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The lower catalase activity is due to nitration and oxidation, which identifies oxidative inactivation as the mechanism of activity loss in vivo [53]

Note also the increase in production of antioxidant rejuvenators like superoxide dismutase and glutathione

Specifically, through the FSP1-CoQ10-NAD (P)H pathway, it adeptly counters CoQ10-mediated ferroptosis, operating in a manner that runs parallel to the well-established GPX4 pathway [53]

This makes S-Acetyl-L-glutathione a promising candidate for conditions involving impaired GSH synthesis, offering a significant advantage in medical research and treatment strategies focusing on oxidative stress and related disorders

These factors may partially explain the paradoxical increase in DCF oxidation observed in the frontal cortex of CT+LipRSV animals