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Lifelong voluntary aerobic exercise protocols have been shown to largely prevent age- and western diet-induced vascular endothelial dysfunction and arterial stiffening throughout the lifespan in mice, and this protective effect appears to be mediated by the mitigation of mitochondrial-derived oxidative stress and inflammation [116]

This paper describes how mitochondria produce ROS

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

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