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Coenzyme Q 10 reduces the toxicity of rotenone in neuronal cultures by preserving the mitochondrial membrane potential
Author(s) -
Menke T.,
Gille G.,
Reber F.,
Janetzky B.,
Andler W.,
Funk R. H. W.,
Reichmann H.
Publication year - 2003
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520180208
Subject(s) - rotenone , biology , coenzyme q10 , mitochondrion , bioenergetics , mitochondrial respiratory chain , membrane potential , apoptosis , microbiology and biotechnology , respiratory chain , neuroprotection , coenzyme q – cytochrome c reductase , biochemistry , pharmacology , cytochrome c
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.