{"title":"铁螯合可防止缺血后的组织损伤","authors":"Steven D. Aust, Blaine C. White","doi":"10.1016/8755-9668(85)90003-1","DOIUrl":null,"url":null,"abstract":"<div><p>Damage to a tissue following ischemia appears top occur during its reperfusion with oxygenated blood. This damage is apparently oxidative in nature and is generally considered to be the result of excessive superoxide (O<sub>2</sub><sup>−</sup> and hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) production. Since neither O<sub>2</sub><sup>−</sup> nor H<sub>2</sub>O<sub>2</sub> cause oxidative damage in the absence of iron, we proposed that the oxidative processes are caused by the released of iron during reperfusion. The damage caused by the iron is exacerbated by hypoperfusion and the loss of calcium homeostasis. Our hypothesis is supported by the finding of significant levels of low molecular weight, chelatable iron in tissues during reperfusion following ischemia. The tissue damage can be ameliorated by techniques that increase the rate of reperfusion (open chest direct heart massage for the cardiac arrest model) and the administration of an iron chelator plus a calcium antagonist. Animals treated in this manner appear to completely recover from 15 minutes of cardiac arrest.</p></div>","PeriodicalId":100046,"journal":{"name":"Advances in Free Radical Biology & Medicine","volume":"1 1","pages":"Pages 1-17"},"PeriodicalIF":0.0000,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/8755-9668(85)90003-1","citationCount":"106","resultStr":"{\"title\":\"Iron chelation prevents tissue injury following ischemia\",\"authors\":\"Steven D. Aust, Blaine C. White\",\"doi\":\"10.1016/8755-9668(85)90003-1\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Damage to a tissue following ischemia appears top occur during its reperfusion with oxygenated blood. This damage is apparently oxidative in nature and is generally considered to be the result of excessive superoxide (O<sub>2</sub><sup>−</sup> and hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) production. Since neither O<sub>2</sub><sup>−</sup> nor H<sub>2</sub>O<sub>2</sub> cause oxidative damage in the absence of iron, we proposed that the oxidative processes are caused by the released of iron during reperfusion. The damage caused by the iron is exacerbated by hypoperfusion and the loss of calcium homeostasis. Our hypothesis is supported by the finding of significant levels of low molecular weight, chelatable iron in tissues during reperfusion following ischemia. The tissue damage can be ameliorated by techniques that increase the rate of reperfusion (open chest direct heart massage for the cardiac arrest model) and the administration of an iron chelator plus a calcium antagonist. Animals treated in this manner appear to completely recover from 15 minutes of cardiac arrest.</p></div>\",\"PeriodicalId\":100046,\"journal\":{\"name\":\"Advances in Free Radical Biology & Medicine\",\"volume\":\"1 1\",\"pages\":\"Pages 1-17\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1985-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/8755-9668(85)90003-1\",\"citationCount\":\"106\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Advances in Free Radical Biology & Medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/8755966885900031\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in Free Radical Biology & Medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/8755966885900031","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Iron chelation prevents tissue injury following ischemia
Damage to a tissue following ischemia appears top occur during its reperfusion with oxygenated blood. This damage is apparently oxidative in nature and is generally considered to be the result of excessive superoxide (O2− and hydrogen peroxide (H2O2) production. Since neither O2− nor H2O2 cause oxidative damage in the absence of iron, we proposed that the oxidative processes are caused by the released of iron during reperfusion. The damage caused by the iron is exacerbated by hypoperfusion and the loss of calcium homeostasis. Our hypothesis is supported by the finding of significant levels of low molecular weight, chelatable iron in tissues during reperfusion following ischemia. The tissue damage can be ameliorated by techniques that increase the rate of reperfusion (open chest direct heart massage for the cardiac arrest model) and the administration of an iron chelator plus a calcium antagonist. Animals treated in this manner appear to completely recover from 15 minutes of cardiac arrest.