Abstract

Axonal and dendrictic degenerations were observed in non-skeleton fluorosis as the neurological manifestations. Microtubules, composed of the assembled tubulin dimers, are the essential cytoskeleton of axon and dendron. However, the effect of fluoride (F) on microtubules status and tubulin dimer expression in central nerves system remains largely unknown. In this study, the ultrastructure of microtubules and expression of TubB1a and TubB2a were detected in hippocampus of mice orally administrated with 25, 50, or 100mgL(-1) NaF for 60d. Results showed that in F treatment groups, microtubules were broken into discrete fragments and bended, which were no longer stretched and went along the axon well. In addition, the expression of TubB1a and TubB2a on both gene and protein levels were significantly reduced in high F group. The visual results of immunocytochemistry also confirmed the decreased protein expressions of TubB1a and TubB2a. These findings suggested that microtubule lesions could be an important cause for neurodegeneration observed in fluorosis, and F may threaten the microtubule stability by affecting the expression of tubulin dimers.

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