Abstract
Vitamin E, such as alpha-tocopherol (ATPH) and alpha-tocotrienol (ATTN), is a chain-breaking antioxidant that prevents the chain propagation step during lipid peroxidation. In the present study, we investigated the effects of ATTN on KA-induced neuronal death using organotypic hippocampal slice culture (OHSC) and compared the neuroprotective effects of ATTN and ATPH. After 15 h KA (5 μM) treatment, delayed neuronal death was detected in the CA3 region and reactive oxygen species (ROS) formation and lipid peroxidation were also increased. Both co-treatment and post-treatment of ATPH (100 μM) or ATTN (100 μM) significantly increased the cell survival and reduced the number of TUNEL-positive cells in the CA3 region. Increased dichlorofluorescein (DCF) fluorescence and levels of thiobarbiturate reactive substances (TBARS) were decreased by ATPH and ATTN treatment. These data suggest that ATPH and ATTN treatment have protective effects on KA-induced cell death in OHSC. ATTN treatment tended to be more effective than ATPH treatment, even though there was no significant difference between ATPH and ATTN in co-treatment or post-treatment.
Highlights
Kainic acid (KA), an agonist for kainate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, is an excitatory neurotoxic substance
We investigated whether KA-induced neuronal death in organotypic hippocampal slice culture (OHSC) can be prevented by ATTN by measuring PI uptake, reactive oxygen species (ROS) generation, and lipid peroxidation levels and compared the neuroprotective effects of ATTN and ATPH
PI uptake was measured to assess the effects of ATPH and ATTN on KA-induced cell death
Summary
Kainic acid (KA), an agonist for kainate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, is an excitatory neurotoxic substance. ROS attacks macromolecules within neurons, resulting in membrane lipid peroxidation, and structural and functional changes in proteins and DNA strand breaks [1,2]. Vitamin E is a chain-breaking antioxidant; it is able to repair oxidizing radicals directly, preventing the chain propagation step during lipid peroxidation [7]. Little is known about the effects of tocotrienols on CNS neurons even though there were several early reports, which showed a protective role for alpha-tocopherol or vitamin E [14,15]. We investigated whether KA-induced neuronal death in OHSC can be prevented by ATTN by measuring PI uptake, ROS generation, and lipid peroxidation levels and compared the neuroprotective effects of ATTN and ATPH
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