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Effects of overexpression of the cytoplasmic copper‐zinc superoxide dismutase on the survival of neurons in vitro
Author(s) -
Schwartz Paul J.,
Coyle Joseph T.
Publication year - 1998
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(199807)29:3<206::aid-syn2>3.0.co;2-a
Subject(s) - superoxide dismutase , oxidative stress , sod1 , antioxidant , chemistry , glutamate receptor , dismutase , biochemistry , microbiology and biotechnology , glutathione peroxidase , biology , receptor
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. Synapse 29:206–212, 1998. © 1998 Wiley‐Liss, Inc.