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Hereditary ceruloplasmin deficiency increases advanced glycation end products in the brain
K Tajima1, T Kawanami, R Nagai
1Third Department of Internal Medicine, Yamagata University School of Medicine, Japan.
Neurology
|August 17, 1999
Abstract:
We investigated the role of ceruloplasmin in the antioxidative process in the brain in a patient with hereditary ceruloplasmin deficiency (HCD). Immunohistochemistry revealed an accumulation of Nepsilon-(carboxymethyl) lysine (CML) in basal ganglia of the HCD brain. In vitro study disclosed that ceruloplasmin inhibited CML formation from glycated proteins through the reaction of Fe2+ with H2O2 by Fenton reaction. These data suggest that ceruloplasmin plays an important role in the protection of neurons against oxidative stress associated with iron metabolism.