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Where NAD+ behaves like a battery that powers cellular reactions, glutathione behaves like a shield that absorbs and clears damage

Mitochondrial impairment serves as a key driver of ferroptosis by elevating reactive oxygen species and promoting the iron-mediated Fenton process, wherein ferrous ions facilitate the transformation of hydrogen peroxide into highly reactive hydroxyl radicals, thereby exacerbating oxidative damage and triggering ferroptotic cell death (121, 125, 126)

Similarly, in the context of diabetes, GPx1 / ApoE / mice had augmented atherosclerosis with increased macrophage infiltration, increased nitrotyrosine levels, and increased expression of proinflammatory and profibrotic markers in mouse aorta [79]

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