Hereditary ceruloplasmin deficiency increases advanced glycation end products in the brain
Abstract
Article 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 Nε-(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.
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© 1999.
Publication History
Received: January 25, 1999
Accepted: April 10, 1999
Published online: August 1, 1999
Published in issue: August 1, 1999
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