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PubMed1993

Growth, copper-tolerant cells, and extracellular protein production in copper-stressed chemostat cultures of Vibrio alginolyticus.

The influence of elevated copper concentrations on cell numbers and extracellular protein production was investigated in chemostat cultures of Vibrio alginolyticus. High (20 microM) copper in the medium reservoir resulted in a dramatic drop in cell numbers which was overcome with time. The copper-stressed cultures established a new equilibrium cell concentration slightly (ca. 20%) lower than control cultures. Copper-stressed chemostat populations contained an increased number of copper-resistant cells, but these averaged only 26% of the copper-adapted population. Previously copper-stressed populations exhibited resistance to a second challenge with copper. Proteins with properties identical to those of copper-induced, copper-binding proteins (CuBPs) observed in batch cultures of V. alginolyticus were observed in the supernatants of copper-stressed chemostat cultures and not in controls. CuBPs from batch and chemostat cultures were identical in terms of their induction by copper, molecular weight, and retention volumes on both immobilized copper ion-affinity chromatography and reverse-phase high-performance liquid chromatography columns. The concentration of CuBP in the chemostat was dependent on copper concentration in the medium reservoir. Either one or two forms of CuBP were observed in various analyses from both batch and chemostat cultures. Gel-to-gel variability was implicated as a factor determining whether one or two forms were resolved in a given analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial Proteins↗

PubMed2006

In long-term bedridden elderly patients with dietary copper deficiency, biochemical markers of bone resorption are increased with copper supplementation during 12 weeks.

BACKGROUND: Although the effect of copper on bone has been tested in animals and healthy subjects, no studies concerning the effect of copper supplementation on bone metabolism in patients with copper deficiency have been reported because of the rarity of these patients. This study was conducted to investigate the effect of copper supplementation on bone metabolism in copper-deficient patients. METHOD: This study included 10 patients (83.7 +/- 8.3 years) with dietary copper deficiency under long-term bed rest for more than 12 months. They had their diets supplemented with copper sulfate (3 mg/day) over 12 weeks in addition to their diet of only one kind of enteral food with a low concentration of copper. Serum copper and ceruloplasmin, urinary deoxypyridinoline (DPD) and collagen-type 1 N-telopeptide (NTX) (biomarkers of bone resorption), serum osteocalcin (OC) and bone-specific alkaline phosphatase (Bone ALP) (biomarkers of bone formation) were analyzed at baseline, 4 and 12 weeks after copper supplementation. RESULTS: DPD and NTX excretion were significantly increased 4 weeks after copper supplementation (p = 0.009 and p = 0.013, respectively). Serum bone ALP and OC were not significantly changed 12 weeks after copper supplementation (p = 0.051 and p = 0.594). CONCLUSIONS: In patients with nutritional copper deficiency, bone resorption markers are increased with copper supplementation.

Aged↗

PubMed1991

Influence of hypertension and dietary copper on indexes of copper status in rats.

The Dahl salt-sensitive rat was used to investigate the effect of hypertension on indexes of copper status and to determine the extent to which dietary manipulation of copper attenuated, or exacerbated, the rate of sodium chloride-induced hypertension. Weanling salt-sensitive rats were fed, in a 2 x 3 factorial design, one of six diets that contained one of three levels of copper (2.0 micrograms/g marginal, 12 micrograms/g adequate, or 50 micrograms/g supplemental) and either control (0.4%) or high (4%) levels of sodium. Diets were fed to the rats for 11 weeks. Rats fed the high sodium diets were characterized by high plasma copper concentrations and ceruloplasmin activities compared with their respective control sodium rats. The magnitude of the sodium-induced rise in plasma copper and ceruloplasmin was affected by dietary copper intake; however, dietary copper intake had no effect on the development of hypertension in the high sodium groups. These results suggest that altered copper metabolism is secondary, rather than primary, to the development of sodium chloride-induced hypertension in the salt-sensitive rat. Red blood cell superoxide dismutase activity was reduced in rats fed the low copper diets compared with the adequate and supplemented copper groups. At the lower levels of copper intake, sodium chloride-induced hypertension increased red blood cell superoxide dismutase activity in a manner consistent with the plasma copper and ceruloplasmin changes observed. However, at adequate or supplemental levels of dietary copper, red blood cell superoxide dismutase activity plateaued, suggesting possible saturation of copper at sites of hematopoeisis.

Animals↗

PubMedDate not supplied

Latent copper deficiency in patients receiving low-copper enteral nutrition for a prolonged period.

BACKGROUND: Copper deficiency has been reported in patients supported with long-term enteral nutrition. Occasionally, this leads to anemia and leukopenia. There is no detailed report relating to the onset time of copper deficiency and how the symptoms develop. This report describes the relation between copper deficiency symptoms and duration of enteral nutrition. METHODS: The study included 55 patients, with 82 measurements, at the neurologic ward of Nagoya Daini Red Cross Hospital. The mean age was 71 +/- 11 years. The daily average dosage of energy was 938 kcal/d. A commercial nutrient for enteral administration that contains 0.13 mg/1000 mL copper was used. Baseline measures on individual patients were taken every month. Blood was collected at 8 am before and after the start of enteral nutrition. Levels of copper, zinc, ceruloplasmin, hemoglobin, and white blood cells were measured. RESULTS: The serum level of copper in the patients was 94.0-181.0 microg/dL before the start of enteral nutrition. The level of serum copper remained within the normal range for about 3 months. The level of serum copper in the patients decreased gradually and was less than the normal level after 3 months, with the exception of 1 patient. The serum level of copper in the patients was 3.0-123.0 microg/dL 3 months after the start of enteral nutrition. The levels of serum copper were below normal in 25 cases out of 82 measurements. However, the number of patients with symptoms of copper deficiency was only 2. Copper deficiency symptoms appeared at 41 and 77 months, the average being 59 months. CONCLUSIONS: Almost all patients showed a latent copper deficiency about 3 months after the start of enteral nutrition. However, only a few patients developed overt symptoms of copper deficiency.

Adult↗

PubMed2004

Cu,Zn-superoxide dismutase is lower and copper chaperone CCS is higher in erythrocytes of copper-deficient rats and mice.

Discovery of a sensitive blood biochemical marker of copper status would be valuable for assessing marginal copper intakes. Rodent models were used to investigate whether erythrocyte concentrations of copper,zinc-superoxide dismutase (SOD), and the copper metallochaperone for SOD (CCS) were sensitive to dietary copper changes. Several models of copper deficiency were studied in postweanling male Holtzman rats, male Swiss Webster mice offspring, and both rat and mouse dams. Treatment resulted in variable but significantly altered copper status as evaluated by the presence of anemia, and lower liver copper and higher liver iron concentrations in copper-deficient compared with copper-adequate animals. Associated with this copper deficiency were consistent reductions in immunoreactive SOD and robust enhancements in CCS. In most cases, the ratio of CCS:SOD was several-fold higher in red blood cell extracts from copper-deficient compared with copper-adequate rodents. Determination of red cell CCS:SOD may be useful for assessing copper status of humans.

Animals↗

PubMed1989

Effects of oral copper administration to pregnant heterozygous brindled mice on fetal viability and copper levels.

Copper (6 ppm) was administered to pregnant heterozygous brindled and normal mice from 13 to 18 days gestation. The copper and zinc concentrations in the cerebrum, cerebellum, liver, and kidneys of mothers and their fetuses were determined. The placental concentrations in fetuses of heterozygous mothers administered copper were also determined. The heterozygous mothers had smaller numbers of live fetuses than the normal mothers, but had the same number as normal mothers when copper was administered. The hepatic copper concentration in the heterozygous mothers was lower than that in the normal mothers and was not increased by the administration. The body and tissue wet weights of all fetuses were unaffected by the maternal genotype or drinking fluid. The cerebral copper concentrations in hemizygous and heterozygous fetuses were increased by the copper administration but did not reach normal levels. The hepatic and renal concentrations remained unchanged. The cerebral copper concentrations in normal fetuses of both heterozygous and normal mothers were increased by the copper administration. The copper administration increased the copper concentrations in liver of normal fetuses of heterozygous mothers and in kidneys of normal fetuses of normal mothers. The placental copper concentration in hemizygous fetuses was higher than those in heterozygous and normal fetuses. These results suggested that oral copper administration to pregnant females could improve an abnormal copper distribution in hemizygous and heterozygous fetuses without affecting fetal growth.

Animals↗

PubMed1999

Studies on the influence of the copper content in the drinking water on the newborn copper burden and transaminases activity.

INTRODUCTION: Clinical parameters for the early diagnosis of a potential development of childhood cirrhosis are not available. A cross-section study was performed to investigate whether the serum copper content and the activities of the newborn's glutamic oxalacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) may be associated with the copper contents of the drinking water and/or the maternal serum and thus could serve as early indicator of an elevated health hazard. MATERIAL AND METHODS: The serum concentration of copper was analyzed in samples of 141 mother-newborn pairs. Additionally, in umbilical cord serum the activities of the transaminases GOT and GPT were determined. Low molecular bound or free copper was quantified in 30 randomly chosen serum filtrates. According to questionnaire data, in 62 of the 141 households the drinking water installations consisted of copper. In these cases, the element was analyzed in drinking water. RESULTS: The copper content of the drinking water was found ranging between 0.02 and 2.5 mg Cu/l (median 0.22 mg Cu/l), the maternal serum copper content ranged from 770-3720 micrograms Cu/l (median 2275 micrograms Cu/l), the neonatal serum from 220 to 1930 micrograms Cu/l (median 500 micrograms Cu/l), respectively. GOT (6-33 U/l); median 14 U/l) and GPT (3-21 U/l; median 6 U/l) activities could be judged as reference range data. In the statistical analysis, an association between the copper content of the drinking water and the maternal or neonatal serum copper content could not be found. Pearson regression analysis revealed slight, yet significant correlations of the neonatal GOT and GPT activities with the maternal serum copper content (GPT: r2 = 0.06; p < 0.05; GOT: r2 = 0.05; p < 0.05; each n = 139). In addition, the copper content of the mother's serum filtrates was correlated with the newborns' serum filtrates (Spearman: r = 0.61; p < 0.001; n = 30). CONCLUSIONS: The prenatal copper exposure of the infant could be mainly determined by low molecular or free serum maternal copper, which seems to be able to penetrate the placental barrier easily. The association between maternal serum copper content and neonatal transaminases activity can be judged as clinically not relevant and might be a physiologic response.

Adult↗

PubMed1976

An investigation of the therapeutic value of the 'copper bracelet'-dermal assimilation of copper in arthritic/rheumatoid conditions.

From over 300 arthritis sufferers, half of whom previously wore 'copper bracelets', three treatment-group-subjects were randomly allocated for a psychological study. This involved wearing 'copper bracelets' and placebo bracelets (amodised aluminum resembling copper) alternately. These groups, as also a control group, answered questionnaires. The copper bracelets were weighed before and after use. Preliminary results show that, to a significant number of subjects, the wearing of the 'copper bracelet' appeared to have some therapeutic value. A study of the components of sweat and the solubility of copper in sweat was carried out. In five sweat samples, the copper concentration was of the order 2 x 10(-5) M and after equilibrating with copper turnings at room temperature for 24 hours the samples turned blue in colour and contained approximately 2 x 10(-3) M copper. The permeability of skin to copper containing solutions has also been discussed. It has also been shown that the wearing of a 'copper bracelet' results in a weight loss in excess of the body's total burden of copper (100-150 mg). A pair of copper bracelets lost 80 mg in 50 days when worn around the ankles and a copper bracelet worn around the wrist also lost about 90 mg in that time.

Administration, Topical↗

PubMed1994

Role of cytosolic copper, metallothionein and glutathione in copper toxicity in rat hepatoma tissue culture cells.

Effects of metallothionein (MT) synthesis inhibiting compounds (actinomycin D, cycloheximide), MT synthesis stimulating compounds (dexamethasone, dibu-cAMP) and interfering metals (Cd, Zn) on copper accumulation were investigated in rat hepatoma tissue culture cells. Copper-metallothionein (Cu-MT) and MT-associated copper levels were determined to find a possible correlation between cytosolic copper concentrations and MT as a Cu-detoxifying protein. Further, intracellular non-MT associated copper levels and levels of GSH and SOD were determined. Cell viability was tested under all experimental conditions by measuring LDH-release, K+ uptake and total cell protein. Administration of dexamethasone and dibu-cAMP showed no effect on MT levels (compared with controls), and only a marginal effect on 64Cu and total Cu accumulation. Administration of actinomycin D resulted in increased copper accumulation in the particulate fraction, possibly due to inhibition of copper secretion processes and/or protein synthesis. Presence of zinc had no effect on MT levels nor on total Cu and 64Cu levels, in contrast with cadmium which drastically enhanced copper accumulation and MT levels in the cells. Cu/MT ratios varied from 1.0 +/- 0.3 to 3.3 +/- 1.2, which is far below the assumed maximum molar ratio of 8-12 mol Cu per mol MT. SOD levels appeared to be enhanced up to 2- or 3-fold in the presence of Cd2+, relative to control values. The role of GSH as Cu-intermediate in intracellular Cu distribution plus its role in copper defence mechanism(s) was tested by application of BSO, an inhibitor of GSH synthesis. It was found that BSO had no effect on intracellular MT level; it was found however that MT-bound copper levels were markedly decreased. The results presented support a model for copper metabolism in hepatoma tissue culture (HTC) cells, where Cu(I) is complexed by GSH immediately after entering the cell. GSH is capable of transferring copper to MT where it is stored. Depletion of GSH (by administration of Cd2+, actinomycin D, cycloheximide) almost instantaneously results in enhanced cellular toxicity. When also MT is depleted (by actinomycin D) non-MT associated, 'free' cytosolic Cu2+ is elevated, and HTC cells rapidly loose their resistance to copper toxicity, as also reflected in loss of cell viability (LDH, K+ and total cell protein).

Animals↗

PubMed2006

Copper transfer studies between the N-terminal copper binding domains one and four of human Wilson protein.

Human Wilson protein functions in the secretory pathway to insert copper ultimately into the multicopper oxidase ceruloplasmin and also plays a role in the excretion of excess copper to the bile. This copper-transporting P-type ATPase possesses six N-terminal cytosolic copper-binding domains contained within an approximately 72 amino acid consensus motif and the first four of these domains, denoted WLN1-4, are implicated in copper acquisition from the metallochaperone HAH1, whereas the domains closest to the membrane portion of the enzyme, WLN5-6, are essential for copper transport across the membrane. In order to test our hypothesis that copper transfer occurs between domains in the N-terminus of Wilson protein, we expressed and purified to homogeneity copper-binding domains 1, 3, 4, 5-6, and 6, denoted by WLN1, WLN3, WLN4, WLN5-6, and WLN6, respectively. Since we determined WLN1 and WLN4 to have the highest and lowest isoelectric points (6.77 and 3.85, respectively) and thus are readily separated via ion exchange chromatography, we developed a copper transfer assay between these domains. We anaerobically incubated either Cu(I)-WLN1 with apo-WLN4 or apo-WLN1 with Cu(I)-WLN4, then separated these domains and quantified the amount of copper that migrates from one domain to another by ICP-MS. Regardless of whether we start with Cu(I)-WLN1 or Cu(I)-WLN4 as the initial copper donor, we demonstrate facile copper transfer between WLN1 and WLN4, thereby demonstrating the feasibility of copper transfer between these domains in vivo.

Adenosine Triphosphatases↗

PubMed2003

The Enterococcus hirae paradigm of copper homeostasis: copper chaperone turnover, interactions, and transactions.

The cop operon is a key element of copper homeostasis in Enterococcus hirae. It encodes two copper ATPases, CopA and CopB, the CopY repressor, and the CopZ metallochaperone. The cop operon is induced by copper, which allows uncompromised growth in up to 5 mM ambient copper. Copper uptake appears to be accomplished by the CopA ATPase, a member of the heavy metal CPx-type ATPases and closely related to the human Menkes and Wilson ATPases. The related CopB ATPase extrudes copper when it reaches toxic levels. Intracellular copper routing is accomplished by the CopZ copper chaperone. Using surface plasmon resonance analysis, it was demonstrated that CopZ interacts with the CopA ATPase where it probably becomes copper loaded. CopZ in turn can donate copper to the copper responsive repressor CopY, thereby releasing it from DNA. In high copper, CopZ is proteolyzed. Cell extracts were found to contain a copper activated proteolytic activity that degrades CopZ in vitro. This post-translational control of CopZ expression presumably serves to avoid the accumulation of detrimental Cu-CopZ levels.

Adenosine Triphosphatases↗

PubMed2007

Copper binding to the N-terminal metal-binding sites or the CPC motif is not essential for copper-induced trafficking of the human Wilson protein (ATP7B).

The Wilson protein (ATP7B) is a copper-translocating P-type ATPase that mediates the excretion of excess copper from hepatocytes into bile. Excess copper causes the protein to traffic from the TGN (trans-Golgi network) to subapical vesicles. Using site-directed mutagenesis, mutations known or predicted to abrogate catalytic activity (copper translocation) were introduced into ATP7B and the effect of these mutations on the intracellular trafficking of the protein was investigated. Mutation of the critical aspartic acid residue in the phosphorylation domain (DKTGTIT) blocked copper-induced redistribution of ATP7B from the TGN, whereas mutation of the phosphatase domain [TGE (Thr-Gly-Glu)] trapped ATP7B at cytosolic vesicular compartments. Our findings demonstrate that ATP7B trafficking is regulated with its copper-translocation cycle, with cytosolic vesicular localization associated with the acyl-phosphate intermediate. In addition, mutation of the six N-terminal metal-binding sites and/or the trans-membrane CPC (Cys-Pro-Cys) motif did not suppress the constitutive vesicular localization of the ATP7B phosphatase domain mutant. These results suggested that copper co-ordination by these sites is not essential for trafficking. Importantly, copper-chelation studies with these mutants clearly demonstrated a requirement for copper in ATP7B trafficking, suggesting the presence of an additional copper-binding site(s) within the protein. The results presented in this report significantly advance our understanding of the regulatory mechanism that links copper-translocation activity with copper-induced intracellular trafficking of ATP7B, which is central to hepatic and hence systemic copper homoeostasis.

Adenosine Triphosphatases↗

PubMed2000

Copper-induced apical trafficking of ATP7B in polarized hepatoma cells provides a mechanism for biliary copper excretion.

BACKGROUND & AIMS: Mutations in the ATP7B gene, encoding a copper-transporting P-type adenosine triphosphatase, lead to excessive hepatic copper accumulation because of impaired biliary copper excretion in Wilson's disease. In human liver, ATP7B is predominantly localized to the trans-Golgi network, which appears incompatible with a role of ATP7B in biliary copper excretion. The aim of this study was to elucidate this discrepancy. METHODS: Immunofluorescence and electron-microscopic methods were used to study the effects of excess copper on ATP7B localization in polarized HepG2 hepatoma cells. RESULTS: ATP7B is localized to the trans-Golgi network only when extracellular copper concentration is low (<1 micromol/L). At increased copper levels, ATP7B redistributes to vesicular structures and to apical vacuoles reminiscent of bile canaliculi. After copper depletion, ATP7B returns to the trans-Golgi network. Brefeldin A and nocodazole impair copper-induced apical trafficking of ATP7B and cause accumulation of apically retrieved transporters in a subapical compartment, suggesting continuous recycling of ATP7B between this vesicular compartment and the apical membrane when copper is increased. CONCLUSIONS: Copper induces trafficking of its own transporter from the trans-Golgi network to the apical membrane, where it may facilitate biliary copper excretion. This system of ligand-induced apical sorting provides a novel mechanism to control copper homeostasis in hepatic cells.

Adenosine Triphosphatases↗

PubMed1980

Serum copper in long-term users of copper intrauterine devices.

A study was undertaken to determine whether long-term use of a copper intrauterine device (IUD) was associated with any alteration in the serum copper levels and thereby whether absorption of copper from the device in utero could result in copper toxicity. Serial estimations in copper IUD wearers showed that there was no alteration in serum copper levels for a period of up to 24 months. The mean range and frequency distribution of serum copper levels in long-term copper IUD wearers was similar to that seen in the normal population. There was no difference in the mean 24-hour urinary copper excretion between the control group and the copper IUD wearers. Data suggest that the copper released from a copper IUD may not be readily absorbed from the uterine fluid. This hypothesis needs verification.

Copper↗

PubMed1985

Copper toxicosis and tolerance in the rat. I--Changes in copper content of the liver and kidney.

Rats can tolerate toxic copper diets; the extent of this adaptation and the changes that take place in the liver and kidney with respect to copper are studied. Rats were fed diets containing 3000-6000 mg/kg copper for 15 weeks and groups were killed at regular intervals. Their livers and kidneys were examined for pathological changes and for their copper content. Liver copper rose rapidly in the 3000 mg/kg trial to 4780 +/- 636 micrograms/g copper between 4 and 5 weeks with marked liver damage. Stainable copper protein was present at 2 weeks in the hepatocytes but had disappeared by 5 weeks. Liver copper subsequently fell with recovery by 15 weeks. Kidney copper rose to plateau from 4 weeks. Stainable copper protein was present from 2 weeks in the cells of the proximal tubules and was apparently excreted. Tubular necrosis occurred at 4-5 weeks followed by regeneration. In the 6000 mg/kg trial the toxicosis was prolonged. Copper toxicosis in the rat can be a temporary phenomenon during the transformation of copper protein synthesis in the liver from a stainable to a non stainable form. Adaptation occurs after the removal of excess liver copper, facilitated probably by renal excretion, and the animals become tolerant.

Animals↗

PubMed2001

Copper-associated liver disease in North Ronaldsay sheep: a possible animal model for non-Wilsonian hepatic copper toxicosis of infancy and childhood.

Indian childhood cirrhosis (ICC), endemic Tyrolean infantile cirrhosis (ETIC) and idiopathic copper toxicosis (ICT), are clinically and pathologically indistinguishable liver disorders of infants and young children linked with exogenous copper and with increasing evidence for a genetic predisposition. North Ronaldsay sheep are a primitive breed which have adapted to a copper impoverished environment (<5 ppm) and display an abnormal sensitivity to copper poisoning when transferred to a copper replete (11 ppm) habitat. The aetiological parallels prompted a study of copper-associated liver disease in North Ronaldsay sheep (RCT) to see if the pathology could contribute to the understanding of the childhood disorder. A retrospective study was performed in which the livers of 22 mainland-bred North Ronaldsay sheep were compared with three island-bred sheep and categorized for liver copper content and pathomorphology. It was found that all the mainland sheep had accumulated liver copper (>300 microg/g), in contrast to the island sheep, although 10 sheep with increased liver copper (mean 600 SD 270 microg/g) showed no evidence of liver damage. A further 10 sheep with liver copper (mean 1276 SD 508 microg/g) exhibited periportal to panlobular histochemical copper retention, a periportal and/or panlobular pericellular fibrosis, a mixed inflammatory infiltrate and cholangioplasia. Steatosis was absent and regeneration was in abeyance. Finally, two sheep (liver copper >2000 microg/g) had a more active hepatitis with a florid pericellular, panlobular fibrosis and cirrhosis. Electron microscopy identified large numbers of collagen-producing hepatic stellate (Ito) cells in periportal regions. The pathological findings were sufficiently reminiscent of ICC, ETIC and ICT to warrant further exploration of RCT as a putative animal model. The North Ronaldsay sheep liver may be a useful tool for the investigation of copper-induced fibrogenesis.

Animals↗

PubMed1999

Effects of promoter mutations on the in vivo regulation of the cop operon of Enterococcus hirae by copper(I) and copper(II).

The cop operon of Enterococcus hirae encodes a repressor, CopY, a copper chaperone, CopZ, and two copper ATPases, CopA and CopB. Regulation of the cop operon is bi-phasic, with copper addition as well as copper chelation leading to induction. Using a plasmid-borne system with a reporter gene, induction of wild-type and mutant cop promoters by high and low copper conditions was investigated. Only mutations that impaired the interaction of CopY with both DNA binding sites had a marked effect on regulation, leading to hyperinduction by copper(I) or copper(II). Chelation of copper(II), but not copper(I), also induced the operon, but induction by copper chelation was not significantly affected by the mutations. E. hirae mutants with reduced extracellular copper reductase activity exhibited the same induction kinetics as wild-type cells. These results show that copper addition and copper chelation induce the cop operon by different routes.

Adenosine Triphosphatases↗

PubMed2002

Runoff rates, chemical speciation and bioavailability of copper released from naturally patinated copper.

The release of copper, induced by atmospheric corrosion, from naturally patinated copper of varying age (0 and 30 years) has been investigated together with its potential ecotoxic effect. Results were generated in an interdisciplinary research effort in which corrosion science and ecotoxicology aspects were combined. The aim of the investigation was to elucidate the situation when copper-containing rainwater leaves a roof in terms of runoff rate, chemical speciation, bioavailability and ecotoxicity effects. Data have been collected during a three-year field exposure conducted in the urban environment of Stockholm, Sweden. The potential environmental effects have been evaluated using a combination of a copper specific biosensor test with the bacterium Alcaligenes eutrophus and the conventional 72-h growth inhibition test with the green alga Raphidocelis subcapitata. The results show annual runoff rates between 1.0 and 1.5 g/m2 year for naturally patinated copper of varying age. The runoff rate increased slightly with patina age, which mainly is attributed to the enhanced first flush effect observed on thicker patina layers. The total copper concentration in investigated runoff samplings ranged from 0.9 to 9.7 mg/l. Both computer modeling and experimental studies revealed that the majority (60-100%) of released copper was present as the free hydrated cupric ion, Cu(H2O)6(2+), the most bioavailable copper species. However, other copper species in the runoff water, such as, e.g. Cu(OH)+ and Cu2(OH)2(2+), were also bioavailable. The copper-containing runoff water, sampled directly after release from the roof, caused significant reduction in growth rate of the green alga. It should be emphasized that the results describe the runoff situation immediately after release from the copper roof and not the real environmental ecotoxicity. Therefore the data should only be used as an initial assessment of the potential environmental effect of copper runoff from building applications. Future risk assessments should also consider dilution effects of copper, changes in its chemical speciation and bioavailability during environmental entry, and type and sensitivity of the receiving ecosystem.

Biological Availability↗