Abstract：
:Exposure chronically to n-hexane produces peripheral-central axonopathy mediated by 2,5-hexanedione (HD). Previous studies have demonstrated decreases in neurofilament (NF) contents of peripheral and central nervous regions from rats intoxicated with HD, and recent analysis has demonstrated that axonal atrophy, instead of NF-filled swellings, is a specific component of morphologic alterations. To deeply investigate the alterations of cytoskeletal proteins in HD peripheral neuropathy, the relative levels of NF-L, NF-M, NF-H, alpha-tubulin, beta-tubulin and beta-actin of rat sciatic-tibial nerves were determined by SDS-PAGE and immunoblotting. HD was administrated to Wistar rats by intraperitoneal injection at dosage of 200 or 400 mg/kg/day (five-times per week). Rats were sacrificed after 6 weeks of treatment, and sciatic-tibial nerves were dissected, homogenized, and used for the determination of cytoskeletal proteins. Except for supernatant NF-L that could not be assayed, the results showed HD intoxication was associated with significant decreases in NF subunits in both of the supernatant and the pellet fractions of sciatic-tibial nerve homogenates (P < 0.01), and obvious reductions in alpha-tubulin, beta-tubulin and beta-actin only in the supernatant (P < 0.05 or P < 0.01). Among these alterations, the falls in the levels of NF subunits tended to be greater compared to those of the other cytoskeletal proteins in all HD-exposed groups, and the trend for decrements in NF-M was greater than those in the other NF subunits. Thus, HD intoxication was associated with significant declines in cytoskeletal protein contents in rat sciatic-tibial nerves, and the decreases might be related to the involvement of the peripheral axonopathy induced by HD.
journal_name
Neurochem Resjournal_title
Neurochemical researchauthors
Zhang T,Zhao X,Zhu Z,Yu L,Han X,Zhang C,Xie Kdoi
10.1007/s11064-004-2439-5keywords:
subject
Has Abstractpub_date
2005-02-01 00:00:00pages
177-83issue
2eissn
0364-3190issn
1573-6903journal_volume
30pub_type
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