中文摘要：

背景我们的以前的研究证明了 apoptosis 和坏死涉及毛细胞(HC ) 在老化 cochleae 的致病。更好理解为 HC 死亡的规定负责的生物机制，我们检验了 succinate 脱氢酶(同步数字系列)的活动， mitochondrial bioenergetic 酶在听觉的 brainstem 反应阀值在 4 点由音调爆炸得到了的老化 cochleae.Methods 的 HC ， 10 和 20 kHz 在幼仔( 2-3 月)和老化( 22-23 月)被测量 Wistar 老鼠。同步数字系列活动用 nitroblue tetrazolium monosodium 盐与比色的试金被评估。Corti 的标记同步数字系列的机关是双的与 propidium 染色了碘化物，设置的 DNA 荧光灯为 HC 原子核的说明的探查。所有标本与荧光显微镜学被检验，共焦的 microscopy.Results 老化老鼠与是的阀值移动展出了 ABR 阀值的重要举起在 20 kHz，在 10 kHz 的 28 dB，和在 4 kHz 的 25 dB 的 34 dB。与在耳蜗的功能的减小一致，老化 cochleae 展出了染色紧张在的同步数字系列的减小顶端并且 cochleae 的基础结束很多 apoptotic，坏死、失踪的 HC 是明显的。在染色的同步数字系列的减小以一种 cell-death-mode 依赖者方式出现了。明确地，标记的同步数字系列留在 apoptotic HC。相反，染色的同步数字系列显著地在变老的蜗在坏死的 HCs.Conclusions 被减少或不在，同步数字系列活动在经历 apoptosis 的 HC 被保存，但是实质地在坏死被减少。这些结果建议那 mitochondrial 精力充沛的功能在老化 cochleae 的致病涉及房间死亡小径的规定。

英文摘要：

Background Our previous studies have shown that both apoptosis and necrosis are involved in hair cell （HC） pathogenesis in aging cochleae. To better understand the biological mechanisms responsible for the regulation of HC death, we examined the activity of succinate dehydregenase （SDH）, a mitochondrial bioenergetic enzyme, in the HCs of aging cochleae. Methods The auditory brainstem response thresholds elicited by tone bursts at 4, 10 and 20 kHz were measured in both young （2-3 months） and aging （22-23 months） Wistar rats. SDH activity was evaluated with a colorimetric assay using nitroblue tetrazolium monosodium salt. The SDH-labeled organs of Corti were double stained with propidium iodide, a DNA intercalating fluorescent probe for illustration of HC nuclei. All the specimens were examined with fluorescence microscopy and confocal microscopy. Results Aging rats exhibited a significant elevation of ABR thresholds with threshold shifts being 34 dB at 20 kHz, 28 dB at 10 kHz, and 25 dB at 4 kHz. Consistent with the reduction in the cochlear function, aging cochleae exhibited the reduction of SDH staining intensity in the apical and the basal ends of the cochleae, where a large number of apoptotic, necrotic, and missing HCs were evident. The reduction in SDH staining appeared in a cell-death-mode dependent fashion. Specifically, SDH labeling remained in apoptotic HCs. In contrast, SDH staining was markedly reduced or absent in necrotic HCs. Conclusions In the aging cochlea, SDH activity is preserved in HCs undergoing apoptosis, but is substantially reduced in necrosis. These results sUggest that mitochondrial energetic function is involved in the regulation of cell death pathways in the pathogenesis of aging cochleae.