{"title":"脂多糖诱导氧化应激过程中l -精氨酸- no途径修饰的血氧功能。","authors":"A Glebov, V Zinchuk","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Our aim was to study the blood oxygen-carrying function during the oxidative stress with a modification of the L-arginine-NO pathway.</p><p><strong>Material and methods: </strong>Oxidative stress was induced by intravenous administration of Escherichia coli lipopolysaccharide (LPS) to rabbits. To modify the L-arginine-NO pathway, animals were administered with NG-nitro-L-arginine methyl ester intravenously 60 min after the LPS. Mixed venous blood was sampled for evaluation of blood oxygen transport before and at 120 and 240 min after the LPS administration; tissue samples (heart, lung, liver, kidney and muscle) were also prepared. The following parameters were measured hemoglobin-oxygen affinity, concentrations of conjugated dienes, Schiff bases, alpha-tocopherol and activity of catalase.</p><p><strong>Results: </strong>During the NO synthase inhibition the oxidative stress was characterized by a shift of hemoglobin oxygen dissociation curve rightwards, more prominent activation of lipid peroxidation and decreased tissue levels of antioxidant defense factors.</p><p><strong>Conclusions: </strong>The inhibition of NO generation induces a shift of prooxidant-antioxidant balance--obviously, not only due its potentially high levels and reactivity with the various target molecules (with a development of oxidative stress), but also because of the lower contribution of other factors including the hemoglobin-oxygen affinity change into the body antioxidant potential.</p>","PeriodicalId":79372,"journal":{"name":"Roczniki Akademii Medycznej w Bialymstoku (1995)","volume":"50 ","pages":"247-51"},"PeriodicalIF":0.0000,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Blood oxygen-carrying function during the oxidative stress induced by lipopolysaccharide with a modification of the L-arginine-NO pathway.\",\"authors\":\"A Glebov, V Zinchuk\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>Our aim was to study the blood oxygen-carrying function during the oxidative stress with a modification of the L-arginine-NO pathway.</p><p><strong>Material and methods: </strong>Oxidative stress was induced by intravenous administration of Escherichia coli lipopolysaccharide (LPS) to rabbits. To modify the L-arginine-NO pathway, animals were administered with NG-nitro-L-arginine methyl ester intravenously 60 min after the LPS. Mixed venous blood was sampled for evaluation of blood oxygen transport before and at 120 and 240 min after the LPS administration; tissue samples (heart, lung, liver, kidney and muscle) were also prepared. The following parameters were measured hemoglobin-oxygen affinity, concentrations of conjugated dienes, Schiff bases, alpha-tocopherol and activity of catalase.</p><p><strong>Results: </strong>During the NO synthase inhibition the oxidative stress was characterized by a shift of hemoglobin oxygen dissociation curve rightwards, more prominent activation of lipid peroxidation and decreased tissue levels of antioxidant defense factors.</p><p><strong>Conclusions: </strong>The inhibition of NO generation induces a shift of prooxidant-antioxidant balance--obviously, not only due its potentially high levels and reactivity with the various target molecules (with a development of oxidative stress), but also because of the lower contribution of other factors including the hemoglobin-oxygen affinity change into the body antioxidant potential.</p>\",\"PeriodicalId\":79372,\"journal\":{\"name\":\"Roczniki Akademii Medycznej w Bialymstoku (1995)\",\"volume\":\"50 \",\"pages\":\"247-51\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2005-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Roczniki Akademii Medycznej w Bialymstoku (1995)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Roczniki Akademii Medycznej w Bialymstoku (1995)","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
目的:通过对l -精氨酸- no通路的修饰,研究氧化应激过程中血液载氧功能。材料与方法:采用静脉注射大肠杆菌脂多糖(LPS)诱导家兔氧化应激。为了改变l -精氨酸- no通路,动物在LPS后60分钟静脉注射ng -硝基- l -精氨酸甲酯。采集混合静脉血,评价LPS给药前、给药后120、240 min血氧运输情况;组织样品(心、肺、肝、肾和肌肉)也准备好了。测定了血红蛋白-氧亲和力、共轭二烯、席夫碱、α -生育酚浓度和过氧化氢酶活性。结果:NO合酶抑制过程中,氧化应激表现为血红蛋白氧解离曲线右移,脂质过氧化活化更为突出,组织抗氧化防御因子水平降低。结论:NO生成的抑制诱导了促氧化-抗氧化平衡的改变——显然,这不仅是因为其潜在的高水平和与各种靶分子的反应性(伴随着氧化应激的发展),还因为其他因素,包括血红蛋白-氧亲和力变化,对机体抗氧化潜能的贡献较低。
Blood oxygen-carrying function during the oxidative stress induced by lipopolysaccharide with a modification of the L-arginine-NO pathway.
Purpose: Our aim was to study the blood oxygen-carrying function during the oxidative stress with a modification of the L-arginine-NO pathway.
Material and methods: Oxidative stress was induced by intravenous administration of Escherichia coli lipopolysaccharide (LPS) to rabbits. To modify the L-arginine-NO pathway, animals were administered with NG-nitro-L-arginine methyl ester intravenously 60 min after the LPS. Mixed venous blood was sampled for evaluation of blood oxygen transport before and at 120 and 240 min after the LPS administration; tissue samples (heart, lung, liver, kidney and muscle) were also prepared. The following parameters were measured hemoglobin-oxygen affinity, concentrations of conjugated dienes, Schiff bases, alpha-tocopherol and activity of catalase.
Results: During the NO synthase inhibition the oxidative stress was characterized by a shift of hemoglobin oxygen dissociation curve rightwards, more prominent activation of lipid peroxidation and decreased tissue levels of antioxidant defense factors.
Conclusions: The inhibition of NO generation induces a shift of prooxidant-antioxidant balance--obviously, not only due its potentially high levels and reactivity with the various target molecules (with a development of oxidative stress), but also because of the lower contribution of other factors including the hemoglobin-oxygen affinity change into the body antioxidant potential.