{"title":"Effects of Exogenous H202 on the Content of Endogenous H₂0₂, Activities of Catalase and Hydrolases, and Cell Ultrastructure in Tobacco Leaves.","authors":"L A Lapshina, A V Reunov, V P Nagorskaya","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>It was shown that tobacco leaf treatment with 100 mM H₂0₂ increased their content ofendogenous H₂0₂ and activities of catalase and hydrolases (acid phosphatase, proteases, and RNase) and also caused'various chang- es in the cell structure. In this case, programmed cell death (PCD) occurred in some cells, which was ob- served as chromatin condensation, cytoplasm collapse, etc. In the meantime, many cells displayed organelle activation rather than PCD. It is suggested that cells that undergo H₂0₂-dependent PCD release signaling molecules inducing protective mechanisms against oxidative stress in neighboring cells not exhibiting PCD.</p>","PeriodicalId":77187,"journal":{"name":"Izvestiia Akademii nauk. Seriia biologicheskaia","volume":" 5","pages":"491-498"},"PeriodicalIF":0.0000,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Izvestiia Akademii nauk. Seriia biologicheskaia","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
Abstract
It was shown that tobacco leaf treatment with 100 mM H₂0₂ increased their content ofendogenous H₂0₂ and activities of catalase and hydrolases (acid phosphatase, proteases, and RNase) and also caused'various chang- es in the cell structure. In this case, programmed cell death (PCD) occurred in some cells, which was ob- served as chromatin condensation, cytoplasm collapse, etc. In the meantime, many cells displayed organelle activation rather than PCD. It is suggested that cells that undergo H₂0₂-dependent PCD release signaling molecules inducing protective mechanisms against oxidative stress in neighboring cells not exhibiting PCD.