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A differential protection was demonstrated in a study, in which an elevated level of GSH decreased the frequency of radiation-induced deletions but increased the frequency of aberrations of the chromosome exchange type [38]

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This destructive oxidative process is considered a central mechanism of ferroptosis, iron overload accelerates the production of ROS via the Fenton reaction, which in turn amplifies lipid peroxidation, compromising the cell membrane and leading to ferroptosis

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