Zhou Yi-de, Ding Da-Lian, Zheng Hong-Liang, Zheng Gui-Liang, Shen Xiao-Hua, Zhang Qing, Salvi Richad J
Department of Otorhinolaryngology Head and Neck Surgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, China.
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2011 Jan;46(1):54-8.
To explore the pattern of hair cell injury and expression of P53 apoptosis protein in intensive impulse noise injured cochlear hair cells in guinea pigs.
Twelve adult guinea pigs were exposed to a series of 40 pairs of impulse noise (2 second intervals) at the intensity of 168 dB (SPL). Animals were terminated at 3, 6 and 12 hours after noise exposure, respectively. Cochlear surface preparations were performed with a double staining of FITC-conjugated phalloidin and propidium iodide for the observations of the stereocilia and the nucleus. P53 immunochemical staining was also performed 12 hours post-noise exposure to observe if there was expression of p53 protein in injured hair cells. Results Three hours after noise exposure, the outer hair cells at the end of basal turn and beginning of second turn were destroyed first with a character of nuclear condensation. Six hours post-noise exposure, many hair cells in the center of damage region had nuclear fragmentations, and the damaging area expanded towards to basal turn and apical turn. Twelve hours after noise exposure, the nucleus in most outer hair cells and inner hair cells at the region of damage center were missing. The nuclear condensation and fragmentation were appeared in hair cells in both sides of the center region of degeneration. P53 immunoreactive products were also found in damaged hair cells, not only in the central damage area, but also in the basal turn and the third turn.
Intensive impulse noise resulted in apoptosis of cochlear hair cells that initiated between the end of basal turn and the beginning of second turn. Hair cell degeneration spread to basal and third turn along the basilar membrane. P53 may play an important role in impulse noise induced-hair cell apoptosis.
探讨强脉冲噪声损伤豚鼠耳蜗毛细胞后毛细胞损伤模式及P53凋亡蛋白的表达情况。
12只成年豚鼠暴露于强度为168 dB（声压级）的一系列40对脉冲噪声（间隔2秒）。分别在噪声暴露后3、6和12小时处死动物。进行耳蜗表面制备，用异硫氰酸荧光素标记的鬼笔环肽和碘化丙啶双重染色观察静纤毛和细胞核。在噪声暴露12小时后还进行P53免疫化学染色，观察损伤毛细胞中是否有p53蛋白表达。结果噪声暴露后3小时，蜗底末端和第二圈起始处的外毛细胞首先受损，表现为核浓缩。噪声暴露后6小时，损伤区域中心的许多毛细胞出现核碎裂，损伤区域向蜗底和蜗顶扩展。噪声暴露后12小时，损伤中心区域的大多数外毛细胞和内毛细胞核消失。退变中心区域两侧的毛细胞出现核浓缩和核碎裂。在受损毛细胞中也发现了P53免疫反应产物，不仅在中央损伤区域，而且在蜗底和第三圈也有。
强脉冲噪声导致耳蜗毛细胞凋亡，起始于蜗底末端和第二圈起始处之间。毛细胞退变沿基底膜向蜗底和第三圈扩散。P53可能在脉冲噪声诱导的毛细胞凋亡中起重要作用。
