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大鼠脊髓神经节神经元对丙烯酰胺细胞内反应的演变。

The evolution of intracellular responses to acrylamide in rat spinal ganglion neurons.

作者信息

Jones H B, Cavanagh J B

出版信息

Neuropathol Appl Neurobiol. 1984 Mar-Apr;10(2):101-21. doi: 10.1111/j.1365-2990.1984.tb00343.x.

DOI:10.1111/j.1365-2990.1984.tb00343.x
PMID:6539426
Abstract

Acrylamide (30 mg or 50 mg/kg/day, 5 days each week) was injected intraperitoneally into rats for up to 4 weeks. Lumbar spinal ganglia, spinal cord and lumbrical muscle spindles were examined by light and electron microscopy at various times during this period. The first abnormalities in spinal ganglion neurons were seen at 7 days when an apparent increase in numbers of mitochondria, some being hypertrophic, were found in a few large light cells. This was 10 days before any significant Wallerian degeneration was found in muscle spindle sensory fibres. Mitochondrial changes became more marked with time and were later associated with RER disruption, loss of neurofilaments and peripheral displacement of the nucleus thus mimicking chromatolysis of the axon reaction. All these changes began, however, before axon degeneration. Evidence of increased satellite cell activity was maximal at 21 days. These changes are discussed in the light of the possibility that calcium entry into the cell may be seriously increased early in the intoxication as a direct result of the presence of acrylamide and that many of these cellular features are secondary responses to such an event. Distal degeneration of axons seems likely to be secondary to the perikaryal changes.

摘要

将丙烯酰胺(30毫克或50毫克/千克/天,每周5天)腹腔注射给大鼠,持续4周。在此期间的不同时间,通过光镜和电镜检查腰段脊神经节、脊髓和蚓状肌梭。在第7天观察到脊神经节神经元的最初异常,此时在一些大的亮细胞中发现线粒体数量明显增加,有些线粒体肥大。这比在肌梭感觉纤维中发现任何明显的华勒氏变性早10天。线粒体变化随时间变得更加明显,随后与粗面内质网破坏、神经丝丢失以及细胞核外周移位相关,从而模拟轴突反应的染色质溶解。然而,所有这些变化都在轴突变性之前开始。卫星细胞活性增加的证据在第21天最为明显。鉴于中毒早期由于丙烯酰胺的存在可能会导致钙大量进入细胞,并且这些细胞特征中的许多可能是对该事件的继发反应,因此对这些变化进行了讨论。轴突的远端变性似乎继发于胞体变化。

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