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Journal articles on the topic 'Liver Copper'

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Published: 3 June 2025

Last updated: 31 July 2025

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1

Kruitwagen, Hedwig S., Hille Fieten, and Louis C. Penning. "Towards Bioengineered Liver Stem Cell Transplantation Studies in a Preclinical Dog Model for Inherited Copper Toxicosis." Bioengineering 6, no. 4 (2019): 88. http://dx.doi.org/10.3390/bioengineering6040088.

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Wilson Disease is a rare autosomal recessive liver disorder in humans. Although its clinical presentation and age of onset are highly variable, hallmarks include signs of liver disease, neurological features and so-called Kayser-Fleischer rings in the eyes of the patient. Hepatic copper accumulation leads to liver disease and eventually to liver cirrhosis. Treatment options include life-long copper chelation therapy and/or decrease in copper intake. Eventually liver transplantations are indicated. Although clinical outcome of liver transplantations is favorable, the lack of suitable donor live

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2

GOONERATNE, S. R., and D. A. CHRISTENSEN. "A SURVEY OF MATERNAL COPPER STATUS AND FETAL TISSUE COPPER CONCENTRATIONS IN SASKATCHEWAN BOVINE." Canadian Journal of Animal Science 69, no. 1 (1989): 141–50. http://dx.doi.org/10.4141/cjas89-017.

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Copper (Cu) status of cattle raised in different soil zones of Saskatchewan was examined with emphasis on the relation between liver Cu concentration in pregnant cows, stage of pregnancy and fetal liver Cu status. Whole fetuses and livers from adult animals were obtained during routine slaughter operation at a local packing plant. Twenty percent of steers, 54% of pregnant cows, 52% of heifers and 77% of nonpregnant cows had liver Cu levels less than 25 mg kg−1 dry matter (DM). Hypocuprosis was most marked in cattle originating from northern regions of Saskatchewan. Fetal liver Cu concentration

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3

Muchenditsi, Abigael, Haojun Yang, James P. Hamilton, et al. "Targeted inactivation of copper transporter Atp7b in hepatocytes causes liver steatosis and obesity in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 313, no. 1 (2017): G39—G49. http://dx.doi.org/10.1152/ajpgi.00312.2016.

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Copper-transporting ATPase 2 (ATP7B) is essential for mammalian copper homeostasis. Mutations in ATP7B result in copper accumulation, especially in the liver, and cause Wilson disease (WD). The major role of hepatocytes in WD pathology is firmly established. It is less certain whether the excess Cu in hepatocytes is solely responsible for development of WD. To address this issue, we generated a mouse strain for Cre-mediated deletion of Atp7b and inactivated Atp7b selectively in hepatocytes. Atp7bΔHep mice accumulate copper in the liver, have elevated urinary copper, and lack holoceruloplasmin

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4

Schultheiss, Patricia C., Cathy L. Bedwell, Dwayne W. Hamar, and Martin J. Fettman. "Canine Liver Iron, Copper, and Zinc Concentrations and Association with Histologic Lesions." Journal of Veterinary Diagnostic Investigation 14, no. 5 (2002): 396–402. http://dx.doi.org/10.1177/104063870201400506.

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Concentrations of iron, copper, and zinc were measured in livers of 95 dogs that were suspected of having liver disease. Iron concentrations ranged from 177 to 7,680 ppm (dry weight basis); 54 dogs had iron concentrations greater than the normal concentration of 1,200 ppm. Iron stores were present in Kupffer cells and macrophages but not hepatocytes. The dogs did not have lesions of hemochromatosis. Dogs with high liver iron tended to have high liver copper and inflammatory lesions. High liver copper concentrations usually were associated with hepatocellular necrosis and fibrosis. High liver z

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5

Sabullah, Mohd Khalizan, Fisal Ahmad, Azlan Jualang Gansau, and Mohd Rosni Sulaiman. "A one dimensional PAGE studies on <i>Puntius javanicus</i> liver proteome affected by copper toxicity." Bioremediation Science and Technology Research 3, no. 2 (2015): 26–29. http://dx.doi.org/10.54987/bstr.v3i2.297.

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Observations on the effects of copper on the liver proteome of Puntius javanicusÂ based on the one dimensional PAGE was carried out. The liver was dissected from each fish, which was separately treated with different concentrations of copper sulfate ranging from 0.1 to 5.0 mg/L. The livers were extracted and one dimensional PAGE was performed under nonreducing (native) and reducing (SDS)-PAGE. Several bands were resolved in the native PAGE with probable candidates for the effect of copper observed showing an increased in the expression and downregulation strongly associated with increasing cop

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6

Wu, Xiaoyan, Hsiaotzu Chien, Monique E. van Wolferen, Hedwig S. Kruitwagen, Loes A. Oosterhoff, and Louis C. Penning. "Reduced FXR Target Gene Expression in Copper-Laden Livers of COMMD1-Deficient Dogs." Veterinary Sciences 6, no. 4 (2019): 78. http://dx.doi.org/10.3390/vetsci6040078.

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Wilson’s disease (WD), an autosomal recessive disorder, results in copper accumulation in the liver as a consequence of mutations in the gene ATPase copper transporting beta (ATP7B). The disease is characterized by chronic hepatitis, eventually resulting in liver cirrhosis. Recent studies have shown that dysregulation of nuclear receptors (NR) by high hepatic copper levels is an important event in the pathogenesis of liver disease in WD. Intracellular trafficking of ATP7B is mediated by COMMD1 and, in Bedlington terriers, a mutation in the COMMD1 gene results in high hepatic copper levels. Her

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7

Thornburg, L. P., M. Beissenherz, M. Dolan, and M. F. Raisbeck. "Histochemical Demonstration of Copper and Copper-Associated Protein in the Canine Liver." Veterinary Pathology 22, no. 4 (1985): 327–32. http://dx.doi.org/10.1177/030098588502200405.

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Three different histochemical methods for copper detection were compared. Atomic absorption analysis was used to substantiate the tissue stains. There was good correlation between rhodanine staining and rubeanic acid-stained tissue sections. The orcein reaction for copper-associated protein did not consistently correlate with the methods demonstrating copper. Prolonged staining (72 hours) with rubeanic acid more consistently and clearly detected increased copper in canine livers than did staining with rhodanine. Seventy-two hour staining with rubeanic acid is the method of choice for histochem

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8

Gabriel, O. Wordu, and Obinna Echem P. "EFFECTS OF ROXARSONE ON COPPER UTILIZATION BY CHICK." Continental J. Food Science and Technology 2 (July 25, 2008): 1–5. https://doi.org/10.5281/zenodo.834639.

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Experiment was conducted to examine the effect of dietary roxarsone (3-nitro-4-hydroxyphemylarsonic acid) on Cu utilization by chick. A fortified corn-soybean meal diet was fed to the chick. Roxarsone dramatically reduced liver cu concentration at all levels of supplemental Cu fed. The level of roxarsone commonly fed, 50 mg/kg diet, resulted in a two-to-four fold depression in liver Cu concentration in chick. The effects of roxarsone on weight gain were more perplexity. In the chick, the diets containing 100 and 250 mg Cu/kg depressed growth in the presence, but not in the absence, of 50mg/kg

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9

Yamkate, Punyamanee, Randi M. Gold, David C. Twedt, Jan S. Suchodolski, Joerg M. Steiner, and Jonathan A. Lidbury. "Assessment of the intracellular distribution of copper in liver specimens from cats." PLOS ONE 17, no. 2 (2022): e0264003. http://dx.doi.org/10.1371/journal.pone.0264003.

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The intracellular distribution of copper in the liver has been investigated in dogs and humans. However, this has not been reported in cats. This study aimed to assess the intracellular copper distribution in liver specimens from cats with a range of hepatic copper concentrations. Twenty-nine frozen liver specimens from cats were included. Each liver specimen was divided into two pieces for overall copper quantification and tissue fractionation. The copper concentrations in liver specimens and liver fractions were measured by flame atomic absorption spectroscopy. Five specimens had copper conc

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10

IVAN, M., J. G. PROULX, R. MORALES, H. C. V. CODAGNONE, and M. DE S. DAYRELL. "COPPER ACCUMULATION IN THE LIVER OF SHEEP AND CATTLE FED DIETS SUPPLEMENTED WITH COPPER SULFATE OR COPPER CHLORIDE." Canadian Journal of Animal Science 70, no. 2 (1990): 727–30. http://dx.doi.org/10.4141/cjas90-089.

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Six groups of 12 pregnant cows were fed barley or grass silage with or without copper sulfate or copper chloride supplements (16 or 14 mg copper kg−1 dry matter (DM)). In addition, five groups of 10 lambs were fed diets supplemented with 5 or 10 mg Cu kg−1 DM as salts of sulfate or chloride. The two Cu salts produced equal increases in the concentration of Cu in the livers of both sheep and cattle. Key words: Sheep, cattle, liver, copper sulfate, copper chloride

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11

Kim, Heejeong, Hwa-Young Son, Sarah M. Bailey, and Jaekwon Lee. "Deletion of hepatic Ctr1 reveals its function in copper acquisition and compensatory mechanisms for copper homeostasis." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 2 (2009): G356—G364. http://dx.doi.org/10.1152/ajpgi.90632.2008.

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Copper is a vital trace element required for normal growth and development of many organisms. To determine the roles for copper transporter 1 (Ctr1) in hepatic copper metabolism and the contribution of the liver to systemic copper homeostasis, we have generated and characterized mice in which Ctr1 is deleted specifically in the liver. These mice express less than 10% residual Ctr1 protein in the liver and exhibit a small but significant growth retardation, which disappears with age. Hepatic copper concentrations and the activities of copper-requiring enzymes are reduced; however, mild copper d

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12

Thornburg, L. P., D. Shaw, M. Dolan, et al. "Hereditary Copper Toxicosis in West Highland White Terriers." Veterinary Pathology 23, no. 2 (1986): 148–54. http://dx.doi.org/10.1177/030098588602300207.

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Histologic, histochemical and atomic absorption studies on liver tissue from 71 West Highland white terriers are reported. Twenty-seven dogs had histologically normal liver and copper concentration comparable to mongrel control dogs. Forty-four dogs had hepatic copper concentrations up to 22 limes the mean copper concentration found in clinically normal mongrel dogs. Hepatitis, hepatic necrosis and cirrhosis were associated with the increased copper concentration in some dogs. Matings between dogs with high liver copper concentration produced pups with high liver concentration. The copper stor

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13

Konovalova, T. V. "The impact of the paternal genetic makeup on the copper concentration in the livers of offspring in cattle." Bulletin of NSAU (Novosibirsk State Agrarian University), no. 1 (April 17, 2024): 196–203. http://dx.doi.org/10.31677/2072-6724-2024-70-1-196-203.

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he copper content in the liver of the progeny of four Holstein breed bulls was investigated. Research was done in Kemerovo, Russia. The identical dietary and lodging conditions were established for all groups of offspring after their birth. The copper concentration was studied using atomic emission spectrometry on the SOLAR M6 series instrument in the Analytical Center of the Institute of Geology and Mineralogy, named by V.S. Sobolev. The determination of the heavy metal content in water, soil, and fodder within the dairy cattle zoning was conducted, with the result that the level did not exce

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14

Day, Patrick Lloyd, Ria Fyffe-Freil, Patrick Vanderboom, et al. "Iron and Copper Liver Concentrations in Wilson Disease." Journal of Gastrointestinal and Liver Diseases 33, no. 4 (2024): 517–23. https://doi.org/10.15403/jgld-5662.

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Background and Aims: Wilson disease (WD) results in the defective incorporation of copper into ceruloplasmin as well as decreased biliary copper excretion. Secondary iron overload has also been associated with WD; however, the prevalence is currently unknown. This study aims to determine the prevalence of potential secondary iron overload in patients suspected to have WD. The secondary aim was to determine whether common laboratory tests were associated with liver copper concentrations or the need for liver transplantation in a subset of patients with confirmed WD. Methods: Using our instituti

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15

Thornburg, Larry P. "Copper-associated liver disease." American Journal of Veterinary Research 47, no. 5 (1986): 1179. https://doi.org/10.2460/ajvr.1986.47.05.1179.

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16

Danks, D. M. "Copper and liver disease." European Journal of Pediatrics 150, no. 3 (1991): 142–48. http://dx.doi.org/10.1007/bf01963553.

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17

Eapen, C. E. "Copper and liver disease." Gut 61, no. 1 (2011): 63. http://dx.doi.org/10.1136/gutjnl-2011-301743.

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18

Hoffmann, Gaby. "Copper-Associated Liver Diseases." Veterinary Clinics of North America: Small Animal Practice 39, no. 3 (2009): 489–511. http://dx.doi.org/10.1016/j.cvsm.2009.02.001.

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19

Youssef, T. H., Y. A. Hefnawy, and H. A. Hassan. "Deposition of copper in cattle and buffaloes edible tissues slaughtered in Assiut city, Egypt." Advance in Biological Research 1, no. 1 (2020): 11–15. http://dx.doi.org/10.26855/abr.2020002.

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A total of 168 samples of livers, kidneys and muscles (part of the diaphragm) were screened. The samples were subjected to preparation and for measurement the level of copper (Cu) by using Atomic Absorption/Flaming Emission Spectrophotometer. Buffaloes organs showed variations in their copper content. As for liver, the mean copper concentrations were 11.52 ± 5.41 with a range varied from 2.34 to 21.88 μg/g wet weight. Whereas in buffalo kidneys copper level varied from 2.34 to 15.13 with a mean value of 5.85 ± 4.34 μg/g wet weight. Moreover, the concentrations of copper in buffalo muscles vari

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20

Sindireva, Anna, Susanna Pashayan, and Mikhail Mikhailov. "FUNCTIONAL CHARACTERISTICS OF THE LIVER." Bulletin of KSAU, no. 9 (October 29, 2024): 121–27. https://doi.org/10.36718/1819-4036-2024-9-121-127.

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The aim of the study is to evaluate the effect of copper- and molybdenum-containing compounds on the morphofunctional state of the body of laboratory mice. The study was conducted in the laboratory of the Department of Anatomy and Physiology of the Northern Trans-Urals State Agrarian University. The expe-riment was conducted on male laboratory mice of the same age. For three weeks, the animals were orally administered solutions of ammonium paramolybdate and copper acetate. The doses of trace elements were 0.0125 (optimal dose for molybdenum) and 5 mg/kg (toxic dose for copper). Based on the ac

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21

Poznański, Jarosław, Dariusz Sołdacki, Bożena Czarkowska-Pączek, et al. "Cirrhotic Liver of Liver Transplant Recipients Accumulate Silver and Co-Accumulate Copper." International Journal of Molecular Sciences 22, no. 4 (2021): 1782. http://dx.doi.org/10.3390/ijms22041782.

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Silver-based materials are widely used in clinical medicine. Furthermore, the usage of silver containing materials and devices is widely recommended and clinically approved. The impact on human health of the increasing use of silver nanoparticles in medical devices remains understudied, even though Ag-containing dressings are known to release silver into the bloodstream. In this study, we detected a widespread and sometimes significant silver accumulation both in healthy and sick liver biopsies, levels being statistically higher in patients with various hepatic pathologies. 28 healthy and 44 c

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22

AGUNBIADE, J. A., and G. M. BABATUNDE. "COPPER AND IRON SUPPLEMENTATION IN THE TROPICAL ENVIRONMENT EFFECTS ON HAEMATOLOGICAL MEASUREMENTS, ORGAN WEIGHTS, TISSUE COPPER AND IRON." Nigerian Journal of Animal Production 22, no. 1 (2021): 49–55. http://dx.doi.org/10.51791/njap.v22i1.2028.

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The study which lasted 3 months was a factorial arrangement in which nine dietary treatments resulting from supplementation of a commercial layers diet with 0, 200 or 400 mg/kg Copper and 0, 100 or 200 mg/kg Iron were fed to 135 fifty two-week old laying hens of the Golden Hubbard Connect Strain. After 12 weeks on the diets, three birds, randomly selected from each treatment, were slaughtered and their blood, liver, spleen and heart analysed for effect of supplementary copper and iron on haemoglobin content, packed cell volume and weights of the liver, spleen and heart and their copper and iro

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23

Tessman, Ronald K. "Liver biopsy procedure and indications." American Association of Bovine Practitioners Conference Proceedings, no. 55 (July 17, 2023): 86–89. http://dx.doi.org/10.21423/aabppro20228609.

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Liver biopsy sampling and subsequent analysis for mineral content can be a valuable diagnostic tool for micronutrient associated illness in cattle. Although there may be some apprehension when using the blind technique, the procedure has little risk of adverse consequences. Utilizing proper biopsy site preparation and appropriate landmarks reduces risk of complications while optimizing the probability of obtaining a sample large enough for micronutrient evaluation. Liver samples are appropriate for evaluating toxicity associated with cobalt, copper, manganese, selenium and zinc and deficien

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24

de Wolf, I. D., A. C. M. Bonné, X. M. Fielmich-Bouman, et al. "Quantitative Trait Loci Influencing Hepatic Copper in Rats." Experimental Biology and Medicine 227, no. 7 (2002): 529–34. http://dx.doi.org/10.1177/153537020222700718.

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Significant differences in liver copper content have been observed between rat inbred strains. To define loci controlling this trait, the offspring (n = 190) from an (LEW/OlaHsd × BC/CpbU) F2-intercross was genetically analyzed. From each F2 animal, liver copper content was determined and genomic DNA was screened with polymorphic DNA markers. We found a major quantitative trait locus (QTL) for liver copper content in females on chromosome 2 and in males on chromosome 10. Both QTLs accounted for approximately 20% of the genetic variance. In addition, suggestive linkage for liver copper content

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25

Thornburg, Larry P. "A Perspective on Copper and Liver Disease in the Dog." Journal of Veterinary Diagnostic Investigation 12, no. 2 (2000): 101–10. http://dx.doi.org/10.1177/104063870001200201.

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Copper is a ubiquitous trace metal necessary for normal function of a variety of cellular proteins. Intracellular copper metabolism is complex, and only a few of the proteins/genes involved are known. Copper deficiency does not appear to be a clinical problem in dogs. Excess copper accumulation in the liver as a cause of hepatitis and cirrhosis was first demonstrated among Bedlington terriers. Subsequently, copper accumulation in the liver has been shown to occur in several other breeds of dogs. Excess hepatic copper has been found in dogs with normal liver histology, dogs with hepatitis, and

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Guigui, Bernard, Philippe Mavier, Marie-Claude Lescs, Won Pinaudeau, Daniel Dhumeaux, and Elie Serge Zafrani. "Copper and copper-binding protein in liver tumors." Cancer 61, no. 6 (1988): 1155–58. http://dx.doi.org/10.1002/1097-0142(19880315)61:6<1155::aid-cncr2820610616>3.0.co;2-6.

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27

SATO, I., N. MATSUSAKA, T. SUZUKI, H. KOBAYASHI, K. SERA, and S. FUTATSUGAWA. "ESSENTIAL METAL CONTENTS IN THE LIVER OF DTPA-TREATED PREGNANT MICE AND THEIR FETUSES." International Journal of PIXE 07, no. 01n02 (1997): 25–29. http://dx.doi.org/10.1142/s0129083597000047.

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Ca -DTPA or Zn -DTPA was injected subcutaneously to pregnant mice once a day for 5 consecutive days from the 13th day to the 17th day of gestation. Maternal and fetal livers were collected 20 hours after the final injection of DTPA, and essential metal contents in the liver samples were determined by PIXE. Both Ca -DTPA and Zn -DTPA don't affect any essential metals in the maternal liver, but Ca -DTPA decreases copper and zinc contents in the fetal liver to 2/3 and 1/2 of the control values, respectively. Although Zn -DTPA does not affect fetal zinc content, it decreases that of copper. It cou

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28

Sadika Kadir, Tamanna Begum, Mohammed Ashraful Haque, et al. "Wilson’s Disease in Children : An Update." Z H Sikder Women’s Medical College Journal 2, Number 1 (2020): 27–30. http://dx.doi.org/10.47648/zhswmcj.2020.v0201.07.

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Wilson’s Disease is an autosomal recessive disorder of copper metabolism due to ATP7B gene defect. This defect result in progressive toxic accumulation of copper in liver, CNS, cornea, skeletal system and other organs. Clinical presentations of Wilson’s disease (WD) in childhood ranges from asymptomatic liver disease to cirrhosis or acute liver failure, whereas neurological and psychiatric symptoms are rare. The basic diagnostic approach includes serum ceruloplasmin and 24-hour urinary copper excretion. Final diagnosis of WD can be established using a diagnostic scoring system based on symptom

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29

Ranganathan, Perungavur N., Yan Lu, Lingli Jiang, Changae Kim, and James F. Collins. "Serum ceruloplasmin protein expression and activity increases in iron-deficient rats and is further enhanced by higher dietary copper intake." Blood 118, no. 11 (2011): 3146–53. http://dx.doi.org/10.1182/blood-2011-05-352112.

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AbstractIncreases in serum and liver copper content are noted during iron deficiency in mammals, suggesting that copper-dependent processes participate during iron deprivation. One point of intersection between the 2 metals is the liver-derived, multicopper ferroxidase ceruloplasmin (Cp) that is important for iron release from certain tissues. The current study sought to explore Cp expression and activity during physiologic states in which hepatic copper loading occurs (eg, iron deficiency). Weanling rats were fed control or low iron diets containing low, normal, or high copper for ∼ 5 weeks,

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Temiz, Mehmet Ali, Atilla Temur, Yusuf Akgeyik, and Ahmet Uyar. "Protective effect of Celtis tournefortii against copper-induced toxicity in rat liver." Acta Veterinaria Brno 90, no. 1 (2021): 91–98. http://dx.doi.org/10.2754/avb202190010091.

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This study aimed to investigate the antioxidant and hepatoprotective effects of Celtis tournefortii fruit extract (Ct) against copper-induced liver damage in rats. Thirty-two Wistar Albino rats were divided into four equal groups (n = 8): Control, Copper (Cu), Copper + C. tournefortii (Cu+Ct), and C. tournefortii (Ct). Superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activities, glutathione (GSH) concentration, malondialdehyde (MDA), total antioxidant status (TAS) and total oxidant status (TOS) were analysed in the liver tissues. Liver histopathology was also evalua

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Binnerts, W. T., H. A. Das, and T. C. Viets. "Liver selenium analysis in cows with a fast method of neutron activation reveals deficiency areas in the Netherlands." Netherlands Journal of Agricultural Science 41, no. 1 (1993): 47–57. http://dx.doi.org/10.18174/njas.v41i1.633.

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A total of 230, 100-g freeze-dried liver samples from the caudal lobe of cows from 13 slaughterhouses in the Netherlands were analysed by irradiating with neutrons in a high flux generator for 5 s followed by measurement of the short-lived isotope 77mSe in a rigid time sequence, under fully automated conditions. Liver Se ranged from 0.16 to 1.82 mg/kg DM and did not appear to relate to geography. 3% of the livers contained Se less than 0.25 mg/kg DM, which is considered critical for development of Se deficiency. Another 20% with less than 0.4 mg/kg DM was considered borderline Se deficiency. T

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Tang, Huaqiao, Min Xu, Fei Shi, et al. "Effects and Mechanism of Nano-Copper Exposure on Hepatic Cytochrome P450 Enzymes in Rats." International Journal of Molecular Sciences 19, no. 7 (2018): 2140. http://dx.doi.org/10.3390/ijms19072140.

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Although nano-copper is currently used extensively, the adverse effects on liver cytochrome P450 (CYP450) enzymes after oral exposure are not clear. In this study, we determined the effects and mechanisms of action of nano- and micro-copper on the expression and activity of CYP450 enzymes in rat liver. Rats were orally exposed to micro-copper (400 mg/kg), Cu ion (100 mg/kg), or nano-copper (100, 200 and 400 mg/kg) daily for seven consecutive days. Histopathological, inflammatory and oxidative stress were measured in the livers of all rats. The mRNA levels and activity of CYP450 enzymes, as wel

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Hassoun, Jeremy, Nathalie Hammer, Giulia Magini, et al. "Management of Acute Wilsonian Hepatitis with Severe Hemolysis: A Successful Combination of Chelation and MARS Dialysis." Case Reports in Hepatology 2021 (May 11, 2021): 1–6. http://dx.doi.org/10.1155/2021/5583654.

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Wilson’s disease is a rare hereditary disorder of copper metabolism leading to progressive accumulation of copper in several organs including the brain and the liver. Acute liver failure is a relatively rare hepatic manifestation of WD which may require urgent liver transplantation if medical treatment fails. We report here the case of a young woman who presented with classic acute Wilsonian hepatitis complicated by liver and renal failure and a severe hemolysis related to massive nonceruloplasmin bound copper accumulation requiring repeated blood transfusions. The early initiation of a combin

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Yun, Sumin, Dohee Lee, Jimin Oh, et al. "Primary copper-associated chronic hepatitis without copper metabolism domain containing 1 mutation in a Dalmatian: a case report." Korean Journal of Veterinary Research 62, no. 4 (2022): e31. http://dx.doi.org/10.14405/kjvr.20220020.

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A 12-year-old intact male Dalmatian dog presented hyporexia and vomiting for 1 week. Blood analysis revealed increased liver enzyme activity. Histopathological examination of the liver confirmed chronic hepatitis with fibrosis and necrosis. Copper staining revealed marked copper accumulation (2,770 ppm; normal range, 200 to 400 ppm), prominent in the centrilobular region, and compatible with copper-associated chronic hepatitis. However, copper metabolism domain containing 1 (COMMD1) mutation predisposing to copper accumulation in the liver tissue was not identified. The dog received medication

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Wu, Dandan, Qiwen Lin, Senao Hou та ін. "Gut Microbiota and Its Metabolite Taurine-β-Muricholic Acid Contribute to Antimony- and/or Copper-Induced Liver Inflammation". International Journal of Molecular Sciences 26, № 7 (2025): 3332. https://doi.org/10.3390/ijms26073332.

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Antimony and copper can contaminate vegetables and enter the human body through the digestive tract, inducing severe and extensive biotoxicity. However, the role of bile acids (BAs) in the pathogenesis of liver inflammation by antimony or copper has not been elucidated. Our results indicated that antimony and/or copper induced liver inflammation, causing the disruption of gut microbiota, with the down-regulation of probiotics and up-regulation of harmful bacteria closely correlated to liver inflammation. Targeted metabolomics of BAs showed that antimony and/or copper significantly up-regulated

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Berzina, Anita, Inese Martinsone, Simons Svirskis, Modra Murovska, and Martins Kalis. "Curcumin Effect on Copper Transport in HepG2 Cells." Medicina 54, no. 2 (2018): 14. http://dx.doi.org/10.3390/medicina54020014.

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Background and Objective: In Wilson’s disease, copper metabolism is impaired due to defective copper transporting protein ATP7B, resulting in copper accumulation in liver and brain and causing damage to liver and brain tissues. Published data suggest that one of the possible treatments for Wilson’s disease is curcumin—a compound found in the root of Curcuma longa. In this study, we tested whether curcumin affects copper transport and excretion in HepG2 hepatocytes carrying wildtype ATP7B. Materials and Methods: We examined the impact of 5 µM and 25 µM curcumin on the transport of copper in Hep

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van Ryssen, J. B. J., and P. R. Barrowman. "Effect of ionophores on the accumulation of copper in the livers of sheep." Animal Science 44, no. 2 (1987): 255–61. http://dx.doi.org/10.1017/s0003356100018626.

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ABSTRACTLambs were allocated to three treatments: control (C), monensin (M) and lasalocid sodium (L) in a concentrate diet containing 36 mg copper per kg food. After 2 months deaths from copper toxicity occurred and the trial was terminated. All lambs were slaughtered. The mean liver copper concentration (mg/kg dry matter) of 1907 in the M treatment was higher than the mean concentrations of 1342 and 1229 in the C and L groups respectively (P < 0·01). Total liver copper was 234, 260 and 230 mg and the retention of dietary copper in the liver was 93·5, 108·5 and 93·3 g/kg for the C, M and L

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Waldrop, G. L., F. A. Palida, M. Hadi, P. A. Lonergan, and M. J. Ettinger. "Effect of albumin on net copper accumulation by fibroblasts and hepatocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 259, no. 2 (1990): G219—G225. http://dx.doi.org/10.1152/ajpgi.1990.259.2.g219.

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The liver accumulates copper rapidly and preferentially from plasma. The effects of albumin on net copper accumulation by fibroblasts and hepatocytes were compared to determine whether preferential uptake involves hepatocyte-specific sequestering of copper. Although albumin inhibits the initial rates (30 s) of copper transport by fibroblasts and hepatocytes similarly, the effects of albumin on net copper accumulation (4 h) by these cell types were strikingly different. Fibroblasts accumulate only approximately 15% as much copper when equimolar albumin is present as from albumin-free media; hep

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Aston, N. S., N. Watt, I. E. Morton, M. S. Tanner, and G. S. Evans. "Copper toxicity affects proliferation and viability of human hepatoma cells (HepG2 line)." Human & Experimental Toxicology 19, no. 6 (2000): 367–76. http://dx.doi.org/10.1191/096032700678815963.

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In Wilson's disease and Indian childhood cirrhosis (ICC) copper accumulates in the liver resulting in poor hepatocyte regeneration and fibrosis. An inhibition of hepatocyte proliferation and an increase in cell death could account for these outcomes. To establish how the toxicity of this metal ion impacts upon the proliferation and viability ofthe HepG2 cells they were cultured in 4-32 jiM copper(II) sulphate (CuS04)). These levels were comparable to the circulatory and tissue concentrations of copper recorded for these two diseases. Specific uptake comparable to levels of copper recorded in t

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Haywood, S., H. C. Rutgers, and M. K. Christian. "Hepatitis and Copper Accumulation in Skye Terriers." Veterinary Pathology 25, no. 6 (1988): 408–14. http://dx.doi.org/10.1177/030098588802500602.

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Livers of nine related Skye terriers with liver disease were evaluated for histological changes and copper content. Lesions ranged from hepatocellular degeneration and necrosis (zone 3) with intracanalicular cholestasis and mild inflammation, to chronic hepatitis with cholangioplasia and cirrhosis. Excess copper (801–2,257 μg/g) was related to the severity of cholestasis. Skye terrier hepatitis is a distinct disease entity and may be derived from a disorder of intracellular bile metabolism culminating in disturbed bile secretion and the accumulation of copper.

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Hutagalung, Caroline Febrina, Ermi Girsang, Maya Sari Mutia, Suhartina Suhartina, and Oliviti Natali. "Liver Protection Effect of Red Rose Petal Methanol Extract in Copper-Induced Liver Injury in Male Wistar Rats." Biology, Medicine, & Natural Product Chemistry 12, no. 2 (2023): 507–13. http://dx.doi.org/10.14421/biomedich.2023.122.507-513.

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The human body requires low amounts of copper to maintain homeostasis, but high copper intake can cause various health problems. Many previous studies have been performed to look for natural products that can neutralize the excessive copper effect; one such natural product is a rose petal. Therefore, this study aims to investigate the liver protection effect of rose petals in copper-induced liver injury in male Wistar rats. This experimental study used thirty male Wistar rats that were grouped into five groups, including control, standard (quercetin), Rose Petal Methanol Extract-1 (400 mg/kg B

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Haider, Rehan. "Wilson's Disease." Cancer Research and Cellular Therapeutics 7, no. 3 (2023): 01–08. http://dx.doi.org/10.31579/2640-1053/149.

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In 1912, Kinnear Wilson was the first to describe an inherited fatal disease associated with progressive lenticular degeneration, chronic liver disease and cirrhosis (Wilson 1912) [1]. In the same year, Kayser and Fleischer found that patients with Wilson's disease (WD) often had brownish deposits of copper on the cornea, now called Kayser-Fleischer rings (Fleischer 1912) [2]. WD is an autosomal recessive metabolic disorder. Its ATP7B gene encodes a copper-transporting ATPase (Bull 1993, Tanzi 1993, Petrukhin 1993, Yamaguchi 1993) [3,4,5,6]. A genetic defect in the ATP7B protein reduces Biliar

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GRIMES, Andrew, Jennifer PAYNTER, Ian D. WALKER, Mrinal BHAVE, and Julian F. B. MERCER. "Decreased carbonic anhydrase III levels in the liver of the mouse mutant ‘toxic milk’ (tx) due to copper accumulation." Biochemical Journal 321, no. 2 (1997): 341–46. http://dx.doi.org/10.1042/bj3210341.

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The mouse mutant ‘toxic milk‘ (tx) is characterized by marked hepatic accumulation of copper, similar to that found in patients with the genetic disorder of copper transport, Wilson disease. In addition, lactating tx females produce copper-deficient milk. To characterize further the biochemical basis of this defect, Western blots of tissue extracts from normal and tx mice were probed with various heavy-metal radioisotopes (63Ni, 65Zn and 64Cu). A 30 kDa Ni/Zn-binding polypeptide was found to be markedly decreased in the livers of the tx mice. This protein was isolated from normal adult mice us

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Corsato Alvarenga, Isabella, Charles Aldrich, and Dennis Jewell. "Influence of Liver Condition and Copper on Selective Parameters of Post-Mortem Dog Tissue Samples." Animals 8, no. 12 (2018): 237. http://dx.doi.org/10.3390/ani8120237.

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One of the liver functions is copper storage, which can be toxic when in excess. The objective of this retrospective study was to determine the relationship between hepatic copper and pathology conditions in stored samples from 55 post-mortem dogs (37 Beagles, 12 Labrador Retrievers, and 6 Labrador Mixes). The analyses evaluated data from blood chemistry and complete blood count (CBC) that were measured immediately before euthanasia, and liver biopsies which were harvested at necropsy and frozen at −80 °C. Slides for microscopic evaluation were prepared, and liver copper and plasma metabolites

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Fimia Duarte, Rigoberto. "Copper and Zinc Levels in the Liver Tissue of Healthy Cattle Affected by Fasciola hepatica in a Slaughterhouse." International Journal of Zoology and Animal Biology 5, no. 2 (2022): 1–7. http://dx.doi.org/10.23880/izab-16000370.

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Fasciolosis is considered the most important liver disease in animals, the most notorious damages are caused by death, it causes a reduction in the production of meat, wool and milk, seizure of affected organs, secondary infections by bacteria, interference with fertility and expenses derived from its treatment. The objective of this research was to determine the relationship of Cu and Zn levels in the liver with the affectation by Fasciola hepatica in slaughterhouse cattle. Determinations of Cu, Zn, ash and dry matter were carried out using the atomic absorption spectrophotometry technique in

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Obayuwana, E., and S. M. Nweke. "Ameliorative effect of vitamin E on copper sulfate-induced liver damage in Wistar rats." Journal of Experimental and Clinical Anatomy 21, no. 2 (2024): 220–26. https://doi.org/10.4314/jeca.v21i2.11.

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BACKGROUND AND AIM: Significant human exposure to heavy metals such as copper sulfate is a major health concern due to its adverse consequences to body tissue. Vitamin E, a potent anti-oxidant is being investigated for its potential to protect against heavy metal toxicity. This study aimed to investigate the role of vitamin E on copper sulfate-induced liver damage. METHOD: Twenty-five (25) adult Wistar rats weighing between 160g and 220g were divided equally into five groups (A to E). They received 1 ml of distilled water, 200 mg/kg of copper sulfate for 30 days, 200 mg/kg of vitamin E for 30

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Tsocheva-Gaitandjieva, N. T., M. P. Gabrashanska, and S. Tepavitcharova. "Trace element levels in the liver of rats with acute and chronic fascioliasis and after treatment with zinc-copper hydroxochloride mixed crystals." Journal of Helminthology 76, no. 1 (2002): 87–89. http://dx.doi.org/10.1079/joh200187.

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AbstractQuantities of trace elements including copper, zinc, cobalt, manganese and iron were investigated in the liver tissue of rats at the acute or chronic stages of fascioliasis following treatment with zinc-copper hydroxochloride mixed crystals. Oral dosing (with food) of zinc–copper mixed crystals to healthy rats increased zinc and copper levels in the liver and decreased the iron content compared with controls. Manganese and cobalt levels did not change significantly. Significant reductions in all trace elements except manganese occurred in the liver of rats with acute or chronic fasciol

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Singh, A. P., J. Batra, S. S. Khan, R. Saxena, and S. Saxena. "Diagnosis and treatment of Wilson disease: An update." CARDIOMETRY, no. 25 (February 14, 2023): 1397–400. http://dx.doi.org/10.18137/cardiometry.2022.25.13971400.

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Wilson’s illness is an autosomal dominant impairment of copper metabolism that results from the lack of or dysfunction of a copper-transporting P-type ATPase, which is expressed on chromosome 13. This ATPase is a component of the trans-Golgi network and is carried by hepatocytes. It transports copper into the secretory route where it is combined with ceruloplasmin and excreted as bile. Affected people gradually develop copper accumulation in the liver since the only pathway for copper excretion in physiological settings is through biliary clearance. Hepatocytes experience cell death when their

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Kubow, Stan, Tammy M. Bray, and William J. Bettger. "Effects of dietary zinc and copper on free radical production in rat lung and liver." Canadian Journal of Physiology and Pharmacology 64, no. 10 (1986): 1281–85. http://dx.doi.org/10.1139/y86-216.

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The effects of dietary copper and zinc on free radical production in lung and liver microsomes were studied in male weanling rats. The rats were fed for 6 weeks on one of seven diets, with different copper and zinc concentrations representing low, adequate, and high dietary levels of copper and low and adequate levels of zinc. Rats were put on diets arranged in a 3 × 2 factorial design with copper and zinc supplementations of 0, 15, and 500 mg/kg and 0.5 or 100 mg/kg, respectively. The low copper diet depressed copper levels in both the lungs and liver, although zinc levels were unchanged in r

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Bakhsh, Shireen, Chia Wei Teoh, Elizabeth A. Harvey, and Damien G. Noone. "Single Pass Albumin Dialysis and Plasma Exchange for Copper Toxicity in Acute Wilson Disease." Case Reports in Nephrology and Dialysis 9, no. 2 (2019): 55–63. http://dx.doi.org/10.1159/000500104.

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Background: Wilson disease (WD) is a disorder of copper metabolism that results in accumulation of copper in tissues. In acute WD, patients present with fulminant hepatic failure, encephalopathy, and hemolytic anemia due to copper release from necrotic hepatocytes. Many will require life-saving liver transplantation. Extracorporeal liver support systems can provide a bridge to transplantation for critically ill patients. We report our experience with 2 patients for whom we used a combination of plasma exchange (PLEX) and single pass albumin dialysis (SPAD), or SPAD alone as a bridge to liver t

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