Hearing loss following exposure during development to polychlorinated biphenyls: A cochlear site of action
Hearing loss following exposure during development to polychlorinated biphenyls: A cochlear site of action
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DOI：
10.1016/s0378-5955(00)00062-9
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发表时间：
2000-06-01
期刊：
影响因子：
2.8
通讯作者：
Henderson, D
中科院分区：
文献类型：
--
作者：
Crofton, KM;Ding, DL;Henderson, D
母亲接触多卤代烃会导致成年后代早期产后低甲状腺血症和低频听力损失（Goldey 等人，1995a. Toxicol. Appl. Pharmacol. 135, 67-76；Herr 等人，1996. Fundam. Appl. Toxicol. 33, 120-128）。目前工作的目的是确定这种听觉障碍的作用部位是否在耳蜗内。从妊娠第 6 天 (GD) 到出生后第 21 天 (PND)，初产 Long-Evans 大鼠每天口服玉米油（对照）或 8 mg/kg 的商用 PCB 混合物 Aroclor 1254 (A1254)。在出生后 (PND) 的年轻成年后代中，使用反射修正测听法评估 1、4、16 和 40 kHz 音调的听觉阈值92-110。听觉评估后大约 6 周，处死一部分动物（每组 4 只）以进行耳蜗的组织学评估。从每只动物的一个耳蜗制备柯蒂氏器的表面制剂，并从相对的耳蜗制备蜗轴切片。与之前的发现一致，暴露于 A1254 的动物中 1kHz 音调的听觉阈值升高了约 25dB。与对照相比，所有较高频率的阈值没有不同。柯蒂氏器的表面处理显示，中上层和顶端转的外毛细胞有轻度至中度的损失。内毛细胞不受影响。蜗轴切片未能揭示任何其他耳蜗结构的变化。神经节细胞也没有明显损失。这些数据清楚地将发育过程中暴露于 A1254 引起的低频听力损失与柯蒂氏器中外毛细胞的损失联系起来。这种发育性耳毒性的机制仍有待确定。这些数据首次证明在发育过程中接触多氯联苯的成年动物的神经系统存在结构性缺陷。 (C) 2000 Elsevier Science B.V. 保留所有权利。
Maternal exposure to polyhalogenated hydrocarbons results in early postnatal hypothyroxenemia and a low-frequency hearing loss in adult offspring (Goldey et al., 1995a. Toxicol. Appl. Pharmacol. 135, 67-76; Herr et al., 1996. Fundam. Appl. Toxicol. 33, 120-128). The purpose of the present work was to determine whether the site-of-action of this auditory impairment was within the cochlea. Primiparous Long-Evans rats were given daily oral doses of corn oil (control) or 8 mg/kg of the commercial PCB mixture Aroclor 1254 (A1254) from gestation day (GD) 6 through postnatal day (PND) 21. Auditory thresholds for 1-, 4-, 16-, and 40-kHz tones were assessed using reflex modification audiometry in young adult offspring on postnatal days (PND) 92-110. Approximately 6 weeks after auditory assessments, a subset of animals (n=4 per group) were killed for histological assessment of the cochlea. Surface preparations of the organ of Corti were prepared from one cochlea per animal and modiolar sections were prepared from the opposite cochlea. Consistent with previous findings, auditory thresholds for 1-kHz tones were elevated by approximately 25 dB in the A1254-exposed animals. Thresholds for all higher frequencies were not different compared to controls. Surface preparations of the organ of Corti revealed a mild to moderate loss of outer hair cells in the upper-middle and apical turns. Inner hair cells were not affected. Modiolar sections failed to reveal alterations in any other cochlear structures. There was also no apparent loss of ganglion cells. These data clearly link the loss of low-frequency hearing caused by exposure during development to A1254 to a loss of outer hair cells in the organ of Corti. The mechanism that underlies this developmental ototoxicity remains to be determined. These data provide the first evidence of a structural deficit in the nervous system of adult animals exposed to PCBs during development. (C) 2000 Elsevier Science B.V. All rights reserved.