Erythrocyte Membrane Fluidity Alterations in Sudden Sensorineural Hearing Loss Patients: The Role of Oxidative Stress
Erythrocyte Membrane Fluidity Alterations in Sudden Sensorineural Hearing Loss Patients: The Role of Oxidative Stress
复制标题
DOI：
10.1160/th17-05-0356
复制
发表时间：
2017-12-01
影响因子：
6.7
通讯作者：
Fiorillo, Claudia
中科院分区：
文献类型：
--
作者：
Becatti, Matteo;Marcucci, Rossella;Fiorillo, Claudia
简介 突发性感音神经性听力损失 (SSNHL) 涉及一种急性、不明原因的听力损失，几乎总是单侧的，发生时间少于 72 小时。 SSNHL 发病机制尚未完全清楚。耳蜗血管闭塞已被认为是听力损伤的潜在机制，并且耳蜗缺血与耳蜗微血管的改变有关。此外，一些研究人员将注意力集中在流变学改变和血液高粘度上。红细胞变形能力在决定血液粘度方面起着关键作用，对耳蜗灌注至关重要。研究表明，氧化应激引起的红细胞膜流动性改变与心血管疾病的进展有关。 方法 为了确定 SSNHL 患者的红细胞是否表现出氧化应激迹象，以及这种情况是否会改变这些患者的血液流变学特征，我们分析了 35 名 SSNHL 患者和 35 名年龄和性别相匹配的健康受试者的血液流变学特征和红细胞氧化应激。荧光各向异性用于评估红细胞膜的流动性。结果我们的结果显示，SSNHL 中红细胞膜的结构和功能改变具有显着的参与，以及膜脂过氧化和细胞内活性氧 (ROS) 产生水平升高。此外，红细胞源性ROS和红细胞脂质过氧化与全血粘度和红细胞变形能力呈正相关。此外，体外实验证明ROS在红细胞膜流动性中发挥关键作用。结论这些发现表明红细胞氧化应激在SSNHL的发病机制中发挥着关键作用，并为新的治疗干预措施铺平了道路。
Introduction Sudden sensorineural hearing loss (SSNHL) involves an acute unexplained hearing loss, nearly always unilateral, that occurs over less than a 72-hour period. SSNHL pathogenesis is not yet fully understood. Cochlear vascular occlusion has been proposed as a potential mechanism of hearing damage and cochlear ischaemia has been related to alterations of cochlear microvessels. In addition, some researchers have focused their attention on the rheological alterations and blood hyperviscosity. Erythrocyte deformability plays a key role in determining blood viscosity, and it is critical to cochlear perfusion. It has been shown that oxidative stress-induced erythrocyte membrane fluidity alterations are linked to the progression of cardiovascular diseases.Methods To determine whether erythrocytes from SSNHL patients show signs of oxidative stress, and whether this condition can modify the haemorheologic profile in these patients, we analysed haemorheologic profile and erythrocyte oxidative stress in 35 SSNHL patients and 35 healthy subjects, matched for age and sex. Fluorescence anisotropy was used to evaluate the fluidity of erythrocyte membranes.Results Our results show a significant structural and functional involvement of erythrocyte membrane alterations in SSNHL, as well as elevated levels of membrane lipid peroxidation and intracellular reactive oxygen species (ROS) production. In addition, erythrocyte-derived ROS and erythrocyte lipid peroxidation positively correlated with whole blood viscosity and erythrocyte deformability. Moreover, in vitro experiments demonstrated that ROS display a key role in erythrocyte membrane fluidity.Conclusion These findings indicate that erythrocyte oxidative stress plays a key role in the pathogenesis of SSNHL and pave the way to new therapeutic interventions.