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

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

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    70 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

    Keywords

    • Aluminium
    • Mitochondria
    • Nicotiana tabacum
    • Programmed cell death

    ASJC Scopus subject areas

    • Biochemistry, Genetics and Molecular Biology(all)
    • Immunology and Microbiology(all)
    • Agricultural and Biological Sciences(all)

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