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Human Molecular Genetics, 2002, Vol. 11, No. 7 815-821
© 2002 Oxford University Press

Frataxin promotes antioxidant defense in a thiol-dependent manner resulting in diminished malignant transformation in vitro

Sarah A. Shoichet, Anselm T. Bäumer1, Djordje Stamenkovic1, Heinrich Sauer2, Andreas F. H. Pfeiffer3, C. Ronald Kahn4, Dirk Müller-Wieland5, Christoph Richter6 and Michael Ristow3,+

Center for Molecular Medicine, 1Clinic III for Internal Medicine and 2Center for Physiology and Pathophysiology, University of Cologne, Germany, 3German Institute for Human Nutrition (DIfE) and Free University of Berlin, Germany, 4Harvard Medical School, Joslin Diabetes Center, Boston, MA, USA, 5Diabetes-Research Institute (DFI), Department of Biochemistry, Düsseldorf, Germany and 6Institute of Biochemistry, Swiss Federal Institute of Technology (ETH), Zürich, Switzerland

Friedreich ataxia is an inherited disorder caused by decreased expression of frataxin protein. Increasing evidence suggests that this protein might detoxify reactive oxygen species (ROS) by an unknown mechanism. Here we demonstrate that transgenic overexpression of human frataxin increases cellular antioxidant defense via activation of glutathione peroxidase and elevation of reduced thiols, thereby reducing the incidence of malignant transformation induced by ROS, as observed by soft agar assays and tumour formation in nude mice. These findings expand the understanding of antioxidant properties of frataxin, and tentatively suggest a role in the early induction of cancer.

+ To whom correspondence should be addressed at: German Institute of Human Nutrition, DIfE, KLE, 114, Arthur-Scheunert-Allee, 14558 Potsdam-Rehbrücke, Germany. Tel: +49 33200 88 787; Fax: +49 33200 88 777; Email: mristow@mristow.org Present address: Sarah A. Shoichet, Max-Planck-Institute (MPI) for Molecular Genetics, Berlin, Germany


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