Skip Navigation


JXB Advance Access originally published online on February 14, 2005
Journal of Experimental Botany 2005 56(413):997-1006; doi:10.1093/jxb/eri093
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
56/413/997    most recent
eri093v1
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (18)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Casolo, V.
Right arrow Articles by Vianello, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Casolo, V.
Right arrow Articles by Vianello, A.
Agricola
Right arrow Articles by Casolo, V.
Right arrow Articles by Vianello, A.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2005]. Published by Oxford University Press [on behalf of the Society for Experimental Biology]. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

RESEARCH PAPER

Involvement of the mitochondrial KATP+ channel in H2O2- or NO-induced programmed death of soybean suspension cell cultures

Valentino Casolo, Elisa Petrussa, Jana Krajnáková *, Francesco Macrì and Angelo Vianello{dagger}

Section of Plant Biology, Department of Biology and Agro-Industrial Economics, University of Udine, via Cotonificio 108, I-33100 Udine, Italy

{dagger} To whom correspondence should be addressed. Fax: +39 0432 558784. E-mail: biolveg{at}dbea.uniud.it

Soybean suspension cell cultures were treated by H2O2 or nitric oxide (NO), to assess the mechanism leading to programmed cell death (PCD). Hydrogen peroxide (5 mM) induced PCD. Cells become necrotic at 20 mM H2O2, with cells exhibiting intermediate hallmarks before that (necrapoptotic cells). The level of ATP and of glucose-6-phosphate remained constant in cells undergoing PCD, while it decreased significantly in the necrotic ones. Mitochondria, isolated from 5 mM H2O2-treated (apoptotic) cells, showed that succinate-dependent oxygen consumption was slightly uncoupled, and the electrical potential difference ({Delta}{Psi}) weakly decreased. The addition of KCl to the {Delta}{Psi} formed determined a partial dissipation, which was higher than the dissipation observed in mitochondria from control cells. The addition of cyclosporin A (CsA) to de-energized mitochondria also induced {Delta}{Psi} formation, due to a K+ efflux from the matrix, which was decreased in mitochondria from treated cells. The same pattern of response was also observed in mitochondria isolated from 1 mM sodium nitroprusside (NO)-treated cells, exhibiting apoptotic symptoms. In mitochondria isolated from 20 mM H2O2-treated (necrotic) cells, succinate-dependent oxygen consumption was completely uncoupled, {Delta}{Psi} generation significantly inhibited, and CsA-dependent {Delta}{Psi} formation prevented. In addition, mitochondria isolated from control cells still underwent swelling, which was partially or completely prevented in mitochondria isolated from apoptotic or necrotic cells, respectively. The moderate swelling was accompanied by a slight rupture of the outer membrane and by a release of cytochrome c. These results point to the involvement of a channel during the manifestation of PCD induced by H2O2 or NO in plants.

Key words: Hydrogen peroxide, channel, mitochondria, nitric oxide, programmed cell death, soybean cells


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Plant Cell PhysiolHome page
M. N. Laus, M. Soccio, D. Trono, L. Cattivelli, and D. Pastore
Plant Inner Membrane Anion Channel (PIMAC) Function in Plant Mitochondria
Plant Cell Physiol., July 1, 2008; 49(7): 1039 - 1055.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
S. Morimoto, Y. Tanaka, K. Sasaki, H. Tanaka, T. Fukamizu, Y. Shoyama, Y. Shoyama, and F. Taura
Identification and Characterization of Cannabinoids That Induce Cell Death through Mitochondrial Permeability Transition in Cannabis Leaf Cells
J. Biol. Chem., July 13, 2007; 282(28): 20739 - 20751.
[Abstract] [Full Text] [PDF]


Home page
J Exp BotHome page
D. Pastore, D. Trono, M. N. Laus, N. Di Fonzo, and Z. Flagella
Possible plant mitochondria involvement in cell adaptation to drought stress: A case study: durum wheat mitochondria
J. Exp. Bot., January 1, 2007; 58(2): 195 - 210.
[Abstract] [Full Text] [PDF]


Home page
Plant Physiol.Home page
D. M. Rhoads, A. L. Umbach, C. C. Subbaiah, and J. N. Siedow
Mitochondrial Reactive Oxygen Species. Contribution to Oxidative Stress and Interorganellar Signaling
Plant Physiology, June 1, 2006; 141(2): 357 - 366.
[Full Text] [PDF]


Home page
Plant Physiol.Home page
F. Van Breusegem and J. F. Dat
Reactive Oxygen Species in Plant Cell Death
Plant Physiology, June 1, 2006; 141(2): 384 - 390.
[Full Text] [PDF]


Home page
J Exp BotHome page
P. C. Bethke, I. G. L. Libourel, and R. L. Jones
Nitric oxide reduces seed dormancy in Arabidopsis
J. Exp. Bot., February 1, 2006; 57(3): 517 - 526.
[Abstract] [Full Text] [PDF]


Home page
J Exp BotHome page
S. Grun, C. Lindermayr, S. Sell, and J. Durner
Nitric oxide and gene regulation in plants
J. Exp. Bot., February 1, 2006; 57(3): 507 - 516.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.