Department of Speech, Language, and Hearing Sciences, University of Florida, Box 100174, Gainesville, FL 32610, USA.
Transl Res. 2011 Jul;158(1):38-53. doi: 10.1016/j.trsl.2011.02.006. Epub 2011 Mar 21.
Oxidative stress has been implicated broadly as a cause of cell death and neural degeneration in multiple disease conditions; however, the evidence for successful intervention with dietary antioxidant manipulations has been mixed. In this study, we investigated the potential for protection of cells in the inner ear using a dietary supplement with multiple antioxidant components, which were selected for their potential interactive effectiveness. Protection against permanent threshold shift (PTS) was observed in CBA/J mice maintained on a diet supplemented with a combination of β-carotene, vitamins C and E, and magnesium when compared with PTS in control mice maintained on a nutritionally complete control diet. Although hair cell survival was not enhanced, noise-induced loss of type II fibrocytes in the lateral wall was significantly reduced (P < 0.05), and there was a trend toward less noise-induced loss in strial cell density in animals maintained on the supplemented diet. Taken together, our data suggest that prenoise oral treatment with the high-nutrient diet can protect cells in the inner ear and reduce PTS in mice. The demonstration of functional and morphologic preservation of cells in the inner ear with oral administration of this antioxidant supplemented diet supports the possibility of translation to human patients and suggests an opportunity to evaluate antioxidant protection in mouse models of oxidative stress-related disease and pathology.
氧化应激被广泛认为是多种疾病状态下细胞死亡和神经退行性变的原因;然而,通过饮食抗氧化剂干预取得成功的证据却存在差异。在这项研究中,我们使用了一种具有多种抗氧化成分的膳食补充剂来研究其对内耳细胞的潜在保护作用,这些成分是根据它们的潜在相互作用效果选择的。与用营养完全的对照饮食饲养的对照组小鼠相比,CBA/J 小鼠在补充了β-胡萝卜素、维生素 C 和 E 以及镁的饮食中,其永久性阈移(PTS)得到了保护。尽管毛细胞的存活率没有提高,但外侧壁Ⅱ型成纤维细胞的噪声诱导性损失明显减少(P<0.05),而且在用补充饮食饲养的动物中,纹状体内细胞密度的噪声诱导性损失也有减少的趋势。综上所述,我们的数据表明,噪声前口服高营养饮食可以保护内耳细胞并降低小鼠的 PTS。这种抗氧化剂补充饮食的口服给药对内耳细胞的功能和形态保存的证明支持了将其转化为人类患者的可能性,并提示有机会在与氧化应激相关疾病和病理学的小鼠模型中评估抗氧化保护作用。