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氟柠檬酸耳毒性。豚鼠耳蜗原发性神经变性的形态学和细胞化学模型。

Fluorocitrate ototoxicity. A morphologic and cytochemical model for primary neural degeneration in the guinea pig cochlea.

作者信息

Spector G J, Carr C D

出版信息

Ann Otol Rhinol Laryngol. 1976 Mar-Apr;85(2 pt.1):185-97. doi: 10.1177/000348947608500202.

DOI:10.1177/000348947608500202
PMID:178265
Abstract

Fluorocitrate, an inhibitor of the tricarboxylic acid cycle at the aconitase reaction, produces a time and dose related neural dystrophy in the guinea pig cochlea. There is direct inhibition of succinic dehydrogenase activity but not nicotinamide adenine dinucleotide dehydrogenase and cytochrome oxidase via cytochrome c activities. The dystrophic neural changes morphologically are similar to those noted in primary neural degeneration and neural presbycusis in man. Neural degeneration in aging appears to be the result of a dissociation of biochemical reactions preventing the proper utilization of organic fuel molecules for generation of energy and direct or indirect inhibition of respiration.

摘要

氟柠檬酸是三羧酸循环中乌头酸酶反应的抑制剂,它在豚鼠耳蜗中会产生与时间和剂量相关的神经萎缩。它直接抑制琥珀酸脱氢酶的活性,但通过细胞色素c活性对烟酰胺腺嘌呤二核苷酸脱氢酶和细胞色素氧化酶没有抑制作用。形态学上,营养不良性神经变化与人类原发性神经变性和神经性老年聋中所观察到的变化相似。衰老过程中的神经变性似乎是生化反应解离的结果,这种解离阻止了有机燃料分子的正常利用以产生能量,并直接或间接抑制呼吸作用。

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