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Coenzyme Q blocks biochemical but not receptor-mediated apoptosis by increasing mitochondrial antioxidant protection
Rizzoli Orthopaedic Institute, Bologna, Italy.
Institute of Experimental Pathology, University of Ancona, Ancona, Italy.
Institute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic.
Institute for Prevention of Cardiovascular Diseases, Ludwig Maximilians University, Pettenkoferstrasse 9, 80336 Munich, Germany.
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2001 (English)In: FEBS Letters, ISSN 0014-5793, Vol. 503, no 1, 46-50 p.Article in journal (Refereed) Published
Abstract [en]

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 a-tocopheryl succinate (a-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 a-TOS, and a mitochondrially targeted coenzyme Q analogue also blocked apoptosis triggered by a-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. © 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

Place, publisher, year, edition, pages
2001. Vol. 503, no 1, 46-50 p.
Keyword [en]
Apoptosis, Coenzyme Q, Lymphoma cell, Reactive oxygen species, Signalling
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-47292DOI: 10.1016/S0014-5793(01)02694-1OAI: diva2:268188
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2011-01-13

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