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Through activation of the SIRT1–PGC-1α axis and related pathways, these agents are likely to influence mitochondrial–ER Ca 2+ communication, β-oxidation in cooperation with peroxisomes, and the cellular capacity to cope with redox stress

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GSH scavenges excess free radicals in the body by oxidizing the sulfhydryl group (-SH) of GSH to produce oxidized GSH (GSSG) through the catalysis of GSH-Px, which consumes H2O2 to produce water (13)