Affiliations: Vestische Kinderklinik Datteln, Universität Witten
Herdecke, 45711 Datteln, Germany | Department of Neurology, TU Dresden, 01307 Dresden,
Germany | Institute of Anatomy, TU Dresden, 01307 Dresden,
Germany
Note: [] Address for correspondence: Dr. Thomas Menke, Vestische
Kinderklinik, Universität Witten/Herdecke, Dr.-Friedrich-Steiner-Str. 5,
D-45711 Datteln, Germany. Tel.: +49 2363 9750; Fax: +49 2363 64211; E-mail:
th.menke@t-online.de
Abstract: Defects in mitochondrial energy metabolism due to respiratory chain
disorders lead to a decrease in mitochondrial membrane
potential (ΔΨ_{m}) and induce apoptosis. Since
coenzyme Q_{10} (CoQ_{10}) plays a dual
role as an antioxidant and bioenergetic agent in the respiratory chain, it has
attracted increasing attention concerning the prevention of apoptosis in
mitochondrial diseases. In this study the potential of
CoQ_{10} to antagonize the apoptosis-inducing effects of the
respiratory chain inhibitor rotenone was explored by video-enhanced microscopy
in SH-SY5Y neuroblastoma cells. The cationic fluorescent dye JC-1 which
exhibits potential-dependent accumulation in mitochondria was used as an
indicator to monitor changes in ΔΨ_{m}. The
relative changes in fluorescence intensity after incubation with rotenone for
15 minutes were calculated. Pre-treatment with CoQ_{10} (10
or 100 μM) for 48h led to a significant reduction of
rotenone-induced loss of ΔΨ_{m}. These results
suggest, that cytoprotection by CoQ_{10} may be mediated by
raising cellular resistance against the initiating steps of apoptosis, namely
the decrease of ΔΨ_{m}. Whether these data may
provide new directions for the development of neuroprotective strategies has to
be investigated in future studies.
