Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Estrogen effects on plasma iron and ferroxidase activity in some mammals and domestic fowl are studied, to investigate a possible estrogen mechanism on iron through its action on the ferroxidase system. Although estrogen generally induces ceruloplasmin, iron mobilization, characterized by a rise in plasma iron, was evident only in rats and chickens. Gonadotrophin treatment confirmed these results. A decreasing affect on plasma iron was noted in rabbits and guinea-pigs, substantiated by some bibliographical data. Ferroxidase activity increased and a copper-dependent factor was evident in copper injected species. Iron mobilization, however, was produced only in rats and chickens. D-penicillamine treatment considerably lowered ferroxidase activity in rats and suppressed the estradiol increasing plasma iron effect. This response to the copper-chelating drug did not take place in the other species. This phenomenon could be explained by the presence of two copper-dependent ferroxidases (ferroxidase I or ceruloplasmin and ferroxidase II) in rat plasma, as recently published.
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PMID:The serum ferroxidase system and the effect of estrogen on plasma iron. 93 20

Alterations of estrogen-inducible hepatic proteins and estrogen receptor proteins were studied in female rats after daily oral administration of vehicle control (0.5% carboxymethylcellulose), the nonsteroidal antiestrogens tamoxifen (TAM; 3, 11, or 45 mg/kg body weight), toremifene (TOR; 3, 12, or 48 mg/kg body weight), or the potent synthetic estrogen diethylstilbestrol (DES; 10 mg/kg body weight) for 1 and 3 months. Serum corticosterone levels were significantly reduced by TAM 11, TOR 12, and DES at 1 month and by TOR 48 and DES at 3 months. Serum ceruloplasmin levels were unchanged at 1 month except for a significant reduction with TOR 48 and a significant increase in the DES-treated group. After 3 months, all doses of TAM and TOR had significant reductions whereas DES had elevations even greater than those at 1 month. The activity of the enzyme alanine aminotransferase in the liver was increased by TAM, TOR, and DES at 1 and 3 months of treatment. Both TAM and TOR caused a slight reduction in cytosolic estrogen receptor protein after 1 month and significant reductions at 3 months. The nuclear estrogen receptor (nER) protein levels were significantly increased at 1 and 3 months for TAM and TOR; whereas DES treatment resulted in nER levels no different than controls. In summary, chronic (up to 3 months) administration of TAM and TOR results in qualitatively and quantitatively similar hormone-related effects on the female rat liver. Thus, other mechanisms must be investigated to ascertain the hepatoproliferative differences seen with TAM administration but not with TOR.
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PMID:The effects of diethylstilbestrol, tamoxifen, and toremifene on estrogen-inducible hepatic proteins and estrogen receptor proteins in female rats. 153 64

Sera were sampled from 83 people (pre- and post-menopausal women and men). Climacteric symptoms of 23 women were treated with conjugated estrogen. Sera were sampled serially until the 21st day of estrogen administration. Serum concentrations of 40 protein components were measured by micro single radial immunodiffusion. The serum proteins were classified into 5 types according to changes after menopause and estrogen therapy, respectively. Type 1 (decreased after menopause and increased by estrogen; alpha 1-antitrypsin, alpha 2-HS - glycoprotein, beta 2-glycoprotein III, Gc-globulin, alpha 1-lipoprotein and alpha 2-AP-glycoprotein), type 2 (unchanged and increased; ceruloplasmin), type 3 (increased and decreased; alpha 1-acid glycoprotein, haptoglobin, serum amyloid P-component, Zn-alpha 2-glycoprotein, beta-lipoprotein and C1-components), type 4 (unchanged and decreased; hemopexin, antithrombin III, beta 2-glycoprotein I, prealbumin and retinol-binding-protein), type 5 (unchanged by estrogen; immunoglobulin M (IgM), IgG and others). Estrogen replacement therapy restored pre-menopausal levels of serum proteins, types 1 and 3. However, estrogen therapy was associated with significantly abnormal levels of proteins, types 2 and 4 in post-menopausal women. Serum levels of type 1 proteins and some type 5 proteins (IgM, alpha 1B-glycoprotein, C9-component and alpha 2-macroglobulin) were higher in pre-menopausal women than in men, whereas type 3 proteins were the opposite.
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PMID:Changes in 40 serum proteins of post-menopausal women. 186 40

Estrogen along with progestogen is the most widely used form of contraceptive by women. Its use in any dose, form or route has been shown to increase serum copper and ceruloplasmin levels in humans and rats. However, its effect on plasma zinc levels is not established unequivocally. We demonstrated in female Long-Evans-Hooded rats that 4 weeks after implantation with 17 beta-estradiol their serum copper and ceruloplasmin and brain copper levels increased while hepatic copper levels decreased significantly. Kidney copper levels increased transitorily after 2 weeks but not after 4 weeks. Zinc levels were affected only in the liver of these animals. It may be concluded that estrogen therapy depletes hepatic stores of these elements with abnormal accumulation of copper in the brain. Health implications of these changes need further investigation.
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PMID:Effect of estrogen on serum and tissue levels of copper and zinc. 262 84

Certain metabolic effects were investigated in post-menopausal women undergoing oral estrogen replacement therapy for 6 months using various substances. The increases in serum concentration of the estrogen-sensitive proteins, pregnancy zone protein (PZP), and sex hormone binding globulin (SHBG) had very similar and dose-dependent patterns. Ethinyl-estradiol was found to be much more potent than the "natural" estrogens. Estriol in various doses did not increase the protein level. Gonadotropin inhibition occurred in a dose-dependent manner. In terms of FSH suppression ethinyl-estradiol was approximately 120 times as potent as the "natural" estrogens. There was a striking resemblance between the "estrogenicity" of four different estrogens when expressed both in inhibition of gonadotropins and in induction of the two serum proteins SHBG and ceruloplasmin. Estriol caused a significant depression of FSH when given orally in a dose of 2 mg three times daily. Prolactin was found to decrease during treatment with low doses of estrogens. Estrogen therapy was found to have only moderate effects on adrenal androgens. Tamoxifen, and anti-estrogen, was found to exert distinctly estrogenic effects during treatment of post-menopausal women. In post-menopausal women with low amounts of circulating estrogens the tamoxifen-receptor complex itself may produce a net estrogenic response. Serum samples from post-menopausal women treated with ethinyl estradiol 0.05 mg and estrone sulphate 2.5 mg daily were found to reduce the lymphocyte reactivity in mixed lymphocyte cultures.
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PMID:Estrogen replacement therapy after the menopause. Estrogenicity and metabolic effects. 628 33

Hematological values, metal content (Fe, Cu, Zn, Cd) in plasma and liver, ceruloplasmin (p-phenylendiamine oxidase) and ferroxidase activity in plasma, were analyzed in chicks, fed during 10 weeks on a commercial diet, supplemented by either 5,000 ppm Zn or 100 ppm Cd. A microcytic and hypochromic anemia was evident in both groups but in the Cd-fed chicks, plasma iron and ceruloplasmin values were normal. Estrogen administration mobilized iron in the Cd-group but not in the Zn-group. The precipitation of plasma phosvitin reduced (90%) the ferroxidase activity that had been previously induced by the estrogens. Correcting copper levels in the Zn-group, by copper injection, restored the ceruloplasmin level. However, the estrogens, in such birds, neither mobilized the plasma iron nor increased the ferroxidase activity. Plasma citrate was determined in laying, non-laying hens and in estrogenized or normal males. The contribution of citrate to the ferroxidase activity of plasma during the laying period, was negligible. It was concluded that plasma phosvitin during laying was the main factor responsible for the ferroxidase activity. However, the ceruloplasmin in chickens, could play a secondary role in iron mobilization.
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PMID:Iron mobilization and plasma ferroxidase factors in chickens. 733 37

Boron deprivation experiments with humans have yielded some persuasive findings for the hypothesis that boron is an essential nutrient. In the first nutritional study with humans involving boron, 12 postmenopausal women first were fed a diet that provided 0.25 mg boron/2000 kcal for 119 days, and then were fed the same diet with a boron supplement of 3 mg boron/day for 48 days. The boron supplementation reduced the total plasma concentration of calcium and the urinary excretions of calcium and magnesium, and elevated the serum concentrations of 17 beta-estradiol and testosterone. This study was followed by one in which five men over the age of 45, four postmenopausal women, and five postmenopausal women on estrogen therapy were fed a boron-low diet (0.23 mg/2000 kcal) for 63 days, then fed the same diet supplemented with 3 mg boron/day for 49 days. The diet was low in magnesium (115 mg/2000 kcal) and marginally adequate in copper (1.6 mg/2000 kcal) throughout the study. This experiment found higher erythrocyte superoxide dismutase, serum enzymatic ceruloplasmin, and plasma copper during boron repletion than boron depletion. The design of the most recent experiment was the same as the second study, except this time the diet was adequate in magnesium and copper. Estrogen therapy increased plasma copper and serum 17 beta-estradiol concentrations; the increases were depressed by boron deprivation. Estrogen ingestion also increased serum immunoreactive ceruloplasmin and erythrocyte superoxide dismutase; these variables also were higher during boron repletion than depletion for all subjects, not just those ingesting estrogen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biochemical and physiologic consequences of boron deprivation in humans. 788 83

The effects of estrogen on synthesis and turnover of ceruloplasmin were studied in adult female Fischer rats. Daily treatment with 140 microgram 17 beta-estradiol resulted in a slow rise of ceruloplasmin concentrations, as measured by p-phenylenediamine oxidase activity, leading to a 70% increase by 7 days and a tripling by Day 14. Ceruloplasmin protein concentrations increased to the same degree, based on yields of the protein obtained during purification. Effects of estrogen on rates of synthesis (incorporation of [3H]leucine) were followed, using immunoprecipitation of total ceruloplasmin or isolation of its two major isoforms (Rfs 0.4 and 0.6 in native gel electrophoresis). Synthesis was increased by 7 days and was 2.5 times that of controls by Day 14. Both forms of ceruloplasmin showed the same specific activities and degree of increase in rate of synthesis. Rates of ceruloplasmin turnover were unaffected, based on double labeling with 3H- and 14C-leucine, but were three- to fourfold faster than for total plasma protein. The enzymatically more active 0.6 Rf form of ceruloplasmin had a faster turnover rate than the 0.4 Rf form. Estrogen treatment doubled ceruloplasmin mRNA levels by 7 days and almost tripled them by Day 14. Most of the ceruloplasmin mRNA was associated with the endoplasmic reticulum-bound polyribosomes. We conclude that estrogen increases the rate of synthesis of two forms of ceruloplasmin by indirectly increasing liver concentrations of its mRNA but has no effect on ceruloplasmin turnover.
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PMID:Synthesis and turnover of ceruloplasmin in rats treated with 17 beta-estradiol. 848 41

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