Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.16.3.1 (ceruloplasmin)
 5,074 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various stages of hypokinesia are marked by specific changes in the level and activity of endogenous metalloproteins with anti- (MAA) and prooxidant action (MPA). In particular, the level of MPA [cytochromes b5 and b558 (III + IV) and suprol] decreases in all stages (except for the level of cytochrome b5 exceeding that in the free control on the 15th and 30th day of hypokinesia). The superoxide production activity of suprol always exceeds that in the control, while the activity of cytochrome b558 (III) exceeds that in the control only on the 30th day of experiment. The level and activity of MAA [ceruloplasmin, transferrin (TF), superoxide dismutase (SOD), and catalase] decrease with the duration of hypokinesia (except for 15th day, when the level of TF and the activity of SOD exceed the values in the free control group). The administration of GABA and pyrrolidone decreases the extent of oxidative stress, which is manifested by leveling of the MAA and MPA content and activity.
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PMID:[Regulating effect of gamma-aminobutyric acid and pyrrolidone-2 on endogenous blood metalloproteins with anti- and pro-oxidant activity in hypoxia]. 1507 5

Oxidative damage and iron redistribution are associated with the pathogenesis and progression of multiple sclerosis (MS), but these aspects are not entirely replicated in rodent experimental autoimmune encephalomyelitis (EAE) models. Here, we report that oxidative burst and injury as well as redistribution of iron are hallmarks of the MS-like pathology in the EAE model in the common marmoset. Active lesions in the marmoset EAE brain display increased expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (p22phox, p47phox, and gp91phox) and inducible nitric oxide synthase immunoreactivity within lesions with active inflammation and demyelination, coinciding with enhanced expression of mitochondrial heat-shock protein 70 and superoxide dismutase 1 and 2. The EAE lesion-associated liberation of iron (due to loss of iron-containing myelin) was associated with altered expression of the iron metabolic markers FtH1, lactoferrin, hephaestin, and ceruloplasmin. The enhanced expression of oxidative damage markers in inflammatory lesions indicates that the enhanced antioxidant enzyme expression could not counteract reactive oxygen and nitrogen species-induced cellular damage, as is also observed in MS brains. This study demonstrates that oxidative injury and aberrant iron distribution are prominent pathological hallmarks of marmoset EAE thus making this model suitable for therapeutic intervention studies aimed at reducing oxidative stress and associated iron dysmetabolism.
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PMID:Oxidative Injury and Iron Redistribution Are Pathological Hallmarks of Marmoset Experimental Autoimmune Encephalomyelitis. 2850 83