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PubMed2003

Copper exposure and potential biomarkers of copper metabolism.

Relevant biological effects associated with mild to moderate copper deficiency and copper excess are unknown. It is difficult to identify markers of these early changes because limits of the homeostatic range are still undefined and early changes may represent adaptive responses that do not imply necessarily risk of damage. We report here a series of studies carried out to shed light on the responses within the homeostatic range, by assessing classic parameters of copper status in humans at different copper exposure. In adult healthy volunteers that had an estimated daily intake of 0.9 mg Cu/day (approximately 15 microg/kg/d), exposure to additional 50-60 microg of copper/kg/day for three months or up to 150 microg/kg/d for two months resulted in no significant changes of SOD activity in erythrocytes, of copper concentration (in serum, erythrocytes and mononuclear cells) and of serum ceruloplasmin (ANOVA). Neither were found differences by gender or age. As in previous studies in infants, the non-ceruloplasmin copper fraction was positively correlated to serum copper (r = 0.58). Assessing variations on copper absorption, infants supplemented/not supplemented with oral copper (80 ug/kg/14 days), at age 1 and 3 months, showed copper absorption close to 80% at both ages; no effect was observed for age or supplementation, suggesting that either these concentrations do not elicit regulatory mechanisms or that at this age down regulation for copper absorption is not efficient. These studies indicate that in the range of the copper homeostasis area the markers tested are not suitable to detect mild changes (within the homeostatic range) of copper metabolism.

Animals↗
PubMed1994

Regional specificity in alterations of rat brain copper and catecholamines following perinatal copper deficiency.

Perinatal copper deficiency was studied in 1-month-old female and male Sprague-Dawley rat offspring to investigate regional changes in brain copper and catecholamine levels. Offspring of dams given the low copper treatment beginning at day 7 of gestation exhibited signs characteristic of deficiency such as impaired growth and 10-fold lower liver copper levels compared with copper-adequate controls. Regional analysis of brain copper by graphite furnace atomic absorption spectroscopy revealed uniform and severe reduction of copper to levels 20 +/- 3% of controls in all regions, except the hypothalamus, where reductions to 56 and 28% of those in copper-adequate females and males, respectively, were measured. HPLC analysis revealed significant reductions in norepinephrine levels in cerebrum, mid-brain, corpus striatum, cerebellum, and medulla-pons of copper-deficient offspring ranging between 39 and 67% of control values. There were no significant differences in norepinephrine concentration in the hypothalamus. There was a significant, one-third reduction of dopamine in the corpus striatum of copper-deficient male rats. Consistent with altered in vivo dopamine beta-monooxygenase activity, there were five-, three-, and twofold elevations of dopamine in cerebellum, medulla-pons, and hypothalamus of copper-deficient rats. Spectrophotometric measurement of in vitro dopamine beta-monooxygenase activity of brain and adrenal homogenates was higher in copper-deficient rats, confirming prior work. An explanation for the in vitro data is unclear. Changes in copper and catecholamine levels were influenced by diet and were regionally selective, especially in the hypothalamus.

Adrenal Glands↗
PubMed2003

A labile regulatory copper ion lies near the T1 copper site in the multicopper oxidase CueO.

CueO, a multicopper oxidase, is part of the copper-regulatory cue operon in Escherichia coli, is expressed under conditions of copper stress and shows enhanced oxidase activity when additional copper is present. The 1.7-A resolution structure of a crystal soaked in CuCl2 reveals a Cu(II) ion bound to the protein 7.5 A from the T1 copper site in a region rich in methionine residues. The trigonal bipyramidal coordination sphere is unusual, containing two methionine sulfur atoms, two aspartate carboxylate oxygen atoms, and a water molecule. Asp-439 both ligates the labile copper and hydrogen-bonds to His-443, which ligates the T1 copper. This arrangement may mediate electron transfer from substrates to the T1 copper. Mutation of residues bound to the labile copper results in loss of oxidase activity and of copper tolerance, confirming a regulatory role for this site. The methionine-rich portion of the protein, which is similar to that of other proteins involved in copper homeostasis, does not display additional copper binding. The type 3 copper atoms of the trinuclear cluster in the structure are bridged by a chloride ion that completes a square planar coordination sphere for the T2 copper atom but does not affect oxidase activity.

Base Sequence↗
PubMed2006

Mechanisms of the copper-dependent turnover of the copper chaperone for superoxide dismutase.

The copper chaperone for superoxide dismutase (CCS) is an intracellular metallochaperone required for incorporation of copper into the essential antioxidant enzyme copper/zinc superoxide dismutase (SOD1). Nutritional studies have revealed that the abundance of CCS is inversely proportional to the dietary and tissue copper content. To determine the mechanisms of copper-dependent regulation of CCS, copper incorporation into SOD1 and SOD1 enzymatic activity as well as CCS abundance and half-life were determined after metabolic labeling of CCS-/- fibroblasts transfected with wild-type or mutant CCS. Wild-type CCS restored SOD1 activity in CCS-/- fibroblasts, and the abundance of this chaperone in these cells was inversely proportional to the copper content of the media, indicating that copper-dependent regulation of CCS is entirely post-translational. Although mutational studies demonstrated no role for CCS Domain I in this copper-dependent regulation, similar analysis of the CXC motif in Domain III revealed a critical role for these cysteine residues in mediating copper-dependent turnover of CCS. Further mutational studies revealed that this CXC-dependent copper-mediated turnover of CCS is independent of the mechanisms of delivery of copper to SOD1 including CCS-SOD1 interaction. Taken together these data demonstrate a mechanism determining the abundance of CCS that is competitive with the process of copper delivery to SOD1, revealing a unique post-translational component of intracellular copper homeostasis.

Animals↗
PubMed1998

Copper intake and assessment of copper status.

The diagnosis of marginal copper deficiency has not been perfected despite an increased understanding of the physiologic roles of copper. The use of nonstandardized procedures and the effects of factors other than copper nutriture have impeded identification of an ideal indicator of copper nutritional status in humans. A review of studies of experimental copper deprivation conducted in adult humans over the past 12 y indicated that between 1.0 and 1.25 mg Cu/d is needed by adults for copper maintenance for periods of up to 6 mo and that < or = 2.6 mg Cu/d for periods of up to 42 d is not sufficient for recovery from copper deprivation. Copper-containing enzymes in blood cells, such as erythrocyte superoxide dismutase and platelet cytochrome-c oxidase, may be better indicators of metabolically active copper and copper stores than plasma concentrations of copper or ceruloplasmin because the enzyme activities are sensitive to changes in copper stores and are not as sensitive to factors not related to copper nutriture.

Adult↗
PubMed2005

Long-term high copper intake: effects on copper absorption, retention, and homeostasis in men.

BACKGROUND: Numerous studies have examined the effect of low and adequate intakes of copper on absorption and retention, but little information is available on the regulation of absorption and retention of copper when intake is high. OBJECTIVE: A study was conducted in men to determine the effect of long-term high copper intake on copper absorption, retention, and homeostasis. DESIGN: Nine men were confined to a metabolic research unit (MRU) for 18 d and were fed a 3-d rotating menu containing an average of 1.6 mg Cu/d. They continued the study under free-living conditions for 129 d, supplementing their usual diets with 7 mg Cu/d. They then returned to the MRU for 18 d and consumed the same diet as during the first period, except that copper intake was 7.8 mg/d. The stable isotope (63)Cu was fed to 3 subjects and infused into the other 6 on day 7 of each MRU period, and complete urine and stool collections were made throughout the study. Total copper and (63)Cu were determined by inductively coupled plasma mass spectrometry. Copper absorption, excretion, and retention were calculated on the basis of dietary, urinary, and fecal copper and (63)Cu. RESULTS: Results were as follows when comparing the high copper intake with the usual intake: fractional copper absorption was significantly lower, but the amount absorbed was significantly higher; excretion of the infused (63)Cu was significantly faster; and total retention was significantly higher. CONCLUSIONS: Homeostatic regulation of copper absorption and retention helped to minimize the amount of copper retained with high copper intake but was not sufficient to prevent retention of >0.6 mg Cu/d.

Administration, Oral↗
PubMed1992

Copper as a cofactor and regulator of copper,zinc superoxide dismutase.

Copper,zinc superoxide dismutase (CuZnSOD), an antioxidant enzyme, is unique in requiring two essential metals for catalytic function. Yet, only one, copper, seems to regulate the expression of functional activity. Restricting dietary copper quickly impairs catalytic functioning of CuZnSOD in numerous tissues. Diets supplemented with copper or small amounts of CuCl2 administered intraperitoneally restore the enzyme activity in animals deprived of copper. Thus, CuZnSOD has been considered a good marker of copper status. A metal-free (apo) form of CuZnSOD could exist in tissues at all times, but especially when an animal is deprived of copper. Restoring CuZnSOD activity with copper permits elucidation of the pathway of copper incorporation into the enzyme. Ceruloplasmin and albumin transport copper to the enzyme in vitro. K562 cells, a human erythroleukemic cell line, can extract copper from ceruloplasmin and incorporate it into CuZnSOD. Ascorbic acid stimulates the transfer of 67Cu transfer from ceruloplasmin to the cells, and somewhat unexpectedly, appears to restrict the amount of transferred copper that becomes bound to the enzyme. Reactivation of CuZnSOD in healthy individuals has the potential of being a useful tool for assessing copper status. This approach has merit, but one must consider that the levels of apo-enzyme that prevail in tissue could be influenced by other metals.

Animals↗
PubMed2000

Changes in liver copper concentration of thoroughbred foals from birth to 160 days of age and the effect of prenatal copper supplementation of their dams.

OBJECTIVES: To monitor the change in liver copper concentration of Thoroughbred foals from birth to 160 days of age and to determine the effects of supplementation by two injections of copper edetate given to dams in late gestation on the liver copper concentration of their foals at birth. PROCEDURE: Ten mares pregnant to the same stallion were randomised into two groups on the basis of age, liver copper concentration and expected foaling date. The treatment group mares were given 100 mg and 250 mg copper edetate intramuscularly during the ninth and tenth months of gestation respectively. Foals had liver biopsies taken weekly in the first month of life, then monthly for four months. Foals were euthanased at 160 days of age; liver samples were taken and the copper concentrations were determined. RESULTS: Two distinct patterns of age dependent decline in liver copper concentration were evident. The mean (+/- SD) liver copper concentration of the foals was high at birth (374 +/- 130 mg/kg DM), and for seven it declined to adult values by 160 days of age (21 +/- 6 mg/kg DM). In three foals the decline was at a slower rate than in the other seven and at 160 days of age the mean concentration was 162 +/- 32 mg/kg DM. Repeated measures analysis showed significant differences between each biopsy (P < 0.01) and between 'normal' and 'accumulator' foals (P < 0.002). Copper injections given to mares in late pregnancy had no effect on the liver copper concentration of foals at birth. CONCLUSIONS: The significance of the two patterns of age dependant decline in liver copper concentration is unknown. Parenteral copper supplementation of the dam in late gestation had no effect on the liver copper concentration of the foal at birth.

Aging↗
PubMed1990

Copper-induced production of copper-binding supernatant proteins by the marine bacterium Vibrio alginolyticus.

Growth of the marine bacterium Vibrio alginolyticus is temporarily inhibited by micromolar levels of copper. During the copper-induced lag phase, supernatant compounds which complex and detoxify copper are produced. In this study two copper-inducible supernatant proteins having molecular masses of ca. 21 and 19 kilodaltons (CuBP1 and CuBP2) were identified; these proteins were, respectively, 25 and 46 times amplified in supernatants of copper-challenged cultures compared with controls. Experiments in which chloramphenicol was added to cultures indicated that there was de novo synthesis of these proteins in response to copper. When supernatants were separated by gel permeation chromatography, CuBP1 and CuBP2 coeluted with a copper-induced peak in copper-binding activity. CuBP1 and CuBP2 from whole supernatants were concentrated and partially purified by using a copper-charged immobilized metal ion affinity chromatography column, confirming the affinity of these proteins for copper. A comparison of cell pellets and supernatants demonstrated that CuBP1 was more concentrated in supernatants than in cells. Our data are consistent with a model for a novel mechanism of copper detoxification in which excretion of copper-binding protein is induced by copper.

Carrier Proteins↗
PubMed2002

Effects of copper supplementation on the copper status of peripartum beef cows and their calves.

The effects of copper supplementation on the copper status of 40 late-pregnant Aubrac beef cows grazing a copper-deficient pasture and later fed a marginally deficient diet were studied for five months. They were divided into four equal groups; the control group received no copper supplement, groups 1 and 2 received copper as copper sulphate at 10 and 30 mg/kg of diet dry matter (DM), respectively, for five months, and group 3 received 120 mg/kg of diet dry matter for 10 days. Plasma copper concentration and the activity of erythrocyte superoxide dismutase (eSOD) were measured at the beginning of the experiment, in the cows and calves during weeks 1 and 3 after calving, and in the calves before they were turned out to pasture at a mean (sd) age of 51 (26) days. In spite of the low dietary copper content (4.2 mg/kg of DM), the plasma copper concentration of the control cows increased during the winter. All the copper supplements resulted in normal and similar plasma copper concentrations in the cows after calving, but the concentration decreased slightly between weeks 1 and 3 after calving in the group supplemented for 10 days. The treatments did not affect the eSOD of the cows. The calves born to the four groups showed the same patterns of plasma copper and eSOD. Compared with the cows, the calves had low plasma copper concentrations at week 1 and values in the normal range at week 3; their eSOD was high at weeks 1 and 3 but decreased after week 3.

Administration, Oral↗
PubMed2005

Effects of copper on bone component in the femoral tissues of rats: anabolic effect of zinc is weakened by copper.

The effects of copper on biochemical components in the femoral-diaphyseal (cortical bone) and -metaphyseal (trabecullar bone) tissues of rats in vivo and in vitro were investigated. Rats were orally administered copper sulfate (50, 100, or 200 microg Cu/100 g body weight) once daily for 7 d. Calcium content in the diaphyseal and metaphyseal tissues was significantly decreased with the administration of copper (200 microg/100 g), while alkaline phosphatase activity in these tissues was not significantly changed by copper administration. The diaphyseal DNA content was significantly decreased with the administration of copper (50, 100, or 200 microg/100 g). Moreover, the femoral-diaphyseal and -metaphyseal tissues were cultured for 48 h in serum-free medium containing either vehicle or copper (10(-7) - 10(-4) M). Culture with copper (10(-7) - 10(-4) M) caused a significant decrease in alkaline phosphatase activity in the diaphyseal and metaphyseal tissues, while calcium and DNA contents in these tissues were not significantly changed. Culture with parathyroid hormone [PTH (1-34); 10(-7) M], a bone-resorbing factor, caused a significant decrease in calcium content in the diaphyseal and metaphyseal tissues. This decrease was completely inhibited in the presence of copper (10(-6) or 10(-5) M). Culture with zinc sulfate (10(-4) M) caused a significant increase in calcium content and alkaline phosphatase activity in the diaphyseal and metaphyseal tissues. The effects of zinc (10(-4) M) in increasing femoral calcium content and alkaline phosphatase activity were not seen in the presence of cycloheximide (10(-6) M), an inhibitor of protein synthesis, suggesting that the effects of zinc are involved in newly synthesized protein components. The effects of zinc in increasing calcium content and alkaline phosphatase activity in the diaphyseal and metaphyseal tissues were significantly weakened in the presence of copper (10(-4) M). The inhibitory effects of copper were further enhanced in the presence of cycloheximide. This study demonstrates that supplementation with copper in adequate copper nutrition does not have anabolic effects on bone components in vivo and in vitro and that copper weakens the anabolic effects of zinc in vitro.

Administration, Oral↗
PubMed2000

Comparative efficacy of several potential treatments for copper mobilization in copper-overloaded rats.

D-Penicillamine (DPA) is effective in the treatment of Wilson's disease, whereas zinc salts are also used as a therapy for this disorder of copper transport. Recently, it has been shown that the copper chelators 1,4,7,11-tetraazaundecane tetrahydrochloride (TAUD) and tetraethylenepentamine pentahydrochloride (TETREN) could be useful for copper mobilization in rats. Because these agents could be potential clinical alternatives to DPA for patients with Wilson's disease who are intolerant to this drug, we examined whether oral administration of TAUD and TETREN could be effective in mobilizing copper in experimental copper-overloaded rats. The efficacy of a combined administration of zinc and DPA, TAUD, or TETREN was also assessed. Rats were copper loaded with 0.125% copper acetate in water for 12 wk. After this period, DPA, TAUD, and TETREN were administered by gavage at 0.67 mmol/kg/d for 5 d, and zinc was given at 2.5 mg Zn/kg/d. Twelve weeks of copper loading resulted in a 32-fold increase in total hepatic copper. TETREN was the most effective chelator in increasing the urinary excretion of copper. However, it did not reduce significantly the hepatic copper levels. In turn, combined administration of zinc and chelating agents significantly reduced the amount of copper found in the feces. Although TAUD and TETREN showed a similar or higher efficacy to DPA in mobilizing copper, concurrent treatment of chelating agents and zinc salts should be discarded according to the current results.

Animals↗
PubMed2002

Excessive hepatic copper accumulation in jaundiced rats fed a high-copper diet.

The response of copper metabolism to dietary copper challenge was investigated in jaundiced rats with elevated plasma concentrations of conjugated bilirubin as a result of impaired canicular transport of bilirubin glucuronides. Control and jaundiced rats were fed purified diets with either normal (64 micromol Cu/kg) or high (640 micromol Cu/kg) concentration of added copper. Copper loading produced a greater increase in hepatic copper concentrations in the jaundiced than in control rats. The greater dietary-copper-induced increase in hepatic copper in the jaundiced rats can be explained by the observed smaller rise in biliary copper excretion and a greater efficiency of dietary copper absorption. In individual rats, there was a positive relationship between hepatic copper concentrations and biliary copper concentrations. It is suggested that not the transport of copper from liver cells to bile but that from plasma to bile is diminished in the jaundiced rats. The elevated plasma copper concentrations in the jaundiced rats may support this suggestion.

Animal Feed↗
PubMed1989

Cellular mechanisms of toxicity and tolerance in the copper-loaded rat. III. Ultrastructural changes and copper localization in the kidney.

The distribution of copper and related changes have been studied in copper-loaded rat kidneys at the ultrastructural level by X-ray electron probe microanalysis, in order to clarify the pathogenesis of copper-induced damage and subsequent recovery in this organ. Male rats fed a high copper diet (1500 ppm) for 16 weeks were killed at intervals; their kidneys were removed and portions of kidney cortex fixed in 4% paraformaldehyde and 2% glutaraldehyde for electron microscopy: other samples were analysed for copper by AA spectrophotometry. Increasing copper accumulation was associated with progressive PCT cell disarray and characterized by irreversible nuclear damage coincident with the intranuclear accumulation of Cu, S, P, and Ca. Copper was also identified within structurally intact lysosomes associated with Zn and Fe (Type I lysosomes) or P and S (Type II lysosomes, putative Cu-MT). Subsequent copper decline and tubular recovery was associated with the facilitated lysosomal sequestration of copper and excretion of copper-containing cell products into the tubule lumina, Cu-MT and alpha-2 urinary protein-copper. The cytotoxicity of copper in the kidney, as well as the liver, is associated primarily with irreversible nuclear damage, whereas lysosomal copper sequestration protects the cell from injury.

Animals↗
PubMed2003

Liveweight gain and copper status of young deer treated or untreated with copper oxide wire particles on ten deer farms in Canterbury.

AIMS: To measure the liveweight response of young deer to copper supplementation on a range of deer farms in the Canterbury region of the South Island, New Zealand, and relate any response to plasma copper concentration. METHODS: On each of 10 farms throughout north and mid-Canterbury, young deer (4-7 months old) were allocated by liveweight to two groups of 45-50. The deer in one group each received 5 g copper oxide wire particles (COWP) at the start of the project (March-June 2000) and a further 10 g COWP 3 months later (+Cu group), while the other group received no copper supplementation (-Cu group). Liveweight (+/-1 kg) of all deer was recorded monthly. A 10 ml blood sample was taken from a sub-sample of 10 animals in each group at the beginning of the trial and from the same animals 3 and 6 months later for measurement of plasma copper concentration. RESULTS: There was no significant effect (p=0.96) of treatment with COWP on liveweight gain (overall mean liveweight gain = 169 g/day). This result was consistent for all farms and for both periods. Mean plasma copper concentration declined from 12.5 (SD 3.4) to 10.3 (SD 3.0) micromol/l in +Cu groups, and to a significantly lower level (p<0.001) of 8.6 (SD 3.2) in -Cu groups after 3 months, at which time 38% of -Cu animals were considered hypocupraemic (<8 micromol/l). At the end of the second 3-month period there was no significant treatment effect on plasma copper concentration, which averaged 9.4 (SD 2.3) micromol/l. Of the feed samples submitted (n=46), only 17% had a copper concentration <5.0 mg/kg dry matter (DM), 13% had a molybdenum concentration >1.0 mg/kg, and 21% had a sulphur content >3.5 g/kg. CONCLUSIONS: Under the conditions of these trials, no response in liveweight gain to copper supplementation was observed despite evidence of hypocupraemia in 38% of -Cu animals, which gained weight at similar rates to those that had adequate plasma copper levels. The extent of the hypocupraemia was either not sufficiently severe, or not maintained for a long enough period to cause copper deficiency resulting in reduced liveweight gain. No other signs of copper deficiency were evident. There is scope for deer farmers to reassess the need for copper supplementation in young deer.

Journal Article↗
PubMed1992

Accumulation of copper and other metals by copper-resistant plant-pathogenic and saprophytic pseudomonads.

Copper-resistant strains of Pseudomonas syringae carrying the cop operon produce periplasmic copper-binding proteins, and this sequestration outside the cytoplasm has been proposed as a resistance mechanism. In this study, strain PS61 of P. syringae carrying the cloned cop operon accumulated more total cellular copper than without the operon. Several other copper-resistant pseudomonads with homology to cop were isolated from plants, and these bacteria also accumulated copper. Two highly resistant species accumulated up to 115 to 120 mg of copper per g (dry weight) of cells. P. putida 08891 was more resistant to several metals than P. syringae pv. tomato PT23, but this increased resistance was not correlated with an increased accumulation of metals other than copper. Several metals were accumulated by both PT23 and P. putida, but when copper was added to induce the cop operon, there was generally no increase of accumulation of the other metals, suggesting that the cop operon does not contribute to accumulation of these other metals. The exceptions were aluminum for PT23 and iron for P. putida, which accumulated to higher levels when copper was added to the cultures. The results of this study support the role of copper sequestration in the copper resistance mechanism of P. syringae and suggest that this mechanism is common to several copper-resistant Pseudomonas species found on plants to which antimicrobial copper compounds are applied for plant disease control.

Journal Article↗
PubMed2005

Differential expression of copper-associated and oxidative stress related proteins in a new variant of copper toxicosis in Doberman pinschers.

BACKGROUND: The role of copper accumulation in the onset of hepatitis is still unclear. Therefore, we investigated a spontaneous disease model of primary copper-toxicosis in Doberman pinschers so to gain insights into the pathophysiology of copper toxicosis, namely on genes involved in copper metabolism and reactive oxygen species (ROS) defences. RESULTS: We used quantitative real-time PCR to determine differentially expressed genes within a target panel, investigating different groups ranging from copper-associated subclinical hepatitis (CASH) to a clinical chronic hepatitis with high hepatic copper concentrations (Doberman hepatitis, DH). Furthermore, a non-copper associated subclinical hepatitis group (N-CASH) with normal hepatic copper concentrations was added as a control. Most mRNA levels of proteins involved in copper binding, transport, and excretion were around control values in the N-CASH and CASH group. In contrast, many of these (including ATP7A, ATP7B, ceruloplasmin, and metallothionein) were significantly reduced in the DH group. Measurements on defences against oxidative stress showed a decrease in gene-expression of superoxide dismutase 1 and catalase in both groups with high copper. Moreover, the anti-oxidative glutathione molecule was clearly reduced in the DH group. CONCLUSION: In the DH group the expression of gene products involved in copper efflux was significantly reduced, which might explain the high hepatic copper levels in this disease. ROS defences were most likely impaired in the CASH and DH group. Overall, this study describes a new variant of primary copper toxicosis and could provide a molecular basis for equating future treatments in dog and in man.

Journal Article↗
PubMed2003

Characterization of copper in uterine fluids of patients who use the copper T-380A intrauterine device.

BACKGROUND: The copper intrauterine device (IUD) is a highly effective method of contraception that requires the dissolution of the copper into uterine cavity. However, there is little information about the amount and form of copper in the fluid and whether the presence of this element produces any change in the protein concentration. METHODS: Twenty-seven women were divided into three groups that had used IUD for about 6 months, 1 year and > or =3 years. The samples were collected during the proliferative phase (Pp), secretory phase (Sp) and menstruation (M). Square-wave anodic stripping voltammetry (SWASV), cyclic voltammetry (CV), high performance liquid chromatography (HPLC) and atomic absorption spectrometry (AAS) were used in this study. RESULTS: Total copper concentrations were between 3.9 and 19.1 micro g/ml. The mean and standard deviations were as follows: 6 months, 11.4+/-4.7 micro g/ml of copper; 1 year, 11.5+/-7.0 micro g/ml of copper; and 3 years, 6.2+/-1.5 micro g/ml of copper. Total proteins were quantified by measuring the area under the chromatographic peaks. The mean areas obtained with uterine fluid samples from women who used IUDs for 6 months, 1 year and 3 years were 290,013, 538,934 and 201,863 arbitrary units (AU), respectively. The control sample was only 22323. CONCLUSIONS: The amount of copper released from IUD, although high, is in the form of complexes with proteins. IUDs have a constant copper release for at least 6-12 months. Copper(I) was not detected in the fluid. Copper induces a change in the total protein concentration. The amount of copper released and the amount of proteins is slightly larger during the menstrual stage.

Body Fluids↗