelial cells. 303 75

Pulmonary artery endothelial cells (PAEC) were isolated from broilers by the method of tissue explantation. The cells were identified using morphological features and immunocytochemical staining using a specific antiserum against factor VIII related antigen. Xanthine/Xanthine oxidase (X/XO) served as the oxygen free radical (OFR) generating system. In vitro model of oxidative injury of PAEC was established based on the X/XO system. The effect of OFR on the growth and viability of PAEC was determined with methylthiazol tetrazolium (MTT) colorimetric assay. Malondialdehyde (MDA, a product of lipid peroxidation) in culture medium of PAEC was detected by a thiobarbituric acid colorimetric assay. The results showed that PAEC survive in vitro and can be subcultured for 5-6 passages. Morphological and immunocytochemical observations of cultured cells demonstrated specific characteristics of endothelial cells. PAECs were severely damaged by OFR. The viability of cells was reduced by the X/XO system, and a dose-dependent decrease in cell viability was found with increasing XO dosages. OFR promoted lipid peroxidation of PAEC and increased the MDA concentration in culture media. These results suggest that OFR can injure the endothelial cells from broiler pulmonary arteries in vitro, which confirms previous results obtained in vivo. Oxidative injury may play an important role in the pathogenesis of pulmonary hypertension syndrome in broiler.
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PMID:The injury effect of oxygen free radicals in vitro on cultured pulmonary artery endothelial cells from broilers. 1705 46