Role of Oxidative Stress in the Neurocognitive Dysfunction of Obstructive Sleep Apnea Syndrome

Figure 1

Schematic demonstration of the important role played by oxidative stress in the development of cognitive dysfunction in OSAS patients: chronic intermittent hypoxia (CIH) resulting from OSAS causes dysfunction of mitochondria and endoplasmic reticulum and overactivation of Nox, iNOS, PAF, and COX-2. All the above induce overproduction of ROS and RNS, as well as attenuated antioxidant capacity, and consequently contribute to imbalance of oxidation-antioxidation and a state of oxidative stress, which result in protein, lipid, and DNA peroxidation damage, and a series of inflammatory responses. Meanwhile, ER stress could upregulate CHOP expression, which could exacerbate production of ROS further. Substantial inflammatory cytokines and peroxidation lead to necrosis and apoptosis of nerve cell, which eventually results in gradual neurocognitive dysfunction of OSA patients. PAF: platelet-activating factor; Nox: NADPH oxidase; ERO1L: endoplasmic reticulum oxidoreductin-1-like; COX-2: cyclooxygenase-2; VEGF: vascular endothelial growth factor; HO-1: heme oxygenase-1; ER: endoplasmic reticulum; IGF: insulin-like growth factor; iNOS: inducible nitric oxide synthase; CHOP: C/EBP-homologous protein; PR: protective factor.