Aladag I, Eyibilen A, Güven M, Atiş O, Erkorkmaz Ü
Department of ORL, Faculty of Medicine, Gaziosmanpasa University, Tokat, Turkey.
J Laryngol Otol. 2009 Sep;123(9):957-63. doi: 10.1017/S0022215109004502. Epub 2009 Feb 9.
Although many clinical investigations have found a relationship between hearing loss and diabetes mellitus, the pathophysiology of this effect remains controversial. To date, the mechanisms of hearing loss in diabetic patients have been explained in terms of microangiopathy, neuropathy and encephalopathy. However, many reports indicate that some diabetic complications are associated with oxidative stress related to the diabetes itself. In the present study, we hypothesised that oxidative stress may be a cause of hearing loss in diabetic patients.
The study group comprised non-insulin dependent diabetic patients with no signs of microangiopathy or peripheral neuropathy. The control group comprised sex-, age- and body weight matched, non-diabetic subjects. Auditory function was evaluated using pure tone audiometry and tympanometry. Subjects with normal hearing and sensorineural hearing loss were included in the study, whereas subjects with conductive hearing loss were excluded. Both the study group (n = 63) and the control group (n = 37) were divided into subgroups based on the presence and absence of hearing loss. Oxidative stress was evaluated by measuring serum indicators of protein oxidation and lipid peroxidation, serum levels of nitric oxide and various non-enzymatic antioxidants, and the activity of various enzymatic antioxidants.
The non-insulin dependent diabetic patients had significantly higher serum levels of protein oxidation products, nitric oxide, enzymatic antioxidant activity (i.e. glutathione peroxidase and superoxide dismutase), compared with the control group (p < 0.05). When we compared the groups in relation to the presence of hearing loss, the nitric oxide level was significantly increased in the diabetic group with good hearing, compared with diabetic patients with hearing loss (p = 0.014). In the diabetic group, a clear, negative correlation was observed between serum levels of nitric oxide and vitamins C and E, and hearing impairment (r = -0.395, r = -0.318, r = -0.500, respectively). There was also a positive correlation between serum vitamin C concentrations and hearing levels in the control group (r = 0.417).
These results suggest that oxidative stress may play an important role in hearing impairment in diabetic patients. In this process, increased protein oxidation appears to be more important than lipid peroxidation. Nitric oxide may have a protective effect on hearing, as may some nonenzymatic antioxidants such as vitamin C and E.
尽管许多临床研究发现听力损失与糖尿病之间存在关联，但其作用的病理生理学仍存在争议。迄今为止，糖尿病患者听力损失的机制已从微血管病变、神经病变和脑病方面进行了解释。然而，许多报告表明，一些糖尿病并发症与糖尿病本身相关的氧化应激有关。在本研究中，我们假设氧化应激可能是糖尿病患者听力损失的一个原因。
研究组由无微血管病变或周围神经病变迹象的非胰岛素依赖型糖尿病患者组成。对照组由性别、年龄和体重匹配的非糖尿病受试者组成。使用纯音听力计和鼓室图评估听觉功能。听力正常和感音神经性听力损失的受试者被纳入研究，而传导性听力损失的受试者被排除。研究组（n = 63）和对照组（n = 37）均根据是否存在听力损失分为亚组。通过测量蛋白质氧化和脂质过氧化的血清指标、血清一氧化氮水平和各种非酶抗氧化剂以及各种酶抗氧化剂的活性来评估氧化应激。
与对照组相比，非胰岛素依赖型糖尿病患者的血清蛋白质氧化产物、一氧化氮、酶抗氧化活性（即谷胱甘肽过氧化物酶和超氧化物歧化酶）水平显著更高（p < 0.05）。当我们比较有听力损失和无听力损失的组时，听力良好的糖尿病组的一氧化氮水平与有听力损失的糖尿病患者相比显著升高（p = 0.014）。在糖尿病组中，血清一氧化氮水平与维生素C和E以及听力障碍之间观察到明显的负相关（分别为r = -
0.395，r = - 0.318，r = - 0.500）。对照组中血清维生素C浓度与听力水平之间也存在正相关（r = 0.417）。
这些结果表明氧化应激可能在糖尿病患者的听力障碍中起重要作用。在此过程中，蛋白质氧化增加似乎比脂质过氧化更重要。一氧化氮可能对听力有保护作用，一些非酶抗氧化剂如维生素C和E也可能有此作用。
