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In both cases, despite the use of different research methodologies, no drastic changes were noted in the functionality of these structures even at high concentrations of DMSO

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However, when production overwhelms the capacity of these containment and buffering systems (e.g., PRX saturation), the same species induce oxidative distress, leading to irreversible macromolecular damage, metabolic dysfunction, and pathological inflammation

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Thus, the oxidative stress-activated import to mitochondria of the GSTA4-4 isoform exhibiting high specificity towards 4-HNEs protects mitochondria from oxidative stress and modulates signal pathways that are affected by 4-hydroxynonenals [127-129]