SLEEP APNEA AND ITS ROLE IN OXIDATIVE STRESS AND INFLAMMATION

Inflammation has been linked with sleep apnea. Sleep apnea is a common comorbidity associated with Parkinson’s disease. Furthermore, both sleep apnea and Parkinson’s disease have been linked with inflammation. A possible mechanism underlying increased inflammation in these disorders is oxidative stress, a hallmark of many neurodegenerative disorders. To examine the role of oxidative stress on inflammation, we used chronic intermittent hypoxia (CIH), an established model for the hypoxemia associated with sleep apnea. CIH consists of recurring events of low oxygen followed by reoxygenation. We hypothesize that CIH causes oxidative stress, which induces inflammation. To test this hypothesis, plasma from adult male rats subjected to 7 days of CIH (3 minute periods of hypoxia (10% oxygen) and 3 minute periods of normoxia (21% oxygen) for 8 hours per day) or normoxia (room air) was tested for AOPP, an indicator of oxidative stress, and circulating inflammatory markers (IL-10, IL-4, IL-6). Our results showed that CIH significantly increased circulating oxidative stress. These results were then correlated with inflammatory markers in the plasma and statistically analyzed for positive associations. IL-6 was found to be significantly increased in CIH, although not associated with oxidative stress. However, CIH did increase IL-4 and IL-10, and these effects were positively associated with circulating oxidative stress. Inflammatory markers IL-4 and IL-6 are generally associated with macrophage-mediated inflammation. Therefore it is possible that CIH-induced oxidative stress underlies macrophage mediated inflammation. These findings suggest that sleep apnea increases oxidative stress and consequently inflammation.