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由2,5 -己二酮（神经毒性工业溶剂甲基正丁基酮的主要代谢产物）引起的实验性神经病变。

Experimental neuropathy produced by 2,5-hexanedione--a major metabolite of the neurotoxic industrial solvent methyl n-butyl ketone.

作者信息

Spencer P S, Schaumburg H H

出版信息

J Neurol Neurosurg Psychiatry. 1975 Aug;38(8):771-5. doi: 10.1136/jnnp.38.8.771.

DOI:10.1136/jnnp.38.8.771
PMID:171344
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC492070/
Abstract

Chronic exposure of rats to 2,5-hexanedione (CH3COCH2CH2COCH3), a major metabolite of the neurotoxic industrial solvent methyl n-buryl ketone (CH3COCH2CH2CH2CH3), has been shown to cause a clinical peripheral neuropathy with dying-back peripheral and central nervous system degeneration characterized by giant axonal swellings filled with neurofilaments. This pattern of disease is similar to that produced by methyl n-butyl ketone.

摘要

大鼠长期接触神经毒性工业溶剂甲基正丁基酮（CH3COCH2CH2CH2CH3）的主要代谢产物2,5 - 己二酮（CH3COCH2CH2COCH3）已被证明会导致一种临床周围神经病变，伴有逆行性周围和中枢神经系统变性，其特征为充满神经丝的巨大轴突肿胀。这种疾病模式与甲基正丁基酮所引发的相似。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5df/492070/45f697f30ee7/jnnpsyc00182-0045-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5df/492070/e16d0fa98351/jnnpsyc00182-0044-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5df/492070/45f697f30ee7/jnnpsyc00182-0045-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5df/492070/e16d0fa98351/jnnpsyc00182-0044-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5df/492070/45f697f30ee7/jnnpsyc00182-0045-a.jpg

相似文献

1
Experimental neuropathy produced by 2,5-hexanedione--a major metabolite of the neurotoxic industrial solvent methyl n-butyl ketone.由2,5 -己二酮（神经毒性工业溶剂甲基正丁基酮的主要代谢产物）引起的实验性神经病变。
J Neurol Neurosurg Psychiatry. 1975 Aug;38(8):771-5. doi: 10.1136/jnnp.38.8.771.
2
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J Neuropathol Exp Neurol. 1977 Mar-Apr;36(2):300-20. doi: 10.1097/00005072-197703000-00006.
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Nervous system degeneration produced by the industrial solvent methyl n-butyl ketone.由工业溶剂甲基正丁基酮引起的神经系统退化。
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Toxic polyneuropathy produced by methyl N-butyl ketone.甲基正丁基甲酮引起的中毒性多发性神经病。
Science. 1974 Aug 30;185(4153):787-9. doi: 10.1126/science.185.4153.787.

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Performance of biomarkers NF-L, NSE, Tau and GFAP in blood and cerebrospinal fluid in rat for the detection of nervous system injury.生物标志物神经丝轻链（NF-L）、神经元特异性烯醇化酶（NSE）、 Tau蛋白和胶质纤维酸性蛋白（GFAP）在大鼠血液和脑脊液中用于检测神经系统损伤的性能。
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本文引用的文献

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The significance of the "dying back" process in experimental and human neurological disease.“逆行性”过程在实验性和人类神经疾病中的意义。
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Giant axonal neuropathy--a unique case with segmental neurofilamentous masses.巨大轴索性神经病——一例伴有节段性神经丝团块的独特病例。
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2,5-Hexanedione mediates neuronal apoptosis through suppression of NGF via PI3K/Akt signaling in the rat sciatic nerve.2,5-己二酮通过抑制神经生长因子（NGF）及其信号通路诱导大鼠坐骨神经神经元凋亡。
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2,5-hexanedione downregulates nerve growth factor and induces neuron apoptosis in the spinal cord of rats via inhibition of the PI3K/Akt signaling pathway.2,5-己二酮通过抑制PI3K/Akt信号通路下调大鼠脊髓中的神经生长因子并诱导神经元凋亡。
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Taurine inhibits 2,5-hexanedione-induced oxidative stress and mitochondria-dependent apoptosis in PC12 cells.牛磺酸抑制2,5 -己二酮诱导的PC12细胞氧化应激和线粒体依赖性凋亡。
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Solvent neurotoxicity.溶剂神经毒性
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Toxic polyneuropathy produced by methyl N-butyl ketone.甲基正丁基甲酮引起的中毒性多发性神经病。
Science. 1974 Aug 30;185(4153):787-9. doi: 10.1126/science.185.4153.787.
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Ultrastructural studies of the dying-back process. I. Peripheral nerve terminal and axon degeneration in systemic acrylamide intoxication.轴突回返性病变的超微结构研究。I. 全身性丙烯酰胺中毒时的周围神经终末及轴突变性
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Ultrastructural studies of the dying-back process. II. The sequestration and removal by Schwann cells and oligodendrocytes of organelles from normal and diseases axons.轴突变性过程的超微结构研究。II. 施万细胞和少突胶质细胞对正常和病变轴突细胞器的隔离与清除
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Giant axonal neuropathy. A clinically and morphologically distinct neurological disease.
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Nervous system degeneration produced by the industrial solvent methyl n-butyl ketone.由工业溶剂甲基正丁基酮引起的神经系统退化。
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