Document Detail


A critical role for ethylene in hydrogen peroxide release during programmed cell death in tomato suspension cells.
MedLine Citation:
PMID:  11925037     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Camptothecin, a topo isomerase-I inhibitor used in cancer therapy, induces apoptosis in animal cells. In tomato (Lycopersicon esculentum Mill.) suspension cells, camptothecin induces cell death that is accompanied by the characteristic nuclear morphological changes such as chromatin condensation and nuclear and DNA fragmentation that are commonly associated with apoptosis in animal systems. These effects of camptothecin can effectively be blocked by inhibitors of animal caspases, indicating that, in tomato suspension cells, camptothecin induces a form of programmed cell death (PCD) with similarities to animal apoptosis (A.J. De Jong et al. (2000) Planta 211:656-662). Camptothecin induced cell death was employed to study processes involved in plant PCD. Camptothecin induced a transient increase in H2O2 production starting within 2 h of application. Both camptothecin-induced cell death and the release of H2O2 were effectively blocked by application of the calcium-channel blocker lanthanum chloride, the caspase-specific inhibitor Z-Asp-CH2-DCB, or the NADPH oxidase inhibitor diphenyl iodonium, indicating that camptothecin exerts its effect on cell death through a calcium- and caspase-dependent stimulation of NADPH oxidase activity. In addition, we show that ethylene is an essential factor in camptothecin-induced PCD. Inhibition of either ethylene synthesis or ethylene perception by L-alpha-(2-aminoethoxyvinyl)glycine or silver thiosulphate, respectively, blocked camptothecin-induced H2O2 production and PCD. Although, in itself, insufficient to trigger H2O2 production and cell death, exogenous ethylene greatly stimulated camptothecin-induced H2O2 production and cell death. These results show that ethylene is a potentiator of the camptothecin-induced oxidative burst and subsequent PCD in tomato cells. The possible mechanisms by which ethylene stimulates cell death are discussed.
Authors:
JongAnkeJ de; Elena T Yakimova; Veneta M Kapchina; Ernst J Woltering
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Planta     Volume:  214     ISSN:  0032-0935     ISO Abbreviation:  Planta     Publication Date:  2002 Feb 
Date Detail:
Created Date:  2002-04-01     Completed Date:  2002-11-25     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  1250576     Medline TA:  Planta     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  537-45     Citation Subset:  IM    
Affiliation:
Agrotechnological Research Institute (ATO), Wageningen University and Research Center, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects,  physiology*
Aspartic Acid / analogs & derivatives*,  pharmacology
Calcium / metabolism
Calcium Channels / metabolism
Camptothecin / pharmacology
Caspases / antagonists & inhibitors
Cells, Cultured
Ethylenes / metabolism,  pharmacology*
Glycine / analogs & derivatives*,  pharmacology
Hydrogen Peroxide / metabolism*
Lanthanum / pharmacology
Lycopersicon esculentum / cytology,  drug effects,  metabolism*
Mitogen-Activated Protein Kinases / metabolism
Oxidation-Reduction
Plant Growth Regulators / metabolism,  pharmacology*
Tosyllysine Chloromethyl Ketone / pharmacology
Chemical
Reg. No./Substance:
0/Calcium Channels; 0/Ethylenes; 0/Plant Growth Regulators; 0/benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene; 10099-58-8/lanthanum chloride; 2104-86-1/Tosyllysine Chloromethyl Ketone; 49669-74-1/aminoethoxyvinylglycine; 56-40-6/Glycine; 56-84-8/Aspartic Acid; 74-85-1/ethylene; 7439-91-0/Lanthanum; 7440-70-2/Calcium; 7689-03-4/Camptothecin; 7722-84-1/Hydrogen Peroxide; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 3.4.22.-/Caspases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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