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目的 确定一个理想的耳蜗氧化损伤模型。方法 对 5只Cu/ZnSOD基因敲除纯合突变 (Cu/ZnSOD无活性 ,Sod1- / - )小鼠和 10只Cu/ZnSOD杂合突变 (5 0 %Cu/ZnSOD失活 ,Sod1+/ - )小鼠及 5只野生小鼠 (Cu/Zn SOD活性正常 ,Sod1+/ +)进行ABR检测及内、外毛细胞计数。应用PCR技术检测Cu/ZnSOD基因敲除小鼠耳蜗mtDNA缺失情况。结果 Cu/ZnSOD基因敲除小鼠耳蜗内外毛细胞大量缺失 (P <0 .0 0 1) ,ABR检测 ,Sod1- / -小鼠ABR阈值在 8,16 ,32kHz及Sod1+/ -小鼠ABR阈值在 16 ,32kHz明显增大 (P <0 .0 0 1)。Cu/ZnSOD基因敲除小鼠耳蜗mtDNA有三种缺失 ,分别为mtDNA 386 7bp、mtDNA 372 6bp及mtDNA 432 6bp缺失。结论 Cu/ZnSOD基因敲除小鼠耳蜗在细胞及分子水平上均表现出受到ROS损伤的改变 ,是一个理想的耳蜗氧化损伤模型。
Objective To determine an ideal cochlear oxidative damage model. Methods Five homozygous mutants of Cu / ZnSOD gene knockout (Cu / ZnSOD inactive Sod1 / -) mice and 10 Cu / ZnSOD heterozygous mutations (50% Cu / ZnSOD inactivation, Sod1 + / - Mice and five wild mice (Cu / Zn SOD activity was normal, Sod1 + / +) ABR detection and inner and outer hair cell count. Detection of cochlear mtDNA deletion in Cu / ZnSOD gene knockout mice by PCR. Results There was a significant loss of inner and outer hair cells in Cochlear / ZnSOD knockout mice (P <0.01). ABR threshold, ABR threshold of Sod1- / - mice at 8, 16, 32 kHz and Sod1 + / - mice ABR threshold At 16, 32kHz significantly increased (P <0. 001). Three types of mtDNA were found in the cochlea of Cu / ZnSOD knockout mice, which were mtDNA 386 7bp, mtDNA 372 6bp and mtDNA 432 6bp deletion, respectively. Conclusion The cochlea of Cu / ZnSOD knockout mice show the changes of ROS injury at the cellular and molecular level, which is an ideal cochlear oxidative damage model.