The investigation of the hypothesis, glutamate-Ca-nitric oxide (NO), in the inner ear disturbance

我们研究了一氧化氮（NO）对内耳障碍的影响。将0.5和0.1摩尔浓度（MC）的1-羟基-2-氧-3-（3-氨基丙基）-3-异丙基-1 -三氮杂烯（NOC-5）作为NO供体放置于豚鼠耳蜗圆窗上，分别于12、28、72 h观察其形态学变化。内耳毛细胞以凋亡方式死亡。谷氨酰胺诱导耳蜗外毛细胞死亡。我们研究了补充胱氨酸对耳蜗外毛细胞（OHCs）变性的影响。长期接触Glu造成的…补充胱氨酸可显著降低死亡OHCs的数量。我们检测了链霉素损伤的前庭毛细胞中细胞色素c的细胞位置。这表明细胞色素c的重新分配参与了氨基糖苷诱导的前庭毛细胞凋亡的途径。我们对慢性暴露于GLU的豚鼠耳蜗进行了检查，以评估Corti器官的退化。同时，NO合成酶（NOS）活性也得到了证实。GLU处理引起OHCs的时间依赖性变性，同时Corti器官中NOS活性的时间性增加。我们使用烟酰胺腺嘌呤二核苷酸磷酸酶染色来监测链霉素作用下豚鼠前庭上皮变性过程中的NOS活性。在受影响的上皮细胞中观察到NUS活性呈剂量和时间依赖性增加，NOS抑制剂可保护毛细胞免于凋亡。此外，环己亚胺显著降低NOS活性和细胞凋亡的发生。这些结果提示NO参与了氨基糖苷引起的前庭上皮退行性变过程。

We investigated effect of Nitric oxide (NO) in the inner ear disturbances.The two concentrations, 0.5 and 0.1 molar concentration (MC) of 1-Hydroxy-2-oxo-3-(3-aminopropyl)-3-isopropyl-1 -triazene (NOC-5) which is NO donor was placed on the round window of the guinea pig cochlea and its morphological changes were investigated at 12, 28, 72 h after the treatment. The inner ear hair cell died in the manner of apoptosis.Glu induced death of cochlear outer hair cells (OHCs). We investigated the effect of cystine supplementation on degeneration of cochlear outer hair cells (OHCs). caused by long-term exposure to Glu.. Supplementation of cystine significantly decreased the number of dying OHCs..We examined the cellular location of cytochrome c in streptomycin-damaged vestibular hair cells. suggesting that redistribution of cytochrome c is involved in the pathway of apoptosis in vestibular hair cells induced by aminoglycosides..We examined guinea pig cochleae following chronic exposure to GLU to evaluate degeneration in the organ of Corti. In parallel, NO synthase (NOS) activity was demonstrated.. GLU treatment caused time-dependent degeneration of OHCs in conjunction with a temporal increase of NOS activity in the organ of Corti..We used nicotinamide adenine dinucleotide phosphate-diapholase staining to monitor NOS activity during degeneration of guinea pig vestibular epithelia affected by streptomycin. Increased NUS activity was observed in affected epithelia in a dose- and time-dependent manner and a NOS inhibitor could protect hair cells from apoptosis. Additionally, cycloheximide significantly reduced NOS activity and the occurrence of apoptosis. These findings suggest tha NO is involved in the degenerative process of vestibular epithelia caused by aminoglycosides.