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They also found that 8-OHdG is significantly correlated with AHI, oxygen desaturation index (ODI), and duration of oxygen saturation EGFR inhibitor Other studies analyzed nitrite/nitrate levels as a measure of circulating NO levels and reported reductions in OSA subjects [91, 93]. However, CPAP treatment of OSA patients restores circulating NO levels and the levels of its substrate L-arginine [94] as well as FMD [95]. Suggested mechanisms for endothelial dysfunction include (1) interaction between NO and superoxide anion leading to increased formation of a highly Dasatinib in vitro unstable RNS peroxynitrite, (2) decreased expression and/or uncoupling of endothelial nitric oxide synthase (eNOS), and (3) increased levels of endogenous eNOS inhibitors such as ADMA [1]. The large volume of distribution and short half-life of peroxynitrite could account for similar levels of nitrotyrosine in OSA and healthy subjects [96, 97]. Microcirculatory endothelial cells (EC) from OSA patients have increased formation of peroxynitrite [98]. In cultured endothelial cells from OSA patients, Jelic and le Jemtel reported a significant decrease in both total and phosphorylated eNOS levels, which were restored by CPAP treatment [99]. Moreover, Tanaka et al. suggested that eNOS activation is regulated by redox status and that Oxygenase increased oxidative stress reduced eNOS activity by suppressing its phosphorylation [100]. Nonetheless, the expression and activity of eNOS have been reported to be upregulated, [101, 102] downregulated, [103, 104], or unchanged [105] in various experimental models of hypoxia and repetitive hypoxia/reoxygenation. Interestingly, Kaczmarek et al. showed that cultured endothelial cells originating from distinct vascular beds in OSA patients and mice responded differently to IH stress in terms of eNOS expression [106]. Another cause of endothelial impairment is the eNOS uncoupling. For production of NO to occur, five cofactor groups (FAD, FMN, heme, Ca2+-calmodulin, and BH4) are needed to incorporate oxygen in L-arginine. A lack of any of these cofactors leads to production of superoxide anion instead of NO and adds insult to injury [18].