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)

To determine whether decrease in serum antioxidants contributes to the increased oxidative stress, we measured the antioxidant activity (AOA), total peroxyl radical-trapping antioxidant parameter (TRAP), and their component individual antioxidants in the serum of diabetic rats. AOA was assayed as the ability of serum to inhibit lipid autoxidation in brain homogenates. TRAP was assayed as the ability to delay lipid peroxidation induced by an azo initiator. Antioxidants measured were ceruloplasmin, unsaturated iron binding capacity (UIBC) and albumin as components of AOA; and uric acid, protein sulfhydryl and alpha-tocopherol as components of TRAP. AOA was decreased markedly in the diabetics due to the decrease in ceruloplasmin, UIBC and albumin. On the other hand, the directly measured TRAP in the diabetics was unaltered. Uric acid and alpha-tocopherol were increased in the diabetics. However, decrease in unidentified scavengers offset the increase brought about by those antioxidants These results suggest that the decreased metal binding capacity contributes to the increased oxidative stress in the diabetic rats.
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PMID:Serum antioxidant status in streptozotocin-induced diabetic rat. 795 5

To investigate the influence of maternal smoke exposure on neonatal and maternal antioxidant status, 39 mothers who were active smokers, 14 mothers exposed to environmental tobacco smoke (ETS), 17 controls, and their newborns were included in a prospective, controlled study. Plasma total antioxidant capacity, measured as total radical-trapping antioxidant parameter (TRAP) and ferric reducing antioxidant power (FRAP), and concentrations of specific antioxidants were measured in cord and in maternal blood. A similar, significant increase in ceruloplasmin concentration was observed in neonates born to actively smoking mothers and in those born to ETS exposed mothers. Uric acid and TRAP concentrations were significantly increased in ETS-exposed newborns and their mothers, compared to newborns and mothers from the active smoking and no-exposure groups with a trend towards increased uric acid, TRAP and FRAP concentrations being observed in the active smokers group. Neonatal and maternal antioxidant concentrations correlated significantly, except for ceruloplasmin. Cord blood vitamin A, E and C concentrations were unaffected by smoke exposure. These results show that maternal active smoking as well as ETS exposure significantly affect neonatal and maternal antioxidant status.
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PMID:Antioxidant status of neonates exposed in utero to tobacco smoke. 1553 69

Wilson disease (WD) is an autosomal recessive disorder due to the defect in ATP7B gene characterized by excessive accumulation of copper in the liver with progressive hepatic damage and subsequent redistribution to various extrahepatic tissues including the brain, kidneys, and cornea. Strikingly, the total serum copper concentration is always low in WD, even though the non-ceruloplasmin copper level is still expected to be high. To assess the role of free radical reactions catalyzed by non-ceruloplasmin copper, we investigated erythrocyte metabolism and oxidative stress as a mechanism for hemolysis in eight WD patients during episodes of acute hemolysis and compared them with eight follow-up cases of WD on d-penicillamine therapy and eight healthy, age-matched children. Elevated levels of non-ceruloplasmin copper were found in all the WD patients during an episode of hemolytic anemia. There was marked inhibition in erythrocyte enzymes, namely, hexokinase, total adenosine triphosphatase (ATPase), and glucose-6-phosphate dehydrogenase (G-6-PD) from WD patients compared with patients on penicillamine and healthy children, indicating altered erythrocyte metabolism during a hemolytic crisis. Antioxidant status was also found to be compromised as is evident from decreased glutathione (GSH) levels, decreased antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase), increased lipid peroxidation, and deranged plasma antioxidants. Uric acid showed maximum decrease followed by ascorbic acid. These findings suggest that the free radical production by elevated non-ceruloplasmin copper through transition metal catalyzed reactions leads to oxidative injury resulting in altered erythrocyte metabolism and severely compromised antioxidant status of WD patients during hemolytic anemia.
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PMID:Erythrocyte metabolism and antioxidant status of patients with Wilson disease with hemolytic anemia. 1654 36

The study was conducted to find out the extent of lipid peroxidation and antioxidant status in ischemic stroke patients (ISPs) with and without diabetes. Malondialdehyde (MDA) was studied as a marker of lipid peroxidation. Glutathione (GSH), uric acid and ceruloplasmin were estimated to study the antioxidant potential of ISPs. Significantly higher levels of MDA were found in both the groups of ISPs and the increase in MDA was more in ISPs without diabetes. GSH levels were decreased significantly in both the groups of ISPs and maximum decline was found in ISPs with diabetes. Uric acid levels were significantly increased in both the groups of ISPs. Ceruloplasmin levels were increased significantly in ISPs without diabetes, whereas its levels were slightly decreased in ISPs with diabetes. A negative correlation was found between MDA and the antioxidants GSH, uric acid and ceruloplasmin in ISPs with diabetes. This study suggests that there is an association between ischemic stroke and increased oxidative stress and the antioxidant potential is impaired in both the groups of ISPs with and without diabetes.
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PMID:A comparative study on oxidative stress and antioxidant status in ischemic stroke patients with and without diabetes. 2310 57

Oxidative stress has been reported to be involved in the onset and development of amyotrophic lateral sclerosis (ALS). Data from clinical studies have highlighted increased peripheral blood oxidative stress markers in patients with ALS, but results are inconsistent. Therefore, we quantitatively pooled data on levels of blood oxidative stress markers in ALS patients from the literature using a meta-analytic technique. A systematic search was performed on PubMed and Web of Science, and we included studies analyzing blood oxidative stress marker levels in patients with ALS and normal controls. We included 41 studies with 4,588 ALS patients and 6,344 control subjects, and 15 oxidative stress marker levels were subjected to random-effects meta-analysis. The results demonstrated that malondialdehyde (Hedges' g, 1.168; 95% CI, 0.812 to 1.523; P < 0.001), 8-hydroxyguanosine (Hedges' g, 2.194; 95% CI, 0.554 to 3.835; P = 0.009), and Advanced Oxidation Protein Product (Hedges' g, 0.555; 95% CI, 0.317 to 0.792; P < 0.001) levels were significantly increased in patients with ALS when compared with control subjects. Uric acid (Hedges' g, -0.798; 95% CI, -1.117 to -0.479; P < 0.001) and glutathione (Hedges' g, -1.636; 95% CI, -3.020 to -0.252; P = 0.02) levels were significantly reduced in ALS patients. In contrast, blood Cu, superoxide dismutase, glutathione peroxidase, ceruloplasmin, triglycerides, total cholesterol, low-density lipoprotein, high-density lipoprotein, coenzyme-Q10, and transferrin levels were not significantly different between cases and controls. Taken together, our results showed significantly increased blood levels of 8-hydroxyguanosine, malondialdehyde, and Advanced Oxidation Protein Product and decreased glutathione and uric acid levels in the peripheral blood of ALS patients. This meta-analysis helps to clarify the oxidative stress marker profile in ALS patients, supporting the hypothesis that oxidative stress is a central component underpinning ALS pathogenesis.
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PMID:Aberrations in Oxidative Stress Markers in Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-Analysis. 3128 67