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This auto-oxidation process generates toxic reactive oxygen species (ROS), quinones, and free radicals that damage intracellular organelles, deplete cellular glutathione, and ultimately trigger apoptotic cell death (Lohr et al., 2014

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Interestingly, BSO treatment did not affect SLC25A39 mRNA levels (Extended Data Fig 1c), but could induce SLC25A39 protein accumulation when an SLC25A39 cDNA lacking UTR elements was expressed ectopically under a viral promoter (Extended Data Fig 1d), thereby suggesting regulation at the post-translational level