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Elevations of the intermediate S-Adenosylhomocysteine (SAH) lead to a feed back inhibition of the function of the cycle and also a reduction in the transsulfuration pathway leading to a deficiency in the production of cysteine and glutathione (James)

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This inhibition may result in the up-regulation of other isoforms, counteracting the intended therapeutic effects and complicating treatment outcomes

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62,109 These examples demonstrate that LPO and ferroptosis may be biologically irrelevant for APAP hepatotoxicity under normal conditions because endogenous defense mechanisms (such as the lipid-soluble antioxidant vitamin E and the iron chelator ferritin) effectively prevent excessive LPO