Effects of overexpression of the cytoplasmic copper-zinc superoxide dismutase on the survival of neurons in vitro

✍ Scribed by Paul J. Schwartz; Joseph T. Coyle

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: English
• Weight: 103 KB
• Volume: 29
• Category: Article
• ISSN: 0887-4476
• DOI: 10.1002/(sici)1098-2396(199807)29:3<206::aid-syn2>3.0.co;2-a

✦ Synopsis

The cytoplasmic copper-zinc superoxide dismutase (Cu, Zn SOD; SOD-1) is an abundant and well-conserved intracellular antioxidant enzyme which has been implicated in a number of oxidative stress mediated phenomena, especially Down Syndrome, in which SOD-1 activity is increased due to triplication of chromosome 21 containing the gene and, in hereditary amyotrophic lateral sclerosis, in which the gene is mutated. Overexpression of SOD-1 could theoretically, therefore, lead to increased vulnerability to oxidative stress in two distinct manners: increasing steady-state hydrogen peroxide levels or increasing toxic side reactions. We used two mouse neuronal culture systems--one in which the murine chromosome containing SOD-1 is triplicated and one in which human SOD-1 is a transgene--to test the effect of overexpression of this enzyme on antioxidant status in general and specifically on glutamate mediated oxidative stress. We found that SOD-1 overexpression increases antioxidant status at the same time it decreases vulnerability to glutamate.