Involvement of apoptosis in progression of cochlear lesion following exposure to intense noise
Involvement of apoptosis in progression of cochlear lesion following exposure to intense noise
复制标题
DOI：
10.1016/s0378-5955(02)00286-1
复制
发表时间：
2002-04-01
期刊：
影响因子：
2.8
通讯作者：
Nicotera, TM
中科院分区：
文献类型：
--
作者：
Hu, BH;Henderson, D;Nicotera, TM
一段时间以来，人们已经知道，噪声诱发的耳蜗外毛细胞（OHC）死亡在噪声暴露终止后仍会继续存在。然而，导致耳蜗病变扩大的潜在机制尚不完全清楚。本研究报告了在110 dB声压下暴露于4 kHz窄带噪声1小时后，鼠耳蜗OHC死亡过程中凋亡通路的参与。OHC核形态学检查显示核凝聚和断裂。典型的细胞凋亡形态学特征：噪声暴露后耳蜗OHC细胞向耳蜗顶端和基底部不对称发展。噪音暴露后两天。耳蜗基底部仍有活跃的OHC病理，核浓缩和碎片化。细胞内凋亡标志物caspase-3的激活检测。凋亡细胞核与活化的caspase-3在空间上一致。这些结果清楚地暗示了暴露后OHC死亡进展中的凋亡途径。(C) 2002 Elsevier Science B.V.版权所有
It has been known for some time that noise-induced outer hair cell (OHC) death in the cochlea continues well after the termination of a noise exposure. However, the underlying mechanisms leading to the expansion of a cochlear lesion are not fully understood. Here we report involvement of the apoptotic pathway in the progression of OHC death in the chinchilla cochlea following exposure to a 4 kHz narrow band noise at 110 dB SPL for 1 h. Morphological examination of OHC nuclei revealed nuclear condensation and fragmentation. typical morphological features of apoptosis, OHC apoptosis developed asymmetrically toward the apical and basal parts of the cochleas following the noise exposure. Two days after the noise exposure. there was still active OHC pathology with condensed and fragmented nuclei in the basal part of the cochleas. Detection of caspase-3 activation, an intracellular marker for apoptosis. showed a spatial agreement between the apoptotic nuclei and activated caspase-3. These results clearly implicate the apoptotic pathway in the post-exposure progression of OHC demise. (C) 2002 Elsevier Science B.V. All rights reserved.