Copper Metabolism and Diseases of Copper Metabolism
René Lontie in Copper Proteins and Copper Enzymes, 1984
In many ways cellular copper metabolism can be approached with the same perspectives as classic metabolic biochemistry. Thus, copper must first be transported across a cell membrane; a series of specific precursor-product steps presumably follows in a specific order within various cell compartments. Ultimately, copper must be stored, mobilized from storage sites, incorporated into essential copper proteins, perhaps be used for a variety of regulatory or other functions, and secreted from the cell. Overall, copper metabolism also includes the regulation of whole body copper homeostasis, i.e., the absorption, distribution, and excretion aspects of copper balance. Metabolic interactions with related trace elements and other key metabolites, especially hormones, constitute yet another aspect of copper metabolism. Several excellent reviews of copper metabolism are available including those written by Sass-Kortsak,3 Evans,4 Mason,5 and others.2,6-14 A major aim of this review is to help identify those aspects of cellular copper metabolism which remain to be elucidated at a molecular biochemistry level. Borrowing again from the experiences of classic metabolic biochemistry, inborn errors of copper metabolism will also be stressed, recognizing that an inherited disease serves as a window to a critical cellular component and metabolic step. Changes during development can provide similar insights.
Postoperative Nutritional Management of the Bariatric-Surgery Patient
Emmanuel C. Opara, Sam Dagogo-Jack in Nutrition and Diabetes, 2019
Although copper deficiency is rare in the general population, anatomic changes from bariatric surgery can lead to copper deficiency in bariatric surgery patients. The reduction in gastric acid from stomach resection and bypassing the duodenum reduces copper bioavailability. Signs of copper deficiency are anemia, leukopenia, neutropenia, thrombocytopenia, and neuropathies affecting muscle weakness, peripheral numbness, and paresthesias. Approximately 20% of RYGB patients were copper deficient at 24 months post-surgery.101 Interestingly, no difference in copper intake was seen between copper-deficient and copper-sufficient patients, suggesting that the reduced bioavailability is the mechanism for compromised copper. Complicating assessment of copper status is that serum copper and ceruloplasmin, both biomarkers for copper status, are elevated with inflammation,102 which may hinder the detection of copper deficiency.
Deficiency of Mineral Nutrients for Mankind
Jul Låg in Geomedicine, 2017
Copper deficiency might be a problem in malnourished children and in patients on long-term parenteral nutrition. Signs of copper deficiency are anemia, leucopenia, skeletal defects, and demyelination and degeneration of the nervous system.12 Animals severely deficient in copper are also hypercholesteremic and their hearts and arteries have abnormal connective tissue.20 Severe copper deficiency in humans is seen in Menkes’ kinky hair disease, an X-linked, recessively inherited disease where the absorption of copper is defective.21 Even if plasma copper can be raised by infusions, these patients usually die before the age of 2 years, probably because of a defective cellular utilization of the element. The biochemical functions of copper are linked to specific cuproenzymes, for example, cytoplasmic superoxide dismutase, cytochrome c oxidase, dopamine-3-monoxygenase, and tyrosinase. Several investigators have pointed out that the average copper intake is marginal or deficient in most of the Western world, compared to the recommended intake of at least 2 mg/d. Based upon results from animal experiments, it has been hypothesized that such marginal intake is of importance in the pathogenesis of ischemic heart disease.22
Theranostic approaches in nuclear medicine: current status and future prospects
Published in Expert Review of Medical Devices, 2020
Luca Filippi, Agostino Chiaravalloti, Orazio Schillaci, Roberto Cianni, Oreste Bagni
Radiopharmacy is a field that is expected to rapidly evolve in the next few years. In this respect, the radionuclide copper-64 (64Cu) is gaining more and more attention in the scientific community. Copper is an essential element in many metabolic processes involving cell differentiation, metabolism, and growth. Furthermore, human copper transporter 1 (CTR1), a transmembrane protein responsible for copper intracellular incorporation, was found to be overexpressed in many malignancies. 64Cu is a cyclotron-produced radionuclide with an intermediate half-life (12.7 h) that decays by both positronic and beta-particles emission, making it suitable for theranostic applications. The radiopharmaceutical 64CuCl2, a substrate for CTR1, is under investigation with promising results as a potential theranostic agent in several pre-clinical and clinical trials regarding tumors such as melanoma or prostate cancer [90,91].
Copper and zinc deficiency in an alcoholic patient: a case report of a therapeutic dilemma
Published in Journal of Addictive Diseases, 2022
Hiroshi Ito, Yasuhiro Ogawa, Nobutake Shimojo, Satoru Kawano
Copper is a trace element essential for the function of human cellular enzymes. The recommended dietary allowance for copper is 0.9 mg daily in adults.1 Although relatively rare, copper deficiency usually presents symptoms including anemia and ataxia.2 The risk factors for copper deficiency include gastrointestinal surgery, excessive zinc ingestion, and malabsorptive conditions. Case reports have suggested an association between alcohol consumption and copper deficiency.3 However, little is known still about the relationship between the two states. Here, we describe a case of copper deficiency in a patient with alcohol use disorder who also had zinc deficiency. Patients with alcohol use disorder can present zinc and copper deficiencies at the same time. Because copper and zinc are competitively absorbed from the jejunum, this condition poses a therapeutic dilemma.
MMP-3 activation is involved in copper oxide nanoparticle-induced epithelial-mesenchymal transition in human lung epithelial cells
Published in Nanotoxicology, 2021
Yuanbao Zhang, Yiqun Mo, Jiali Yuan, Yue Zhang, Luke Mo, Qunwei Zhang
Copper exposure has been shown to cause acute adverse health effects in workers including fever, dyspnea, chills, headache, and nausea. The symptoms appeared less than 5 h after exposure and increased urine copper level was detected in five of twelve exposed workers (Armstrong et al. 1983). Nano-CuO has manifested more toxic effects than its micro-sized particles and can cause oxidative stress, mitochondrial damage, oxidative DNA lesions, and cell death (Juganson et al. 2015; Wang et al. 2012). Recently, studies also verified that intranasal or inhalation exposure of mice to Nano-CuO caused pulmonary inflammation after short-term exposure and fibrosis after long-term exposure (Costa et al. 2018; Gosens et al. 2016; Ilves et al. 2019; Lai et al. 2018; Park et al. 2016). However, the detailed mechanisms of Nano-CuO-induced pulmonary injury and fibrosis is still unclear.
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