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Collectively, these results indicate that iodide may increase intracellular ferrous iron, leading to the accumulation of ROS and increased ferroptosis

The magnitude and severity of age-associated mitochondrial impairment in these organs becomes clear via the molecular data which shows that old mice had abnormalities in mitochondrial biogenesis and energy metabolism (PGC1), and impaired mitochondrial -oxidation of fatty-acids (PPAR), ATP synthesis (ATP5A), and mitophagy (PINK1)

They state that it offers a strong possibility for transducing oxidative information from intracellular oxidants via the GSH redox buffer to individual proteins containing regulatory thiols

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