| Home | E-Submission | Sitemap | Editorial Office |  
top_img
Ann Clin Neurophysiol > Volume 8(1); 2006 > Article
Ann Clin Neurophysiol. 2006; 8(1): 63-70.
Testosterone-mediated Neuroprotection in NO Induced CellDeath of Motor Neuron Cells Expressing Wild Typeor Mutant Cu/Zn Superoxide Dismutase
Nam Hee Kim, Hyun Jung Kim, Manho Kim, Kyung Seok Park, and Kwang-Woo Lee
Copyright © 2006 The Korean Society of Clinical Neurophysiology
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
ABSTRACT
Background: Testosterone is reported to have neuroprotective effect in various neurological diseases. Recently, the mechanism involved in nitric oxide (NO)-mediated motor neuron death is under extensive investigation. The Cu/Znsuperoxide dismutase (SOD1) mutations has been implicated in selective motor neuron death of amyotrophic lateral sclerosis (ALS) and it is said to play an important role in NO-mediated motor neuron death. However, neuroprotective effect of testosterone on motor neuron exposed to NO has rarely been studied.

Methods: Motor neuron-neuroblastoma hybrid cells expressing wild-type or mutant (G93A or A4V) SOD gene were treated with 200
Key words: Amyotrophic lateral sclerosis, Testosterone, Nitric Oxide, Neuroprotection, Cu/Zn superoxide dismutase, Cell viability
TOOLS
PDF Links  PDF Links
Download Citation  Download Citation
  Print
Share:      
METRICS
1,436
View
3
Download
Related article
Editorial Office
Department of Neurology, Seoul National University (SNU) College of Medicine
SMG-SNU Boramae Medical Center
20 Boramaero-5-Gil, Dongjak-Gu, Seoul 07061, Republic of Korea
TEL : +82-2-2266-7238    FAX : +82-2-831-2826   E-mail: acn.journal@e-acn.org
About |  Browse Articles |  Current Issue |  For Authors and Reviewers
Copyright © The Korean Society of Clinical Neurophysiology.           Developed in M2PI