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Hepatic effects that are considered adverse include death, abnormal clinical chemistry parameters, obvious functional organ impairment, DNA and mitochondrial alteration, glutathione depletion, hepatocyte necrosis, enhanced replicative DNA synthesis, generation of reactive oxygen species, and increased peroxisome proliferation (in rodents) (Williams and Iatropoulos 2002)

One potential mechanism is that H 2 S 2 and H 2 S 3 produced by 3MST readily react with free cysteine and GSH to produce Cys-SSH and GSSH, and react with cysteine residues of proteins to generate persulfurated proteins (Figs 2 and 8a)

109 Thus, a ferroptosis inhibitor alone cannot be used to support the conclusion of ferroptosis

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