Acrylamide and 2,5-hexanedione induce collapse of neurofilaments in SH-SY5Y human neuroblastoma cells to form perikaryal inclusion bodies.
Neurofilament accumulations are characteristic of a number of neurological conditions including amyotrophic lateral sclerosis, giant axonal neuropathies and several chemically-induced neuropathies. Although the mechanism(s) leading to neurofilament accumulation are unknown, it is possible that similar processes occur both in disease and in chemically-induced neuropathies. Understanding the mechanism(s) of chemically-induced neurofilament accumulation, which is more amenable to experimental manipulation, may give insight into the neurological diseases they mimic. We have compared the effects of two chemically-dissimilar neurotoxins, 2,5-hexanedione and acrylamide, on neurofilaments in the human neuroblastoma cell line, SH-SY5Y. Both undifferentiated and differentiated SH-SY5Y cells were exposed to 2,5-hexanedione or acrylamide and changes in cytoskeletal organization examined by immunofluorescence and electron microscopy. Although distinct morphological differences have previously been characterized in the neuropathies induced by 2,5-hexanedione and acrylamide in vivo, we have found that both compounds had similar direct effects on neurofilaments in SH-SY5Y cells, inducing formation of perikaryal inclusion bodies. In addition, differentiated SH-SY5Y cells were more sensitive to both 2,5-hexanedione and acrylamide compared with undifferentiated cells. These similar effects of 2,5-hexanedione and acrylamide lend further support that a common mechanism(s) may lead to neurofilament accumulation in these neuropathies. SH-SY5Y cells provide a useful model to investigate further the biochemical basis of neurofilament accumulation.[1]References
- Acrylamide and 2,5-hexanedione induce collapse of neurofilaments in SH-SY5Y human neuroblastoma cells to form perikaryal inclusion bodies. Hartley, C.L., Anderson, V.E., Anderton, B.H., Robertson, J., Anderson, B.H. Neuropathol. Appl. Neurobiol. (1997) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg