Document Detail

Mitochondrial alterations related to programmed cell death in tobacco cells under aluminium stress.
MedLine Citation:
PMID:  18606389     Owner:  NLM     Status:  MEDLINE    
The present investigation was undertaken to verify whether mitochondria play a significant role in aluminium (Al) toxicity, using the mitochondria isolated from tobacco cells (Nicotiana tabacum, non-chlorophyllic cell line SL) under Al stress. An inhibition of respiration was observed in terms of state-III, state-IV, succinate-dependent, alternative oxidase (AOX)-pathway capacity and cytochrome (CYT)-pathway capacity, respectively, in the mitochondria isolated from tobacco cells subjected to Al stress for 18 h. In accordance with the respiratory inhibition, the mitochondrial ATP content showed a significant decrease under Al treatment. An enhancement of reactive oxygen species (ROS) production under state-III respiration was observed in the mitochondria isolated from Al-treated cells, which would create an oxidative stress situation. The opening of mitochondrial permeability transition pore (MPTP) was seen more extensively in mitochondria isolated from Al-treated cells than in those isolated from control cells. This was Ca(2+) dependent and well modulated by dithioerythritol (DTE) and Pi, but insensitive to cyclosporine A (CsA). The collapse of inner mitochondrial membrane potential (DeltaPsi(m)) was also observed with a release of cytochrome c from mitochondria. A great decrease in the ATP content was also seen under Al stress. Transmission electron microscopy analysis of Al-treated cells also corroborated our biochemical data with distortion in membrane architecture in mitochondria. TUNEL-positive nuclei in Al-treated cells strongly indicated the occurrence of nuclear fragmentation. From the above study, it was concluded that Al toxicity affects severely the mitochondrial respiratory functions and alters the redox status studied in vitro and also the internal structure, which seems to cause finally cell death in tobacco cells.
Sanjib Kumar Panda; Yoko Yamamoto; Hideki Kondo; Hideaki Matsumoto
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-06-02
Journal Detail:
Title:  Comptes rendus biologies     Volume:  331     ISSN:  1631-0691     ISO Abbreviation:  C. R. Biol.     Publication Date:  2008 Aug 
Date Detail:
Created Date:  2008-07-08     Completed Date:  2008-10-31     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101140040     Medline TA:  C R Biol     Country:  France    
Other Details:
Languages:  eng     Pagination:  597-610     Citation Subset:  IM    
Research Institute for Bioresources, Okayama University, Kurashiki, Japan. <>
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MeSH Terms
Adenosine Triphosphate / metabolism
Aluminum / toxicity*
Apoptosis / drug effects*
Blotting, Western
Cells, Cultured
Electrophoresis, Polyacrylamide Gel
Hydrogen Peroxide / toxicity
In Situ Nick-End Labeling
Membrane Potentials / drug effects
Microscopy, Electron, Transmission
Mitochondria / drug effects*,  metabolism*
Mitochondrial Membranes / drug effects,  metabolism
Oxygen Consumption / drug effects
Peptide Hydrolases / metabolism
Reactive Oxygen Species / metabolism
Superoxides / metabolism
Tobacco / cytology*,  drug effects
Reg. No./Substance:
0/Reactive Oxygen Species; 11062-77-4/Superoxides; 56-65-5/Adenosine Triphosphate; 7429-90-5/Aluminum; 7722-84-1/Hydrogen Peroxide; EC 3.4.-/Peptide Hydrolases

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

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