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Patients with insufficient glutathione stores (e.g., alcoholics and acquired immunodeficiency syndrome patients) and patients with induced cytochrome P-450 enzymatic activity (e.g., alcoholics and those taking concurrent anticonvulsant or antituberculous medications) may be at greater risk for developing acetaminophen-induced hepatotoxicity following overdose (as opposed to therapeutic dosing described earlier)

The current evidence base points to several overlapping molecular pathways operating in parallel: VEGFR2/Akt/eNOS Angiogenic Signalling A primary mechanistic axis involves upregulation of vascular endothelial growth factor receptor 2 (VEGFR2), leading to activation of the Akt/eNOS (endothelial nitric oxide synthase) downstream pathway

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Glutathione analogue sorbents selectively bind glutathione S-transferase isoenzymes [PMID: 8503872] Laboratory literature summary: Glutathione analogue sorbents selectively bind glutathione S-transferase isoenzymes