Wali S O, Bahammam A S, Massaeli H, Pierce G N, Iliskovic N, Singal P K, Kryger M H
Sleep Disorders Center, St. Boniface General Hospital, Winnipeg, Manitoba.
Sleep. 1998 May 1;21(3):290-6.
Cardiovascular diseases are more common in patients with obstructive sleep apnea (OSA) than in the general population. We hypothesized that severe hypoxemia during sleep in these patients may cause an imbalance between reactive oxygen species and the antioxidant reserve that is important for the detoxification of these molecules. We tested the hypothesis that low-density lipoproteins (LDL) in hypoxic OSA patients may be more susceptible to oxidative stress than LDL of nonhypoxic OSA patients and normal controls. Fifteen OSA patients were included in this study, six with severe hypoxia (hypoxic group) who spent more than 10 minutes during sleep with SaO2 < 85% (mean 96 minutes), and nine OSA patients (nonhypoxic group) who spent less than 10 minutes during sleep with SaO2 < 85% (mean 1.1 minutes). Six healthy nonsmoking males of the same age group were included as a control group. The susceptibility of each individual's LDL to oxidative stress was examined after free-radical challenge in vitro by assessing changes in levels of conjugated dienes. The LDL in OSA patients with severe hypoxia was not more susceptible to oxidative stress compared to the LDL of nonhypoxic OSA patients and normal controls. After 6 hours of exposure to an oxidative agent, the changes in the mean conjugated diene were not different among the three groups (p = 0.75). The time required to reach 50% of maximal absorbance was also not different, p = 0.199. Glutathione peroxidase and catalase activities in red blood cells in the hypoxic and nonhypoxic patient groups were not significantly different. One night of CPAP therapy in each patient group did not significantly change the level of the antioxidant enzymes. Our results did not show any difference in the susceptibility to oxidative stress between hypoxic and nonhypoxic OSA patients and normal controls.
心血管疾病在阻塞性睡眠呼吸暂停（OSA）患者中比在普通人群中更为常见。我们推测，这些患者睡眠期间的严重低氧血症可能会导致活性氧与抗氧化储备之间的失衡，而这种失衡对于这些分子的解毒至关重要。我们检验了这样一个假设：低氧OSA患者的低密度脂蛋白（LDL）可能比非低氧OSA患者和正常对照的LDL更容易受到氧化应激的影响。本研究纳入了15例OSA患者，其中6例有严重低氧（低氧组），其睡眠期间血氧饱和度（SaO2）<85%的时间超过10分钟（平均96分钟），另外9例OSA患者（非低氧组）睡眠期间SaO2<85%的时间少于10分钟（平均1.1分钟）。纳入6名同年龄组健康非吸烟男性作为对照组。通过评估共轭二烯水平的变化，在体外自由基攻击后检测每个人的LDL对氧化应激的敏感性。与非低氧OSA患者和正常对照的LDL相比，严重低氧OSA患者的LDL对氧化应激并不更敏感。暴露于氧化剂6小时后，三组的平均共轭二烯变化无差异（p=0.75）。达到最大吸光度50%所需的时间也无差异，p=0.199。低氧和非低氧患者组红细胞中的谷胱甘肽过氧化物酶和过氧化氢酶活性无显著差异。每个患者组进行一晚的持续气道正压通气（CPAP）治疗并未显著改变抗氧化酶的水平。我们的结果显示，低氧和非低氧OSA患者与正常对照之间在氧化应激易感性方面没有任何差异。
