Decreased level of ATP7A contributes to endothelial dysfunction Using type 1 diabetic mice: (1) Decrease in SOD3 activity, yet with increase SOD3 protein levels (2) Unaltered SOD1 activity and protein levels (3) Increase O2-· production (4) Restoration of SOD3 activity after copper addition (5) Reduction in endothelium-dependent Ach relaxation (6) Decrease expression of ATP7A (7) Insulin increase ATP7A expression and restore SOD3 activity. The gene discussed is SOD1; the disease is endothelial dysfunction.