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The latter observation also indicates that cell death caused by prolonged ER stress is not linked to H 2 O 2 production (Haynes et al , 2004), as HGT1 ire1 cells did not generate H 2 O 2 when exposed to GSH, but were much more sensitive to its toxicity

The copper center's accessibility to redox cycling enables GHK-Cu to modulate oxidative stress responses in tissues experiencing inflammation or ischemic conditions

However, this is currently determined on a case-by-case basis

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This paper describes how mitochondria produce ROS

Dev Comp Immunol (2018) 81:16779