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)

Cervical carcinoma is the second most common cancer worldwide. The extent of free radical induced oxidative stress can be exacerbated by the decreased efficiency of antioxidant defense mechanisms. Low levels of essential antioxidants in the circulation have been found to be associated with an increased risk of cancer. The aim of our study was to assess the extent of oxidative stress, the levels of antioxidants like superoxide dismutase (SOD), catalase (CAT), ceruloplasmin and to evaluate tumor markers such as aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP) and total sialic acid (TSA) levels in circulation of women with cervical carcinoma and to compare our findings with age matched controls. Low levels of SOD and CAT observed in the circulation of cervical cancer patients may be due to their increased utilization to scavenge lipid peroxides as well as sequestration by tumor cells. Higher levels of TSA, AST, ALT and ALP, in the circulation of cervical cancer patients may be used in the diagnosis and treatment monitoring of patients with cervical carcinoma.
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PMID:Oxidative stress and tumor markers in cervical cancer patients. 1497 92

Two hundred and sixteen weanling gilts (6.65+/-0.08 kg) were used to determine the effects of decreasing supplemental concentrations of Zn, Cu, Fe, and Mn, and trace mineral source (inorganic vs. chelated) on growth performance, mineral status, and fecal mineral concentrations from weaning through development. The study was conducted over three trials with 72 pigs in each trial. Gilts were blocked by weight and randomly assigned to either 1) control, 2) reduced inorganic, or 3) reduced chelated trace minerals. The control diet was supplemented with 25, 150, 180, and 60 mg/kg of Cu, Zn, Fe, and Mn (in sulfate forms), respectively, during the nursery phase and 15, 100, 100, and 40 mg/kg of supplemental Cu, Zn, Fe, and Mn, respectively, during the growing and gilt-developer phases. Reduced inorganic and reduced chelated treatments were supplemented during all phases with 5, 25, 25, and 10 mg/kg of Cu, Zn, Fe, and Mn, respectively. The reduced chelated treatment supplied 50% of the supplemental Cu, Zn, Fe, and Mn in the form of metal proteinates, with the remainder from sulfate forms. Performance by control pigs did not differ from pigs fed the reduced trace mineral treatments during the nursery and grower-development periods. Gain:feed was lower (P < 0.05) for pigs fed the reduced inorganic compared with those fed the reduced chelated treatment during the nursery period. Trace mineral source did not affect performance during the growing or gilt-developer phase. Plasma Zn concentration and alkaline phosphatase activity were higher (P < 0.01) in control pigs than in those receiving reduced trace minerals during the nursery and growing phases. Plasma Cu concentration and ceruloplasmin activity were generally not affected by treatment. Hemoglobin concentrations were lower (P < 0.05) for the reduced inorganic compared with the reduced chelated treatment in the nursery phase. Fecal concentrations of Cu, Zn, and Mn were lower (P < 0.05) in pigs fed reduced trace minerals than in controls during all production phases. Fecal Zn concentration during the nursery and fecal Cu concentrations during the growing and gilt-developer phases were lower (P < 0.05) in pigs fed the reduced chelated compared with the reduced inorganic treatment. Results indicate that reducing the concentrations of Zn, Cu, Mn, and Fe typically supplemented to pig diets will greatly decrease fecal mineral excretion without negatively affecting pig performance from weaning through development.
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PMID:Effect of dietary trace mineral concentration and source (inorganic vs. chelated) on performance, mineral status, and fecal mineral excretion in pigs from weaning through finishing. 1530 62

Epidemiological studies have indicated incidences of 32.9% and 27.8% for rickets and osteomalacia, respectively, in Bactrian camels (Camelus bactrianus), but there is an increased incidence under drought conditions, sometimes reaching 75%. We have found that concentrations of phosphorus and copper in forage and soil samples in a drought affected area were significantly lower than in a control area or normal reference values (P < 0.01) ; the mean Ca:P ratio in the forages was 50:1. The phosphorus content of blood and hair from affected camels was significantly less than that in controls (P < 0.01) and concentrations of copper in the liver and kidney were significantly lower in affected camels than control animals (P < 0.01); the concentrations of triiodothyronine (T(3)), thyroxine (T(4)) and parathyroid hormone (PTH) in the serum from affected animals were significantly higher than those from healthy controls (P < 0.01); serum inorganic phosphorus and ceruloplasmin levels were lower than those in the controls (P < 0.01 or P < 0.05); the concentrations of serum alpha-globulin and beta-globulin were significantly higher in the affected camels than in the healthy controls (P < 0.01). The pathological changes seen in camels affected with rickets included porous, brittle, light, osteoporotic bones that were susceptible to fractures and had less resistance to cutting and sawing. Wrist joints were enlarged with an apparent bowing of the long bones in forelimb and with typical broadening of the epiphyses. In adult female camels, many enlarged scars were often seen in ribs indicating earlier fractures. The disease could be cured with supplementary bone meal, phosphate or mineral mixtures and in field investigations clinical signs disappeared within 15 days. Over the same period, the concentrations of phosphorus and alkaline phosphatase in blood returned to normal. The disease may be effectively prevented by use of mineral blocks (block salt licks) or dosing orally with copper, selenium and cobalt soluble glass boluses. We conclude that rickets and osteomalacia are mainly caused by phosphorus and copper deficiencies in the pasture.
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PMID:Studies on rickets and osteomalacia in Bactrian camels (Camelus bactrianus). 1584 87

A survey was conducted in 10 districts of northern India. Significant deficiency of zinc was observed in soil, fodders and (cattle) serum samples. The animals showed typical signs of zinc deficiency, namely stiff gait, swelling of hocks and knees, subcutaneous fluid accumulation, rough coat, etc. of variable intensity. A clustered model therapeutic trial was conducted and zinc-deficient cattle were divided into three groups. Group A was provided with mineral mixture containing zinc sulphate. Group B was given mineral mixture without zinc sulphate and group C was given no mineral mixture. Significant improvement (p < 0.01) was observed in the haemoglobin (Hb), total white blood cells (WBC) and total erythrocyte count (TEC) levels at the 7th day of treatment in the animals of group A. Significant improvement in enzyme serum alkaline phosphatase (SAP) was observed in group A animals at the 7th day, while improvement in asparatate aminotransferase (AST), alanine aminotransferase (ALT) and ceruloplasmin (Cp) was observed after 21 days of treatment. Regarding hormones, significant improvement was observed in thyroxine (T3) and triiodothyronine (T4), oestrogen and progesterone in group A animals within 14 days of treatment. The values of vitamin A showed a highly significant (p < 0.01) improvement within 7 days of treatment in group A animals and that of vitamin E on the 21 st day of treatment. The milk yield of lactating cattle and body weight of growing calves in group A showed highly significant (p < 0.01) increases at about 14 and 30 days, respectively. It is concluded that zinc sulphate supplementation is highly effective in alleviating zinc deficiency and improving various biochemical and production parameters in cattle. The clustered model treatment provides a better indicator of the most limiting element under field conditions where simultaneous deficiency of various minerals is prevalent.
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PMID:Therapeutic efficacy of zinc sulphate used in clustered model treatment in alleviating zinc deficiency in cattle and its effect on hormones, vitamins and production parameters. 1614 8

In the present study we used patient data to calculate laboratory-specific indirect reference intervals. These values were compared with reference intervals obtained for a healthy group according to recommendations of the International Federation of Clinical Chemistry and Laboratory Medicine and manufacturer suggestions. Laboratory results (422,919 records) from all subjects of 18-45 years of age over a 1-year period were retrieved from our laboratory information system and indirect reference intervals for 40 common analytes were estimated using a modified Bhattacharya procedure. Indirect reference intervals for most of the biochemical analytes were comparable, with small differences in lower [alkaline phosphatase (ALP) (male), alanine aminotransferase (ALT), creatine kinase, iron (male), total iron-binding capacity, folic acid, calcium (female), lactate dehydrogenase (LDH), lipoprotein (a) [Lp(a)], thyroid-stimulating hormone (TSH), total triiodothyronine (T(3)), direct bilirubin, apolipoprotein A-I (apoA-I), glucose, homocysteine, total cholesterol, ferritin, total protein, ceruloplasmin, sodium, blood urea nitrogen (BUN) and uric acid (female)] and/or upper limits [albumin, ALP (male), amylase, apoA-I, creatine kinase-MB (CK-MB), total iron-binding capacity, phosphorus, glucose, total cholesterol, gamma-glutamyltransferase (gamma-GT), magnesium, total protein, high-density lipoprotein cholesterol (HDL-C), total T(3), ALP (male), ALT, aspartate aminotransferase (AST) (male), direct bilirubin (male), creatine kinase, iron, folic acid (female), Lp(a), uric acid and triglycerides], to the reference intervals determined for healthy subjects in our laboratory. The indirect reference intervals, with the exception of a few parameters (creatinine, direct total bilirubin, calcium, BUN and potassium), were not similar to the reference intervals suggested by the manufacturers. We conclude that laboratory-specific reference intervals can be determined from stored data with a relatively easy and inexpensive method. Indirect reference intervals derived from stored data may be particularly suitable for the evaluation of results for the presenting population.
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PMID:Use of total patient data for indirect estimation of reference intervals for 40 clinical chemical analytes in Turkey. 1677 35

Estimation of serum copper to indicate copper status in the human system in the context of moderate chronic occupational copper exposure requires a sophisticated and expensive method. Hence, a search for a suitable marker has been made and few studies have found potential in serum ceruloplasmin. In this context, the present study was initiated to explore whether ceruloplasmin could serve as a predictor of occupational copper exposure. An interviewer-administered questionnaire survey (personal, occupational and health-related information) was undertaken involving 185 employees of a copper handling industry. Serum alkaline phosphatase, serum glutamic pyruvic transaminase (SGPT), serum ceruloplasmin and serum copper were estimated in all the subjects. Multivariate analysis was undertaken using a linear regression model to understand the contribution of serum copper on serum ceruloplasmin values adjusting for the role of other confounders. Serum copper and serum ceruloplasmin values were found to have a statistically significant positive correlation (R=0.169, adjusted R(2)=0.024) after adjustment for other predictors like age, nature of job (department), job duration, smoking, serum alkaline phosphatase and SGPT. This study concludes that the serum ceruloplasmin level can act as a reliable indicator of copper status in the human body following copper exposure in cases of chronic moderate occupational exposure to copper.
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PMID:Ceruloplasmin as a marker of occupational copper exposure. 1828 39

Oxidative stress plays a pivotal role in the pathogenesis and progression of gamma-irradiation induced cellular damage and the administration of dietary antioxidants has been suggested to protect against the subsequent tissue damage. Here, we present the data to explore the hepatoprotective and antioxidant effect of hesperidin, a naturally occurring citrus flavanoglycone, against gamma-irradiation induced oxidative damage in the liver of rats. Healthy male Sprague-Dawley rats were exposed to gamma-irradiation (1 Gy, 3 Gy and 5 Gy) and were administered hesperidin (50 mg/kg and 100 mg/kg, b.w, orally) for 7 days post irradiation. The changes in body weight, liver weight, spleen index, serum and liver aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma-glutamyl transpeptidase (gamma-GT) and serum ceruloplasmin levels were determined along with differences in the liver histopathology. Liver thiobarbuturic acid reactive substance as an index for lipid peroxidation and the levels of enzymatic antioxidants like superoxide dismutase, catalase, glutathione peroxidase and the status of non-enzymatic antioxidants as an index for oxidative stress were also determined. Exposure to gamma-irradiation resulted in hepatocellular damage in a dose-dependent manner, featuring a significantly decreased body weight and liver weight and higher levels of serum AST, ALT, ALP, LDH and gamma-GT levels and a simultaneous decrease in their levels in the liver tissue. Oxidative stress was evidenced by elevated levels of lipid peroxidation and a decrease in the levels of key enzymatic and non-enzymatic antioxidants in the liver. However, the gamma-irradiation induced toxic effects were dramatically and dose-dependently inhibited by hesperidin treatment as observed by the restoration in the altered levels of the marker enzymes, lipid peroxidation, enzymatic and non-enzymatic antioxidants. The results of the biochemical observations were supported by the histopathological findings. Thus, oral administration of hesperidin was found to offer protection against gamma-irradiation induced hepatocellular damage and oxidative stress in rats, probably by exerting a protective effect against hepatocellular necrosis via its free radical scavenging and membrane stabilizing ability.
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PMID:Hesperidin a flavanoglycone protects against gamma-irradiation induced hepatocellular damage and oxidative stress in Sprague-Dawley rats. 1848 45

Vascular calcification plays a role in the pathogenesis of atherosclerosis, diabetes, and chronic kidney disease. Human aortic smooth muscle cells (HSMCs) undergo mineralization in response to elevated levels of inorganic phosphate (Pi) in an active and well-regulated process. This process involves increased activity of alkaline phosphatase and increased expression of core binding factor alpha-1, a bone-specific transcription factor, with the subsequent induction of osteocalcin. Mounting evidence suggests an essential role for the heme oxygenase 1 (HO-1)/ferritin system to maintain homeostasis of vascular function. We examined whether induction of HO-1 and ferritin alters mineralization of HSMCs provoked by high Pi. Upregulation of the HO-1/ferritin system inhibited HSMC calcification and osteoblastic differentiation. Of the products of the system, only ferritin and, to a lesser extent, biliverdin were responsible for the inhibition. Ferritin heavy chain and ceruloplasmin, which both possess ferroxidase activity, inhibited calcification; a site-directed mutant of ferritin heavy chain, which lacked ferroxidase activity, failed to inhibit calcification. In addition, osteoblastic transformation of HSMCs provoked by elevated Pi (assessed by upregulation of core binding factor alpha-1, osteocalcin, and alkaline phosphatase activity) was diminished by ferritin/ferroxidase activity. We conclude that induction of the HO-1/ferritin system prevents Pi-mediated calcification and osteoblastic differentiation of human smooth muscle cells mainly via the ferroxidase activity of ferritin.
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PMID:Ferritin prevents calcification and osteoblastic differentiation of vascular smooth muscle cells. 1942 91

Hemochromatosis is a known cause of osteoporosis, and iron overload has deleterious effects on bone. Although iron overload and its association with osteoporosis has long been recognized, the pathogenesis and exact role of iron have been undefined. Bone is an active tissue with constant remodeling capacity. Osteoblast (OB) development and maturation are under the influence of core binding factor alpha-1 (CBF-alpha1), which induces expression of OB-specific genes, including alkaline phosphatase, an important enzyme in early osteogenesis, and osteocalcin, a noncollagenous protein deposited within the osteoid. This study investigates the mechanism by which iron inhibits human OB activity, which in vivo may lead to decreased mineralization, osteopenia, and osteoporosis. We demonstrate that iron-provoked inhibition of OB activity is mediated by ferritin and its ferroxidase activity. We confirm this notion by using purified ferritin H-chain and ceruloplasmin, both known to possess ferroxidase activity that inhibited calcification, whereas a site-directed mutant of ferritin H-chain lacking ferroxidase activity failed to provide any inhibition. Furthermore, we are reporting that such suppression is not restricted to inhibition of calcification, but OB-specific genes such as alkaline phosphatase, osteocalcin, and CBF-alpha1 are all downregulated by ferritin in a dose-responsive manner. This study corroborates that iron decreases mineralization and demonstrates that this suppression is provided by iron-induced upregulation of ferritin. In addition, we conclude that inhibition of OB activity, mineralization, and specific gene expression is attributed to the ferroxidase activity of ferritin.
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PMID:Ferritin ferroxidase activity: a potent inhibitor of osteogenesis. 1982 64

The multifactor outcome of hypoandrogenemia with the impact of oxidative stress induced by glucose intolerance, fascioliasis with or without schistosomiasis and cumulative smoking influence on bone remodeling and the early development of osteoporotic manifestations were studied. The effect on vascular endothelium immune mediated mechanisms and antioxidant capacity were monitored in cases of youth aged selected male smokers involving 20 with hypoandrogenemia who were either subjected to sedentary life style, glucose intolerance fascioliasis hepatic fibrosis (FHF) (G1) or without (G2) and GI after following 6 months therapy (G3). Monitoring of clinical picture and biochemical assessments of osteoporotic indices (osteocolcin, bone alkaline phosphatase, parathyroid hormone, urinary cyclic AMP), hypoandrogenism (dehydroepiandrosterane sulphate or DHEAS & testosterone) glycemic determinant (insulin) immuno-inflammatory response (interleukein-6, tumor necrosis factor alpha, E-selectin, ceruloplasmin) smoking index (serum cotinine), total antioxidant capacity (AOC) and lipid peroxidation (malonedialdehyde) was done before and after 6 months therapeutic program involving supplement of DHEAS, mirazid, chromium picolinate, and megavit zinc alongside smoking cessation and physical exercise daily for at least 30 minutes. Treatment with Mirazid supplied as 10 mg/kg for 6 successive days resulted in 100% cure of fascioliasis whether single or combined with schistosomiasis.
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PMID:Early development of osteoporosis in male smokers with hypoandrogenism due to fascioliasis with or without schistosomiasis added by life style. 2012 Jul 45


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