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Due to the fact that ACTL6A did not regulate NRF2, we could reach the conclusion that ACTL6A functions in conjunction with NRF2 to regulate GCLC expression at the transcriptional level

It may be useful when precursor availability is limiting, but its effect depends on the bodys ability to synthesize glutathione

In more severe patients in whom airway GSH reserves are depleted, this may result in a detrimental cascade with a shift toward GSSG formation and oxidation of thioredoxins, leading to post-translational protein modifications through oxidation of protein-methionine residues and formation of protein disulfides from glutathionylation or other mechanisms (Fig

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