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ROS can oxidize cysteine residues allowing formation of disulfide bridges with one another or with GSH leading to S-glutathionylation

In the context of ovarian aging, impaired mTORC1 and AMPK activity or localization disrupts autophagy regulation, delays mitochondrial turnover, and diminishes metabolic adaptability, exacerbating the imbalance between energy homeostasis and mitochondrial quality control [230, 294]

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