Coenzyme Q10 reduces the toxicity of rotenone in neuronal cultures by preserving the mitochondrial membrane potential

Defects in mitochondrial energy metabolism due to respiratory chain disorders lead to a decrease in mitochondrial membrane potential (ΔΨm) and induce apoptosis. Since coenzyme Q10 (CoQ10) plays a dual role as an antioxidant and bioenergetic agent in the respiratory chain, it has attracted increasing...

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Veröffentlicht in:BioFactors (Oxford) 2003, Vol.18 (1-4), p.65-72
Hauptverfasser: Menke, T., Gille, G., Reber, F., Janetzky, B., Andler, W., Funk, R. H. W., Reichmann, H.
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Sprache:eng
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Zusammenfassung:Defects in mitochondrial energy metabolism due to respiratory chain disorders lead to a decrease in mitochondrial membrane potential (ΔΨm) and induce apoptosis. Since coenzyme Q10 (CoQ10) 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 CoQ10 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 ΔΨm. The relative changes in fluorescence intensity after incubation with rotenone for 15 minutes were calculated. Pre‐treatment with CoQ10 (10 or 100 μM) for 48h led to a significant reduction of rotenone‐induced loss of ΔΨm. These results suggest, that cytoprotection by CoQ10 may be mediated by raising cellular resistance against the initiating steps of apoptosis, namely the decrease of ΔΨm. Whether these data may provide new directions for the development of neuroprotective strategies has to be investigated in future studies.
ISSN:0951-6433
1872-8081
DOI:10.1002/biof.5520180208