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Biochem Biophys Res Commun. 1998 Aug 19;249(2):542-5.

Increase in intracellular hydrogen peroxide and upregulation of a nuclear respiratory gene evoked by impairment of mitochondrial electron transfer in human cells.

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Laboratory of Molecular Biology and Biotechnology, Fukui Prefectural University, 4-1-1 Kenjojima, Matsuoka-cho, Yoshida-gun, Fukui, 9101195, Japan.


We have investigated an interorganelle communication pathway between the nucleus and mitochondria. We loaded a stress specific to mitochondria of human fibroblast cells by antimycin A (AA), an inhibitor of the mitochondrial cytochrome bc1 complex. AA inhibited cellular respiration in a dose-dependent manner. When the respiratory capacity was reduced to 50-70% of the original one, mRNA levels of cytochrome c1 as well as cytochrome b increased at 24 h after AA treatment, resulting in maintenance of the cell viability. In contrast, the cells retaining less than 40% of the original capacity showed no increase in either mRNA level and were targeted for death. Intracellular H2O2 level monitored by the fluorescence of dichlorofluorescein increased within 3 h in both the cases, although this increase was higher in the cells where the mRNA levels increased. An antioxidant N-acetylcysteine repressed the increases of not only H2O2 but also cytochrome c1 mRNA levels. These results suggest that the cells can respond to a limited impairment of electron transfer by promoting expression of nuclear and mitochondrial genes, probably through an H2O2-dependent signaling pathway.

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