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The research to date shows a relatively favorable safety profile in limited human studies, but long-term safety and large-scale clinical trials are lacking

[DOI] [PMC free article] [PubMed] [Google Scholar] Kadoglou, N

Specifically, p66Shc can generate ROS through the oxidation of cytochrome c by utilizing the reducing equivalents of the mitochondrial ETC, playing a crucial role in carcinogenesis and aging [44]

Without adequate glutathione to neutralize ROS, superoxide radicals collide with and damage the mitochondria's inner membrane (specifically a lipid called cardiolipin) and the mitochondrial DNA itself