Vitamin E prevents hyperoxia-induced loss of soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor proteins in the rat neuronal cytoplasm
| Autor: | Shiro Urano, Nozomi Kaneai, Taisuke Koike, Koji Fukui |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Vitamin
Male Vesicle-associated membrane protein 8 Cytoplasm medicine.medical_treatment Pharmaceutical Science Hyperoxia medicine.disease_cause Antioxidants chemistry.chemical_compound medicine Animals Vitamin E Rats Wistar N-Ethylmaleimide-Sensitive Proteins Pharmacology biology Brain General Medicine N-ethylmaleimide sensitive fusion protein Fusion protein Cell biology Rats Soluble N-Ethylmaleimide-Sensitive Factor Attachment Proteins Membrane docking Oxidative Stress chemistry biology.protein medicine.symptom SNARE Proteins Oxidative stress Synaptosomes |
| Zdroj: | Biologicalpharmaceutical bulletin. 36(9) |
| ISSN: | 1347-5215 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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