Coenzyme Q blocks biochemical but not receptor-mediated apoptosis by increasing mitochondrial antioxidant protection

Renata Alleva, Marco Tomasetti, Ladislav Andera, Nina Gellert, Battista Borghi, Christian Weber, Michael P. Murphy, Jiri Neuzil

Research output: Contribution to journalArticle

Abstract

Generation of free radicals is often associated with the induction and progression of apoptosis. Therefore, antioxidants can prove anti-apoptotic, and can help to elucidate specific apoptotic pathways. Here we studied whether coenzyme Q, present in membranes in reduced (ubiquinol) or oxidised (ubiquinone) forms, can affect apoptosis induced by various stimuli. Exposure of Jurkat cells to α-tocopheryl succinate (α-TOS), hydrogen peroxide, anti-Fas IgM or TRAIL led to induction of apoptosis. Cell death due to the chemical agents was suppressed in cells enriched with the reduced form of coenzyme Q. However, coenzyme Q did not block cell death induced by the immunological agents. Ubiquinol-10 inhibited reactive oxygen species (ROS) generation in cells exposed to α-TOS, and a mitochondrially targeted coenzyme Q analogue also blocked apoptosis triggered by α-TOS or hydrogen peroxide. Therefore, it is plausible that ubiquinol-10 protects cells from chemically-induced apoptosis by acting as an antioxidant in mitochondria. Our results also indicate that generation of free radicals may not be a critical step in induction of apoptosis by immunological agents.

Original languageEnglish
Pages (from-to)46-50
Number of pages5
JournalFEBS Letters
Volume503
Issue number1
DOIs
Publication statusPublished - Aug 10 2001

Keywords

  • Apoptosis
  • Coenzyme Q
  • Lymphoma cell
  • Reactive oxygen species
  • Signalling

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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