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John Buse, Director of the Diabetes Care Center at the University of North Carolina and a principal investigator in GLP-1 outcomes trials, has noted in published commentary that "the antioxidant milieu in type 2 diabetes is genuinely impaired, but whether exogenous supplementation corrects the underlying defect or simply raises circulating levels without tissue impact remains unresolved." [9] That distinction shapes the practical advice: correcting a documented deficiency (measured low whole-blood glutathione in a patient with poorly controlled diabetes) is a different clinical decision from empirically adding glutathione to a well-controlled patient already benefiting from dulaglutide's own oxidative-stress effects

Bateman DN, Dear JW, Thanacoody HKR, et al

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NEDD4L decreased the viability of KGN cells and increased the levels of MDA and ROS

In addition, AsGGT2 may function in the breakdown of glutathione S -conjugates in the vacuole in a similar manner as Arabidopsis AtGGT4 ( Figures 7A,C ), suggesting that AsGGT1 and AsGGT3 have no apparent signal sequence for targeting to the cellular organelles in their N-terminal peptides