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does oxidation state of glutathione depends on cysteine residue Oxidation/regeneration a typical reactive of a Selenocysteine
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The mechanism involves reductions in the SAM-dependent methylation cycle and selective suppression of mTORC1 signaling, which collectively reduce anabolic activity in favor of catabolic processes like autophagy and mitophagy—crucial cellular renewal processes that become dysregulated with age.[7] The challenge, of course, is that complete methionine restriction is neither practical nor entirely beneficial for most individuals, as methionine is an essential amino acid required for protein synthesis and numerous other functions
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