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00?��mol/L with LVH and 1.88?��mol/L without LVH) and were correlated with left ventricular mass (r = 0.26, P Selleckchem Dasatinib that OSA is a cardiovascular risk factor and that ADMA has the potential to exacerbate cardiovascular disease. But does OSA influence ADMA levels? Many studies show increases in ADMA levels in OSA patients; Barcel�� et al. measured plasma ADMA in 23 OSA patients and found it to be significantly higher (1.17?��mol/L) compared to control (0.87?��mol/L, P Oxygenase one or more unpaired electrons in their molecular or atomic orbitals. At low concentrations, these species play an important role in cellular signaling, specifically in defense against infectious agents and induction of mitogenic response [64]. Overproduction of ROS/RNS or deficiency of enzymatic and nonenzymatic antioxidants can lead to oxidative and nitrosative stress. Consequently, oxidative stress leads to an imbalance between prooxidant/antioxidant reactions related to oxygen metabolism. ROS can oxidize lipids, protein, or DNA, so inhibiting their function and disturbing many cellular processes [64]. As a result, oxidative stress has been implicated in many human diseases (e.g., cardiovascular diseases, cognitive impairment, Gefitinib purchase and diabetes) [65�C67] as well as in the aging process [68]. Intermittent hypoxia (IH), a hallmark of OSA, is characterized by repeated episodes of hypoxia interspersed with episodes of normoxia, potentially similar to the ischemia/reperfusion (I/R) that results in injury due to the burst of ROS production during the reperfusion period [69]. It is well established that oxidative stress is a major consequence of I/R injuries [70]. Similarly, cycles of IH in OSA patients promote ROS generation and oxidative stress through comparable pathways and various sources, as described in the next section. 5. Sources of ROS/RNS in OSA During aerobic respiration, approximately 3�C5% of the oxygen consumed by the mitochondria is converted to superoxide anion, a major form of ROS.