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

The various risk factors for peripheral arterial disease (PAD) are almost identical to those for atherosclerosis and include abnormal levels of lipids or lipoproteins. Lipid peroxidation parameters and total antioxidant capacity in the serum of male patients with PAD before surgery as well as 3-5 days and 7-10 days after surgery were measured. We also compared these parameters with those in a group of patients receiving simvastatin therapy. Concentrations of lipid hydroperoxides (LOOHs) and malondialdehyde, the total antioxidant capacity (assessed by ferric reducing antioxidant power assay), concentration of thiol (-SH) groups, and ceruloplasmin activity were determined spectrophotometrically in PAD patients treated surgically (Group I) or pharmacologically (Group II). The patients before surgical treatment had significantly higher concentrations of malondialdehyde but lower ceruloplasmin activity than those observed in Group II, treated with simvastatin. No significant differences before surgery in ferric reducing antioxidant power or thiol concentrations were found between the two groups. However, in Group I, both ferric reducing antioxidant power and thiol group concentrations decreased 3-5 days postoperatively, and ceruloplasmin activity increased 7-10 days after surgical treatment. The presented results demonstrate diverse oxidative stress responses to surgical treatment and confirm the beneficial effects of statin therapy in PAD.
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PMID:Effect of surgical treatment on lipid peroxidation parameters and antioxidant status in the serum of patients with peripheral arterial disease. 2430 9

The effect of iron on the progress of atherosclerosis is still controversial. To explore the relationship between atherosclerotic plaques and iron metabolism and how iron is accumulated in plaque macrophages, we performed Oil red O staining to detect the lipid of the atherosclerotic plaques, enzyme-linked immunosorbent assay to detect the intracellular lipids (total cholesterol, free cholesterol) and serum hepcidin, Western-blot to examine the iron-related proteins, immunohistochemical and immunofluorescence assays to localize ferroportin 1 in macrophages. The contents of serum iron and transferrin saturation were measured. The results confrimed that atherosclerotic plaques were all lipid-rich. Compared to normal vessel wall, atherosclerotic plaques had significantly higher levels of ferritin and ferroportin 1. Strikingly, we found the much lower levels of ferroxidases ceruloplasmin and hephaestin in plaque tissue than the normal vessel, while the content of serum hepcidin, iron and transferrin saturation were similar in these two groups. The novel finding suggests that the inability of ferrous iron to be oxidized into ferric iron might be a potential mechanism for iron retention in plaques.
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PMID:Low expression of ferroxidases is implicated in the iron retention in human atherosclerotic plaques. 2620 58

Changes in the blood serum proteins were assessed in men with coronary atherosclerosis and without coronary heart disease. Proteins were separated by 2D-electrophoresis, protein fractions were identified by their peptide fingerprint by MALDI method; fractions with more than twofold increase in protein level were determined. In blood serum of patients with coronary atherosclerosis, the content of C4 complement protein increased and ceruloplasmin level decreased, which is typical of heart failure and coronary heart disease.
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PMID:Proteomic Study of Blood Serum in Coronary Atherosclerosis. 2809 99

The prevalence of vascular disorders continues to rise worldwide. Parallel with that, new pathophysiological pathways have been discovered, providing possible remedies for prevention and therapy in vascular diseases. Growing evidence suggests that endoplasmic reticulum (ER) stress is involved in a number of vasculopathies, including atherosclerosis, vascular brain events, and diabetes. Heme, which is released from hemoglobin or other heme proteins, triggers various pathophysiological consequence, including heme stress as well as ER stress. The potentially toxic free heme is converted by heme oxygenases (HOs) into carbon monoxide (CO), iron, and biliverdin (BV), the latter of which is reduced to bilirubin (BR). Redox-active iron is oxidized and stored by ferritin, an iron sequestering protein which exhibits ferroxidase activity. In recent years, CO, BV, and BR have been shown to control cellular processes such as inflammation, apoptosis, and antioxidant defense. This review covers our current knowledge about how heme induced endoplasmic reticulum stress (HIERS) participates in the pathogenesis of vascular disorders and highlights recent discoveries in the molecular mechanisms of HO-mediated cytoprotection in heme stress and ER stress, as well as crosstalk between ER stress and HO-1. Furthermore, we focus on the translational potential of HIERS and heme oxygenase-1 (HO-1) in atherosclerosis, diabetes mellitus, and brain hemorrhage.
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PMID:Heme, Heme Oxygenase, and Endoplasmic Reticulum Stress-A New Insight into the Pathophysiology of Vascular Diseases. 3135 46


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