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4.2 Healthy-tissue antioxidant shielding and the antioxidant paradox Many standard therapies cause systemic oxidative injury (e.g., cardiotoxicity from anthracyclines), prompting antioxidant shielding strategies ( 4.3 Safety implications of dual redox programming The same formulation feature that is attractive for tumor sensitization, namely, prolonged intracellular residence or stimulus-linked release, can magnify liability when exposure occurs in non-target tissues

To further test the crucial role of GSH in the acute phase of colitis, we analyzed the effect of NAC, a GSH precursor, on mucosal GSH levels in relation with the TNBS-induced colitis

Alongside NLRP3 activation, circulating cell-free mitochondrial DNA (ccf-mtDNA) release was also significantly reduced by similar levels following MCC950 and BFE treatment, indicating that both interventions mitigated mitochondrial stress in BD and CT COs (Fig

Changes in the levels of both thiols led to the activation of defense responses in nodules