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Additionally, to avoid homocysteine accumulation, which is potentially cytotoxic, SAM stimulates homocysteine catabolism by increasing CBS activity (Fig

Toxicity of DCVC to kidney cells has been associated with (1) covalent modification of macromolecules, (2) depletion of nonprotein thiols (presumably mostly GSH), (3) lipid peroxidation (Beuter et al., 1989, Chen et al., 1990, Groves et al., 1991), and (4) carbonylation of susceptible proteins (Fan et al., 2014)

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