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Specifically, APOC1 mitigates iron-mediated cytotoxicity by upregulating the NRF2/HO-1 axis

At this point, the enzyme L-gulono-1, 4-lactone dehydrogenase catalyze the conversion of L-gulose into L-gulono-1, 4-lactone which is then finally converted to AsA (Smirnoff et al., 2001)

Several data are available indicating that the overproduction of NO and iNOS is responsible for inflammatory myopathies, muscle wasting, cachexia, muscle dystrophy and injuries [95,96,97]

Retrospective detection of sulfur mustard exposure by mass spectrometric analysis of adducts to albumin and hemoglobin: an in vivo study

However, probably, a large part of these effects is due to its main antifibrotic effect