scholarly journals Hepatic Copper Accumulation: A Novel Feature in Transient Infantile Liver Failure Due to TRMU Mutations?

2014 ◽  
pp. 109-113 ◽  
Author(s):  
Z. Grover ◽  
P. Lewindon ◽  
A. Clousten ◽  
A. Shaag ◽  
O. Elpeleg ◽  
...  
Keyword(s):  
Liver Failure ◽  
Copper Accumulation ◽  
Hepatic Copper

Assessment of copper accumulation in archived liver specimens from cats

2020 ◽  
pp. 1098612X2096135
Author(s):  
Punyamanee Yamkate ◽  
Randi M Gold ◽  
Panagiotis G Xenoulis ◽  
Katja Steiger ◽  
David C Twedt ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Hepatic Steatosis ◽  
Dry Weight ◽  
Reference Interval ◽  
Copper Accumulation ◽  
Zonal Distribution ◽  
Tissue Samples ◽  
Hepatic Copper ◽  
Liver Copper ◽  
Flame Atomic Absorption

Objectives The aim of this study was to assess hepatic copper concentrations and zonal distribution in cat liver specimens. Methods For this study, 121 archived, formalin-fixed, paraffin-embedded liver specimens from cats were used. Tissue sections were stained for copper with rhodanine and scored from 0 (no copper accumulation) to 5 (panlobular copper accumulation). The tissue specimens were then deparaffinized and hepatic copper concentrations were measured using flame atomic absorption spectroscopy. Results Tissue samples were categorized into four groups based on histopathologic findings: (1) no significant histopathologic hepatic changes (n = 66); (2) hepatic steatosis (n = 18); (3) inflammatory or infectious disease (n = 24); and (4) neoplasia (n = 13). Of the 121 specimens, 13 (11%) stained positive for copper, with three having a score ⩾3. Thirty-seven specimens (31%) had copper concentrations above the reference interval ([RI] <180 µg/g dry weight liver). Copper concentrations in cats with hepatic inflammatory or infectious disease were significantly higher than cats with hepatic steatosis ( P = 0.03). Copper-staining score and concentration were positively correlated ( rs = 0.46, P <0.001). Conclusions and relevance Despite the fact that 31% of specimens had copper concentrations above the RI, only 11% showed positive copper staining and only 2.5% had a score ⩾3. Our findings suggest that hepatic copper concentrations greater than the upper limit of the RI are relatively common in cats. Further studies to determine the factors that influence hepatic copper staining in cats and to establish contemporary RIs for hepatic copper in healthy cats are warranted.

Hepatic Copper Accumulation Induces DNA Strand Breaks in the Liver Cells of Long-Evans Cinnamon Strain Rats

2000 ◽  
Vol 276 (1) ◽  
pp. 174-178 ◽  
Author(s):  
Masanobu Hayashi ◽  
Tomoko Kuge ◽  
Daiji Endoh ◽  
Kenji Nakayama ◽  
Jiro Arikawa ◽  
...  
Keyword(s):  
Dna Strand Breaks ◽  
Liver Cells ◽  
Copper Accumulation ◽  
Strand Breaks ◽  
Hepatic Copper ◽  
Long Evans ◽  
Dna Strand

scholarly journals Regulation of murine copper homeostasis by members of the COMMD protein family

2020 ◽  
Vol 14 (1) ◽  
pp. dmm045963
Author(s):  
Amika Singla ◽  
Qing Chen ◽  
Kohei Suzuki ◽  
Jie Song ◽  
Alina Fedoseienko ◽  
...  
Keyword(s):  
Copper Homeostasis ◽  
Copper Accumulation ◽  
Copper Transporter ◽  
Copper Excretion ◽  
Copper Absorption ◽  
Hepatic Copper ◽  
High Copper ◽  
Molecular Machinery ◽  
And Function

ABSTRACTCopper is an essential transition metal for all eukaryotes. In mammals, intestinal copper absorption is mediated by the ATP7A copper transporter, whereas copper excretion occurs predominantly through the biliary route and is mediated by the paralog ATP7B. Both transporters have been shown to be recycled actively between the endosomal network and the plasma membrane by a molecular machinery known as the COMMD/CCDC22/CCDC93 or CCC complex. In fact, mutations in COMMD1 can lead to impaired biliary copper excretion and liver pathology in dogs and in mice with liver-specific Commd1 deficiency, recapitulating aspects of this phenotype. Nonetheless, the role of the CCC complex in intestinal copper absorption in vivo has not been studied, and the potential redundancy of various COMMD family members has not been tested. In this study, we examined copper homeostasis in enterocyte-specific and hepatocyte-specific COMMD gene-deficient mice. We found that, in contrast to effects in cell lines in culture, COMMD protein deficiency induced minimal changes in ATP7A in enterocytes and did not lead to altered copper levels under low- or high-copper diets, suggesting that regulation of ATP7A in enterocytes is not of physiological consequence. By contrast, deficiency of any of three COMMD genes (Commd1, Commd6 or Commd9) resulted in hepatic copper accumulation under high-copper diets. We found that each of these deficiencies caused destabilization of the entire CCC complex and suggest that this might explain their shared phenotype. Overall, we conclude that the CCC complex plays an important role in ATP7B endosomal recycling and function.

scholarly journals Soy Protein Isolate Enhances Hepatic Copper Accumulation and Cell Damage in LEC Rats

2003 ◽  
Vol 133 (5) ◽  
pp. 1250-1254 ◽  
Author(s):  
Kayo Yonezawa ◽  
Sachiko Nunomiya ◽  
Mitsue Daigo ◽  
Yasumitsu Ogra ◽  
Kazuo T. Suzuki ◽  
...  
Keyword(s):  
Soy Protein ◽  
Cell Damage ◽  
Soy Protein Isolate ◽  
Protein Isolate ◽  
Copper Accumulation ◽  
Hepatic Copper ◽  
Lec Rats

Variations in ATP7B in cats with primary copper-associated hepatopathy

2019 ◽  
Vol 22 (8) ◽  
pp. 753-759
Author(s):  
Hajime Asada ◽  
James K Chambers ◽  
Mari Kojima ◽  
Yuko Goto-Koshino ◽  
Taisuke Nakagawa ◽  
...  
Keyword(s):  
The Other ◽  
Copper Accumulation ◽  
Limited Information ◽  
Single Nucleotide ◽  
Serum Ceruloplasmin ◽  
Hepatic Copper ◽  
Single Nucleotide Variations ◽  
Tissue Specimens ◽  
Ceruloplasmin Activity ◽  
Low Serum

Objectives Primary copper-associated hepatopathy (PCH) has been reported in young cats. Although our group recently reported a young cat with PCH harbouring single-nucleotide variations in ATP7B, limited information is available regarding its association with the pathogenesis of feline PCH. The objective of this study was to investigate the prevalence of ATP7B variations in cats with PCH. Methods Rhodanine staining was performed to detect hepatic copper accumulation (HCA) in intraoperative liver tissue specimens from 54 cats. In cats with HCA, variations in ATP7B and COMMD1 and serum ceruloplasmin activity were analysed. Results Based on age, liver histopathological findings and hepatic distribution of accumulated copper, PCH was suspected in 4/54 cats. Sequence analysis of ATP7B and COMMD1 revealed single-nucleotide variations in ATP7B in 3/4 cats with PCH. Among the cats with PCH, one showed remarkably low serum ceruloplasmin activity, while the other three did not. Conclusions and relevance The results of this study suggest that some cats with PCH harbour single-nucleotide variations in ATP7B, suggesting that feline PCH is an equivalent disorder to human Wilson’s disease. This study provides basic evidence facilitating further studies of the pathophysiology and treatment of feline PCH.

Excessive Hepatic Copper Accumulation in Jaundiced Rats Fed a High-Copper Diet

2002 ◽  
Vol 88 (3) ◽  
pp. 255-270
Author(s):  
A. C. Beynen ◽  
S. Yu ◽  
R. Van Der Meer
Keyword(s):  
Copper Accumulation ◽  
Hepatic Copper ◽  
High Copper

scholarly journals Spontaneous hepatic copper accumulation in Long-Evans Cinnamon rats with hereditary hepatitis. A model of Wilson's disease.

1991 ◽  
Vol 87 (5) ◽  
pp. 1858-1861 ◽  
Author(s):  
Y Li ◽  
Y Togashi ◽  
S Sato ◽  
T Emoto ◽  
J H Kang ◽  
...  
Keyword(s):  
Hepatitis A ◽  
Wilson’S Disease ◽  
Wilson's Disease ◽  
Copper Accumulation ◽  
Hepatic Copper ◽  
Long Evans

ABCB4 deficiency is causative for hepatic copper accumulation in a patient with features of Wilson Disease

2012 ◽  
Vol 50 (01) ◽  
Author(s):  
C Jüngst ◽  
F Lammert ◽  
V Zimmer
Keyword(s):  
Wilson Disease ◽  
Copper Accumulation ◽  
Hepatic Copper

scholarly journals Effects of Super Nutritional Hepatic Copper Accumulation on Hepatocyte Health and Oxidative Stress in Dairy Cows

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Jaimie M. Strickland ◽  
Doug Lyman ◽  
Lorraine M. Sordillo ◽  
Thomas H. Herdt ◽  
John P. Buchweitz
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Dairy Cows ◽  
Inductively Coupled Plasma ◽  
Copper Concentration ◽  
Tissue Level ◽  
Copper Accumulation ◽  
Serum Samples ◽  
Inductively Coupled ◽  
Hepatic Copper

Concerns regarding excessive hepatic copper concentrations in dairy cows have increased. The objective of this study was to determine the association of hepatic copper concentrations with evidence of liver disease. Blood and liver samples were collected at the time of slaughter in cull dairy cows (n=100). Liver samples were analyzed for copper using inductively coupled plasma mass spectrometry and crude fat using liquid-liquid extraction and gravimetry. Serum samples were analyzed for glutamate dehydrogenase,γ-glutamyltransferase, sorbitol dehydrogenase, aspartate aminotransferase activities, and bile acid concentrations. Liver samples were examined histologically for inflammation, fibrosis, and rhodanine staining. Animals were stratified by hepatic copper concentration and samples in the highest and lowest quintiles (Q5 and Q1) were evaluated for oxidative stress. Systemic indices of oxidative stress included serum reactive oxygen and nitrogen species (RONS) and total antioxidant potential (AOP). Tissue-level oxidative stress was assessed by immunohistochemistry using 4-hydroxynonenal (4HNE) and 3-nitrotyrosine (3NIT) stains to score the relative abundance and distribution of oxidized lipid and protein products, respectively. Mean hepatic copper concentration was 496.83μg/g and median 469.72μg/g and ranged from 70.56 to 1264.27μg/g dry tissue. No association was found between hepatic copper concentrations and clinicopathological or histological evidence of hepatic damage or dysfunction. There was a significant increase in the amount of IHC staining of 4HNE and 3NIT in Q5 compared with Q1. Moreover, the IHC staining mirrored the distribution of the copper-specific stain rhodanine. These results demonstrate that cows with elevated hepatic copper concentrations had no evidence of active liver disease but had increased hepatic oxidative stress.

Presumed primary and secondary hepatic copper accumulation in cats

2014 ◽  
Vol 244 (1) ◽  
pp. 68-77 ◽  
Author(s):  
Brandi M. Hurwitz ◽  
Sharon A. Center ◽  
John F. Randolph ◽  
Sean P. McDonough ◽  
Karen L. Warner ◽  
...  
Keyword(s):  
Copper Accumulation ◽  
Hepatic Copper
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