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The research focused on oxidative stress models induced by prooxidant compounds and evaluated the capacity of GHK to support radical-associated signaling pathways

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, the covalent binding of NAPQI to the thiol groups of critical cellular proteins (following glutathione depletion), oxidative stress induced directly by NAPQI or via coproduction of reactive oxygen species (superoxide radical and hydrogen peroxide) through redox cycling between the paracetamol semiiminoquinone radical and NAPQI) (1, 2), and vice versa, these processes counteraction may be involved in BPC 157 beneficial effects