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Due to the activation of metabolic pathways related to OS protection, inflammation, regulation of excitotoxicity and preservation of neuronal functions, PTER is a protective factor against neurodegenerative diseases (Poulose et al., 2015)

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Indeed, it was observed that xanthine dehydrogenase was converted to the oxidase in the liver after APAP overdose, and mice pretreated with the xanthine oxidase inhibitor allopurinol attenuated the oxidative stress and liver injury [48], [49], arguing for a potential involvement of xanthine oxidase in the pathophysiology of APAP hepatotoxicity