Vitamin e prevents hyperoxia-induced loss of soluble n-ethylmaleimide- sensitive fusion protein attachment protein receptor proteins in the rat neuronal cytoplasm

Nozomi Kaneai, Koji Fukui, Taisuke Koike, Shiro Urano

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)

Abstract

This study examines the ability of vitamin E to inhibit hyperoxia-induced loss of soluble N-ethylmaleimide- sensitive fusion protein attachment protein receptor (SNARE) proteins in the neuronal cytoplasm. Here, the effects of vitamin E on hyperoxia-induced changes in the expressions of N-ethylmaleimide-sensitive factor (NSF) and soluble NSF-attachment protein α (α-SNAP) in the rat brain were analyzed. When rats were subjected to hyperoxia, the expression of both SNARE proteins was markedly decreased compared to normal rats. Vitamin E significantly inhibited the decrease in the expression of NSF in rats subjected to hyperoxia. Rats showed the tendency to improve the loss of α-SNAP by vitamin E-supplementation, although it was not statistically significant. On the other hand, vitamin E deficient rats showed marked loss of these proteins in the brain in the absence of oxidative stress. These results suggest that hyperoxia induces a loss of SNARE proteins, which are involved in membrane docking between synaptic vesicles and pre-synaptic membranes, and that vitamin E prevents the oxidative damage of SNARE proteins. Consequently, it is implied that vitamin E inhibits impaired neurotransmission caused by oxidative stress through the prevention of oxidative damage to SNARE proteins by probably its antioxidant effect.

Original languageEnglish
Pages (from-to)1500-1502
Number of pages3
JournalBiological and Pharmaceutical Bulletin
Volume36
Issue number9
DOIs
Publication statusPublished - 2013 Sept

Keywords

  • Membrane fusion
  • N-ethylmaleimide-sensitive fusion protein attachment protein receptor
  • Neurodegeneration
  • Neurotransmission
  • Vitamin e

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science

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