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These results indicate that the metabolic shift from glucose substrate-dependent pathway to FAO or glutaminolysis was induced under the exposure to H 2 O 2 regarding the mitochondrial damage, whereas the promotion was not enough to compensate respiratory capacity decrease and was rather a marker of H 2 O 2 -exposed stress, and this shift was held to the nearly normal state with PQQ pretreatment protection

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Detailed individual longitudinal data are provided in Supplementary Tables 1 and 2