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• W2163670131 abstract "Abstract Activity of the oxidative phosphorylation (OXPHOS) is decreased in patients and mice with non-alcoholic steatohepatitis. Nitro-oxidative stress seems to be involved in its pathogenesis. The aim of this study was to determine whether fatty acids are implicated in the pathogenesis of this mitochondrial defect. In HepG2 cells, we analyzed the effect of saturated (palmitic and stearic acids) and monounsaturated (oleic acid) fatty acids on the OXPHOS activity, OXPHOS complexes and their subunits, gene expression and half-life of OXPHOS complexes, nitro-oxidative stress, NADPH oxidase gene expression and activity. We also studied the effects of inhibiting or silencing NADPH oxidase on the palmitic acid-induced nitro-oxidative stress and OXPHOS inhibition. Exposure of cultured HepG2 to saturated fatty acids resulted in a significant decrease in the OXPHOS activity. This effect was prevented in the presence of a mimic of manganese superoxide dismutase. Palmitic acid reduced fully assembled OXPHOS complexes and the amount of complex subunits. This reduction was due mainly to an accelerated degradation of these subunits, which was associated with a 3-tyrosine nitration of mitochondrial proteins. Pretreatment of cells with uric acid, an antiperoxynitrite agent, prevented protein degradation induced by palmitic acid. A reduced gene expression also contributed to decrease mitochondrial DNA (mtDNA)-encoded subunits. Saturated fatty acids induced oxidative stress and caused mtDNA oxidative damage. This effect was prevented by inhibiting NADPH oxidase. These acids activated NADPH oxidase gene expression and increased NADPH oxidase activity. Silencing this oxidase abrogated totally the inhibitory effect of palmitic acid on OXPHOS complex activity. We conclude that saturated fatty acids caused nitro-oxidative stress, reduced OXPHOS complex half-life and activity, and decreased gene expression of mtDNA-encoded subunits. These effects were mediated by activation of NADPH oxidase. That is, these acids reproduced mitochondrial dysfunction found in human and animal with non-alcoholic steatohepatitis." @default.
• W2163670131 created "2016-06-24" @default.
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• W2163670131 date "2014-01-01" @default.
• W2163670131 modified "2023-10-18" @default.
• W2163670131 title "<i>In vitro</i> treatment of HepG2 cells with saturated fatty acids reproduces mitochondrial dysfunction found in non-alcoholic steatohepatitis" @default.
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• W2163670131 doi "https://doi.org/10.1242/dmm.018234" @default.
• W2163670131 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4314783" @default.
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• W2163670131 hasPublicationYear "2014" @default.
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