Yang Wei Ping, Henderson Donald, Hu Bo Hua, Nicotera Thomas M
Center for Hearing and Deafness, State University of New York at Buffalo, 137 Cary Hall, 3435 Main Street, Buffalo, NY 14214, USA.
Hear Res. 2004 Oct;196(1-2):69-76. doi: 10.1016/j.heares.2004.04.015.
We have reported that by 2 days after noise exposure the size of cochlear lesion was expanding by outer hair cells (OHCs) dying either by apoptosis or necrosis. The current study was designed to compare the prevalence of the two cell death pathways as a function of time after exposure to noises of different levels. Chinchillas were exposed to a narrow band noise at either 104 or 108 dB SPL for 1 h. At three time points (1, 4 and 30 days) after the noise exposure, the numbers of missing, apoptotic and necrotic OHCs in the cochleas were identified and documented with a combination of TUNEL, caspase-3 and propidium iodide labeling. The subjects exposed to the 108-dB noise showed significantly more apoptotic OHCs than necrotic OHCs in the cochleas examined at days 1 and 4 after the noise exposure. By day 30, apoptotic and necrotic pathologies continued, although in small quantity, with no significant difference in quantity between two types of cell death. The subjects exposed to the 104-dB noise showed a significant difference in the numbers of apoptotic and necrotic OHCs at day 1 after the noise exposure, whereas the difference became statistically insignificant at day 4 and day 30 after the noise exposure. The results of the study indicate that the early expansion of cochlear lesion is attributed primarily to apoptosis, whereas the later stage of lesion expansion is likely the result of an equal contribution from apoptosis and necrosis.
我们曾报道，噪声暴露后2天，耳蜗损伤范围因外毛细胞（OHC）通过凋亡或坏死死亡而扩大。本研究旨在比较暴露于不同强度噪声后，两种细胞死亡途径的发生率随时间的变化情况。将毛丝鼠暴露于104或108 dB SPL的窄带噪声中1小时。在噪声暴露后的三个时间点（1、4和30天），结合TUNEL、半胱天冬酶-3和碘化丙啶标记，识别并记录耳蜗中缺失、凋亡和坏死的OHC数量。在噪声暴露后第1天和第4天检查的耳蜗中，暴露于108 dB噪声的受试动物显示凋亡的OHC比坏死的OHC明显更多。到第30天，凋亡和坏死病变仍在继续，尽管数量很少，两种细胞死亡类型的数量没有显著差异。暴露于104 dB噪声的受试动物在噪声暴露后第1天凋亡和坏死的OHC数量有显著差异，而在噪声暴露后第4天和第30天，这种差异在统计学上不显著。研究结果表明，耳蜗损伤的早期扩大主要归因于凋亡，而损伤扩大的后期阶段可能是凋亡和坏死同等作用的结果。
