Increasing evidence has demonstrated that ROS via various pathways triggers systemic inflammation and endothelial cell dysfunction through several mechanisms, such as mitochondrial dysfunction and uncoupling, raised FAO, up-regulation of NOX activity, impaired antioxidant capacity, and cardiac metabolic memory
The effect of mitochondrial oxidative stress on POCD Neurons are particularly susceptible to ROS and reactive nitrogen species (RNS) damage owing to their high metabolic rate, fatty acids prone to peroxidation, abundant transition metals that catalyze ROS formation, and low antioxidant levels [154, 155]
Despite that mitochondria are exposed to the generation of oxidant species, the existence of an efficient antioxidant defense system, of which mGSH is a critical component, prevents or repairs oxidative damage generated during normal aerobic metabolism (Mari et al., 2013)
The ACCEPT study: ustekinumab versus etanercept in moderate-to-severe psoriasis patients
Verghese, J., Abrams, J., Wang, Y
The flexibility of proanthocyanidin biosynthesis in plants
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