Selective vulnerability of the cochlear Basal turn to acrylonitrile and noise.

Selective vulnerability of the cochlear Basal turn to acrylonitrile and noise.
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DOI:
10.1155/2009/908596
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发表时间:
2009
影响因子:
2.9
通讯作者:
Fechter LD
Fechter LD
中科院分区:
其他
文献类型:
--
作者:
Pouyatos B;Gearhart CA;Nelson-Miller A;Fulton S;Fechter LD

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暴露于丙烯腈,一种高产的工业化学品,可以促进大鼠的噪声性听力损失(NIHL),即使这种药剂本身不会产生永久性听力损失。丙烯腈促进NIHL的机制包括氧化应激,因为抗氧化剂药物可以部分保护耳蜗免受丙烯腈+噪声的影响。丙烯腈消耗谷胱甘肽水平,而噪音可以增加活性氧的形成。先前注意到,当倍频程带噪声(OBN)以8 kHz为中心时,耳蜗的高频或基回特别容易受到丙烯腈和噪声的组合影响。正常情况下,这样的噪声会在耳蜗的更顶端区域产生损伤。本研究旨在确定基底耳蜗是否对丙烯腈选择性敏感,或者通过调整噪声频带的频率,是否有可能控制听觉障碍的区域。将大鼠暴露于以不同频率(4 kHz,110 dB和8或16 kHz,97 dB)为中心的三种不同OBN中的一种,持续5天,给予和不给予丙烯腈(50 mg/kg/天)。噪声被设置为自身引起有限的NIHL。通过记录畸变产物、复合动作电位和进行耳蜗组织学检查来监测听觉功能。虽然仅ACN和仅噪声暴露未诱导或几乎未诱导永久性听觉丧失,但丙烯腈+噪声的三次暴露在16 kHz以上产生了相似的听觉和耳蜗损伤,尽管噪声暴露覆盖了2个倍频程。这些观察结果表明,基底耳蜗比顶端分区对丙烯腈+噪声更敏感。他们提供了一个初步的基础,以区分耳蜗损伤的模式,导致噪声暴露,由于噪声和化学污染物的综合影响而发生的。
Exposure to acrylonitrile, a high-production industrial chemical, can promote noise-induced hearing loss (NIHL) in the rat even though this agent does not itself produce permanent hearing loss. The mechanism by which acrylonitrile promotes NIHL includes oxidative stress as antioxidant drugs can partially protect the cochlea from acrylonitrile + noise. Acrylonitrile depletes glutathione levels while noise can increase the formation of reactive oxygen species. It was previously noted that the high-frequency or basal turn of the cochlea was particularly vulnerable to the combined effects of acrylonitrile and noise when the octave band noise (OBN) was centered at 8 kHz. Normally, such a noise would be expected to yield damage at a more apical region of the cochlea. The present study was designed to determine whether the basal cochlea is selectively sensitive to acrylonitrile or whether, by adjusting the frequency of the noise band, it would be possible to control the region of the auditory impairment. Rats were exposed to one of three different OBNs centered at different frequencies (4 kHz, 110 dB and 8 or 16 kHz at 97 dB) for 5 days, with and without administration of acrylonitrile (50 mg/kg/day). The noise was set to cause limited NIHL by itself. Auditory function was monitored by recording distortion products, by compound action potentials, and by performing cochlear histology. While the ACN-only and noise-only exposures induced no or little permanent auditory loss, the three exposures to acrylonitrile + noise produced similar auditory and cochlear impairments above 16 kHz, despite the fact that the noise exposures covered 2 octaves. These observations show that the basal cochlea is much more sensitive to acrylonitrile + noise than the apical partition. They provide an initial basis for distinguishing the pattern of cochlear injury that results from noise exposure from that which occurs due to the combined effects of noise and a chemical contaminant.
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