Emerging evidence suggests that oxidative stress might contribute to demyelination and axonal damage in multiple sclerosis (MS). Ferroxidase (FeOx) activity of ceruloplasmin prevents the formation of free radicals from Fe2+ by promoting the incorporation of this pro-oxidant ion to transferrin. The aim of our study was to investigate serum FeOx activity in a cohort of patients with MS and neurological controls. Serum FeOx activity was determined in 69 relapsing-remitting patients with MS and in 62 patients with other inflammatory neurological disorders (OIND) and 52 patients with other non-inflammatory neurological disorders (NIND) as controls. Serum FeOx activity was lower (p<0.01) in MS and OIND than in NIND, without any significant differences among MS patients grouped according to clinical and magnetic resonance evidence of disease activity. A reduced serum FeOx activity, which can potentially lead to a rise in oxidative stress-induced biomolecular damage, seems to be a shared condition in inflammatory disorders of the central nervous system including MS.