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Redox Rep. 2013;18(6):238-44. doi: 10.1179/1351000213Y.0000000065.

Tocotrienol prevents AAPH-induced neurite degeneration in neuro2a cells.

Author information

1
Shibaura Institute of Technology, Fukasaku 307, Minuma-ku, Saitama 337-8570, Japan; Shibaura Institute of Technology, Saitama 337-8570, Japan.

Abstract

OBJECTIVES:

Reactive oxygen species induce neurite degeneration before inducing cell death. However, the degenerative mechanisms have not yet been elucidated. While tocotrienols have a known neuroprotective function, the underlying mechanism remains unclear and may or may not involve antioxidant action. In this study, we hypothesize that free radical-derived membrane injury is one possible mechanism for inducing neurite degeneration. Therefore, we examined the potential neuroprotective effect of tocotrienols mediated through its antioxidant activity.

METHODS:

Mouse neuroblastoma neuro2a cells were used to examine the effect of the water-soluble free radical generator 2,2'-azobis(2-methylpropionamide) dihydrochloride (AAPH) on neurite dynamics. After 24 hours of AAPH treatment, cell viability, neurite number, and the number of altered neurites were measured in the presence or absence of α-tocotrienol.

RESULTS:

Treatment of neuro2a cells with a low concentration of AAPH induces neurite degeneration, but not cell death. Treatment with 5 µM α-tocotrienol significantly inhibited neurite degeneration in AAPH-treated neuro2a cells. Furthermore, morphological changes in AAPH-treated neuro2a cells were similar to those observed with colchicine treatment.

CONCLUSIONS:

α-Tocotrienol may scavenge AAPH-derived free radicals and alkoxyl radicals that are generated from AAPH-derived peroxyl radicals on cell membranes. Therefore, α-tocotrienol may have a neuroprotective effect mediated by its antioxidant activity.

PMID:
24112959
DOI:
10.1179/1351000213Y.0000000065
[Indexed for MEDLINE]

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