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)

Previous studies have proposed that oxygen radicals may play a role in the triggering of ischemic preconditioning. However, studies evaluating the effects of radical scavengers have yielded conflicting results, possibly because of differences in the number of preconditioning episodes used. The present study tested whether N-2-mercaptopropionylglycine (MPG) could block protection of both single and multiple episodes of preconditioning in in situ and in vitro rabbit hearts. All hearts were subjected to 30 min of regional ischemia followed by reperfusion for 2 (in vitro) or 3 (in situ) h. Infarct size was measured by tetrazolium. Infarction in control in situ hearts was 37.5+/-3.5% of the risk zone. A single cycle of preconditioning (PC1), with 5 min ischemia/10 min reperfusion, reduced infarct size to 12.3+/-2.0% (P<0.05). Four cycles of preconditioning (PC4) were equally protective. MPG (1 mg/kg/min i.v.) alone had no effect on infarction but abolished protection afforded by PC1 (35.4+/-3.9%). However, MPG failed to block protection in the PC4 group. In isolated control hearts, infarct size was 31.1+/-1.8% and was reduced to 10.2+/-2.2% (P<0.05) by preconditioning. MPG (300 microM) aborted protection. Infusion of hypoxanthine or xanthine oxidase separately in lieu of preconditioning had no effect on infarct size, but induced protection when combined (14.1+/-2.2%; P<0.05). Polymyxin B, an inhibitor of protein kinase C (PKC), abolished this protection (53.1+/-4.1%). In conclusion, oxygen radicals contribute to ischemic preconditioning in the rabbit and appear to do so via activation of PKC. The fact that MPG could not block protection by PC4 suggests that oxygen radicals act in concert with other triggers of preconditioning such as adenosine and bradykinin.
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PMID:Oxygen radicals released during ischemic preconditioning contribute to cardioprotection in the rabbit myocardium. 904 35

Trends of polycyclic aromatic hydrocarbons (PAHs) for 1992-1996 (cold season) and their mutagenic activity were investigated in organic extracts from the Santiago, Chile, inhalable particles (PM(10)). The highest PAH concentrations were observed in 1992 and declined dramatically in the following years. During this period, total PAHs decreased 85%, carcinogenic PAHs 82%, and benzo[a]pyrene, the most potent carcinogen, 85%. In spite of this significant decrease, PAH levels in respirable particles were higher than those reported in recent studies in Australia, Europe, and the United States. PAH profiles were analyzed by principal component (PC) analysis and Pearson correlation analysis. PC1 represents 71% of the variance, suggesting that most PAHs might originate predominantly from one main generic source. Higher correlations were obtained for the major carcinogenic PAHs. Most of the samples assayed were highly mutagenic to Salmonella typhimurium both in the presence and in the absence of metabolic activation system (S9), especially in the coarse fraction, but direct mutagenicity did not decline significantly. Incubation of calf thymus DNA with organic extracts from particulate matter and xanthine oxidase allowed the detection of five nitro-PAH-DNA adducts. Thus, nitroarenes might play an important role in the mutagenic activity of inhalable particles in Santiago, representing a high risk for human health.
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PMID:Trends of polycyclic aromatic hydrocarbon levels and mutagenicity in Santiago's inhalable airborne particles in the period 1992-1996. 1111 88