Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/13843
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dc.contributor.authorOPDENAKKER, Kelly-
dc.contributor.authorREMANS, Tony-
dc.contributor.authorKEUNEN, Els-
dc.contributor.authorVANGRONSVELD, Jaco-
dc.contributor.authorCUYPERS, Ann-
dc.date.accessioned2012-07-25T09:16:39Z-
dc.date.available2012-07-25T09:16:39Z-
dc.date.issued2012-
dc.identifier.citationENVIRONMENTAL AND EXPERIMENTAL BOTANY, 83, p. 53-61-
dc.identifier.issn0098-8472-
dc.identifier.urihttp://hdl.handle.net/1942/13843-
dc.description.abstractMetals, like cadmium (Cd) and copper (Cu), have the ability to induce the production of reactive oxygen species (ROS) at the cellular level. It is widely known that these ROS can cause irreversible damage to cellular components, like DNA, proteins and lipids. On the other hand, ROS can also act as signaling molecules and in this way they play an essential role in many normal physiological processes, but also in defense responses against stress. ROS signaling in plants uses mitogen-activated protein kinase (MAPK) pathways leading to the transcriptional control of target genes involved in the scavenging or production of ROS. Here, oxidative signaling induced by exposure to excess Cd or Cu was investigated in relation to antioxidative defense responses to these metals. Three-week-old Arabidopsis thaliana plants were exposed to environmentally realistic concentrations of Cu and Cd and immediate responses were measured at the level of hydrogen peroxide (H2O2) content, lipid peroxidation and transcript levels of genes involved in ROS homeostasis and signaling. Our findings show immediate (after 2 h exposure) effects in the roots following Cu exposure, whereas effects in the leaves were generally more delayed. Effects of Cd exposure in leaves and roots were observed only after 24 h exposure. On one hand, exposure of roots to Cu leads via activation of NADPH oxidases and Fenton reactions to H2O2 production that can induce MAPK and oxylipin signaling to control the cellular redox status. On the other hand, conversion of H2O2 to the more damaging hydroxyl radical by Fenton and Haber-Weiss reactions can initiate lipid peroxidation leading to membrane damage. In roots exposed to elevated Cd concentrations only oxidative signaling was initiated, possibly via NADPH oxidase-mediated ROS production. In leaves, time-dependent activation of MAPK and oxylipin signaling was seen after exposure to both metals. Cu or Cd, independent of changes in H2O2 content. (C) 2012 Elsevier B.V. All rights reserved.-
dc.language.isoen-
dc.publisherPERGAMON-ELSEVIER SCIENCE LTD-
dc.subject.otherPlant Sciences; Environmental Sciences; Cadmium; Copper; Oxidative stress; Signal transduction; Arabidopsis thaliana; MAPkinases-
dc.subject.otherCadmium; Copper; Oxidative stress; Signal transduction; Arabidopsis thaliana; MAPkinases-
dc.titleExposure of Arabidopsis thaliana to Cd or Cu excess leads to oxidative stress mediated alterations in MAPKinase transcript levels-
dc.typeJournal Contribution-
dc.identifier.epage61-
dc.identifier.spage53-
dc.identifier.volume83-
local.format.pages9-
local.bibliographicCitation.jcatA1-
dc.description.notes[Opdenakker, Kelly; Remans, Tony; Keunen, Els; Vangronsveld, Jaco; Cuypers, Ann] Hasselt Univ, Ctr Environm Sci, B-3590 Diepenbeek, Belgium.-
local.publisher.placeOXFORD-
local.type.refereedRefereed-
local.type.specifiedArticle-
dc.bibliographicCitation.oldjcatA1-
dc.identifier.doi10.1016/j.envexpbot.2012.04.003-
dc.identifier.isi000305767500006-
item.fullcitationOPDENAKKER, Kelly; REMANS, Tony; KEUNEN, Els; VANGRONSVELD, Jaco & CUYPERS, Ann (2012) Exposure of Arabidopsis thaliana to Cd or Cu excess leads to oxidative stress mediated alterations in MAPKinase transcript levels. In: ENVIRONMENTAL AND EXPERIMENTAL BOTANY, 83, p. 53-61.-
item.accessRightsRestricted Access-
item.contributorOPDENAKKER, Kelly-
item.contributorREMANS, Tony-
item.contributorKEUNEN, Els-
item.contributorVANGRONSVELD, Jaco-
item.contributorCUYPERS, Ann-
item.fulltextWith Fulltext-
item.validationecoom 2013-
crisitem.journal.issn0098-8472-
crisitem.journal.eissn1873-7307-
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