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. Author manuscript; available in PMC: 2008 Dec 1.
Published in final edited form as: Exp Neurol. 2007 Aug 3;208(2):216–227. doi: 10.1016/j.expneurol.2007.07.017

Figure 2. Decreased Expression of SOD2 Increases Glucose-Mediated O2•− and Apoptosis.

Figure 2

DRG neurons from adult SOD2+/+ and SOD2+/− mice were exposed to 20 mM added glucose. A) O2•− generation was measured using an in vitro Amplex Red oxidation reaction at 5 h (Vincent et al., 2005a). **p < 0.001 compared to SOD2+/+ in basal glucose; +p < 0.01 compared to SOD2+/+ in basal glucose; *p < 0.05 compared to SOD+/− in basal glucose. B) DRG neurons were loaded with TMRM (50 nM), then mitochondrial membrane potential assessed through the increase in red fluorescence. In the presence of 20 mM glucose, hyperpolarization was greater and depolarization occurred earlier in SOD2+/− compared to SOD2+/+ neurons. C) Caspase-3 activation was determined by counting the percent of DRG neurons labeled with a fluorescent caspase-3 substrate (CaspaTag). Glucose-induced caspase-3 activation was increased in both the SOD2+/−and SOD+/+ cultures, compared to basal glucose, ***p < 0.001. D) Neurites were measured in DRG neurons 12 h after plating in control or hyperglycemia (20 mM added glucose) media. Mean neurite length was shorter in 20 mM added glucose than basal glucose, ***p < 0.001 for SOD2+/+ and ###p < 0.05 for SOD2+/−.