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- W2025100814 abstract "Malfunction of mitochondrial complex I caused by nuclear gene mutations causes early-onset neurodegenerative diseases. Previous work using cultured fibroblasts of complex-I-deficient patients revealed elevated levels of reactive oxygen species (ROS) and reductions in both total Ca2+ content of the endoplasmic reticulum (ERCa) and bradykinin(Bk)-induced increases in cytosolic and mitochondrial free Ca2+ ([Ca2+]C; [Ca2+]M) and ATP ([ATP]C; [ATP]M) concentration. Here, we determined the mitochondrial membrane potential (Δψ) in patient skin fibroblasts and show significant correlations with cellular ROS levels and ERCa, i.e., the less negative Δψ, the higher these levels and the lower ERCa. Treatment with 6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox) normalized Δψ and Bk-induced increases in [Ca2+]M and [ATP]M. These effects were accompanied by an increase in ERCa and Bk-induced increase in [Ca2+]C. Together, these results provide evidence for an integral role of increased ROS levels in complex I deficiency and point to the potential therapeutic value of antioxidant treatment." @default.
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- W2025100814 date "2009-03-03" @default.
- W2025100814 modified "2023-09-23" @default.
- W2025100814 title "The antioxidant Trolox restores mitochondrial membrane potential and Ca2+-stimulated ATP production in human complex I deficiency" @default.
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- W2025100814 doi "https://doi.org/10.1007/s00109-009-0452-5" @default.
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