Mitochondrial alterations related to programmed cell death in tobacco cells under aluminium stress

Sanjib Kumar Panda, Yoko Yamamoto, Hideki Kondo, Hideaki Matsumoto

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

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 Ca2+ dependent and well modulated by dithioerythritol (DTE) and Pi, but insensitive to cyclosporine A (CsA). The collapse of inner mitochondrial membrane potential (Δ Ψm) 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. To cite this article: S.K. Panda et al., C. R. Biologies 331 (2008).

Original languageEnglish
Pages (from-to)597-610
Number of pages14
JournalComptes Rendus - Biologies
Volume331
Issue number8
DOIs
Publication statusPublished - Aug 2008

Fingerprint

Tobacco
Cell death
Aluminum
aluminum
Mitochondria
Cell Death
tobacco
apoptosis
mitochondria
Cells
cells
cell respiration
Toxicity
Respiration
Dithioerythritol
Adenosine Triphosphate
toxicity
Membranes
Oxidative stress
cyclosporine

Keywords

  • Aluminium
  • Mitochondria
  • Nicotiana tabacum
  • Programmed cell death

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Developmental Biology

Cite this

Mitochondrial alterations related to programmed cell death in tobacco cells under aluminium stress. / Panda, Sanjib Kumar; Yamamoto, Yoko; Kondo, Hideki; Matsumoto, Hideaki.

In: Comptes Rendus - Biologies, Vol. 331, No. 8, 08.2008, p. 597-610.

Research output: Contribution to journalArticle

Panda, Sanjib Kumar ; Yamamoto, Yoko ; Kondo, Hideki ; Matsumoto, Hideaki. / Mitochondrial alterations related to programmed cell death in tobacco cells under aluminium stress. In: Comptes Rendus - Biologies. 2008 ; Vol. 331, No. 8. pp. 597-610.
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