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Free Radicals and Antioxidants
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Copper can act both as an antioxidant and as a pro-oxidant. As an antioxidant, Cu scavenges or neutralizes free radicals and may reduce or help prevent oxidative stress caused by free radicals. When copper acts as a pro-oxidant at times, it promotes free radical damage and may contribute to the development of chronic diseases such as Alzheimer’s disease (212). Deficiency or excess of copper in the human body can cause diverse kinds of diseases. Excessive copper intake can cause nausea, vomiting, abdominal pain and cramps, headache, dizziness, weakness, and diarrhea. Since excess copper is excreted through bile, copper toxicity is most likely to occur in individuals with liver disease or bile disease (212). Maintaining the proper dietary balance of Cu, along with other minerals such as zinc and manganese, is important for maintaining good health. Beyond its role in iron metabolism, Cu also is involved in myriad biological processes, including antioxidant defense, neuropeptide synthesis, and immune function. It empowers the immune system, participates in the formation of enzymes, proteins, and brain neurotransmitters, and is an anti-inflammatory and anti-infectious agent. Similarly, it facilitates the synthesis of collagen and elastin (necessary constituents of the blood vessels, lungs, skin). In addition, it facilitates calcium and phosphorous fixation (15, 111, 209–212). The Tolerable Upper Intake Level (UL), and the recommended dietary allowances (RDAs), as well as the dietary source of copper are cited in Chapter 2 of this book.
Trace Minerals
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
Ingestion of copper from foods or simple salts appears to be relatively safe in humans. Estimates of safe intakes for indefinite time periods range from 10 to 35 mg Cu per d.808 Even 200 mg/d appears to be safe for short time periods.808 Acute copper toxicity may be more feasible. As little as 10 mg of copper (as a salt) may produce nausea, and 64 mg copper as 250 mg copper sulfate produces vomiting.808 Lethal doses in humans are thought to be 3.5 to 35 g. Acute toxicity symptoms are nausea, vomiting, jaundice, intravascular hemolysis, gastric hemorrhage, and hepatic necrosis. Situations where copper supplements should not be given are (1) Wilson’s disease (rare congenital disorder of excess tissue copper), (2) Indian childhood cirrhosis, (3) biliary atresia, (4) α1-antitrypsin deficiency, and (5) primary biliary cirrhosis.958 These conditions all cause copper to accumulate in tissues.
Non-viral liver disease
Published in Michael JG Farthing, Anne B Ballinger, Drug Therapy for Gastrointestinal and Liver Diseases, 2019
John ML Christie, Roger WG Chapman
Copper toxicity plays a primary role in the pathogenesis of this disorder.76 Affected organs invariably exhibit elevated copper levels, and reduction in the copper content results in improvement. Maintenance of normal copper homeostasis depends on the balance between gastrointestinal absorption and biliary excretion. Intestinal copper absorption is not different from normal individuals in Wilson’s disease; however, biliary excretion is reduced. Studies in a rat model (Long-Evans Cinnamon rat) indicate a possible defect in the entry of copper into lysosomes but with normal delivery into bile. It is thought that the Wilson gene product may be essential for the routing of copper into the trans-Golgi apparatus and thus be essential for copper excretion by the lysosomal pathway.77 The low ceruloplasmin level seen in Wilson’s disease is unlikely to have a pathological role and it is now believed that the low level is simply the result of a lack of incorporation of copper into apocaeruloplas-min, which has a shorter half-life than the copper-bound caeruloplasmin. Excess copper appears to exert toxic effects by the generation of free radicals.
Assay in serum of exchangeable copper and total copper using inductively coupled plasma mass spectrometry (ICP-MS): development, optimisation and evaluation of a routine procedure
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2020
Richard Daymond, Sarah L. Curtis, Vinita Mishra, Norman B. Roberts
A precise and reproducible method has been established using ICP-MS for the measurement of total copper and exchangeable copper in human serum with values for ExCu and REC compared in normal and states of increased CRP as a marker of inflammatory response. Overall no clear relationship to CRP was observed other than grossly elevated CRP resulting in raised ExCu and REC. Further studies are clearly needed to check for any increase of the copper toxic fraction in patients administered copper supplements with total parenteral nutrition where increased inflammation is associated. The conditions in which copper toxicity has been indicated such as liver disease, Alzheimer’s disease and pregnancy will also be important to assess. As regards application to WD it will be important to continue collection of data to establish cut-offs for ExCu and REC on newly diagnosed patients as well as those on treatment.
The Use of Trace and Essential Elements in Common Clinical Disorders: Roles in Assessment of Health and Oxidative Stress Status
Published in Nutrition and Cancer, 2019
David Calderón Guzmán, Hugo Juárez Olguín, Norma Osnaya Brizuela, Ernestina Hernández Garcia, Miroslava Lindoro Silva
Cu is an essential trace element required for the normal development of living organisms and their redox potential has been associated to human hepatopathies (62). However, copper is a very reactive element that, in free state, triggers the production of a large amount of free radicals, which consequently leads to the damage of proteins and DNA (63,64). Copper deficiency induced alterations in the oxidant defense system which ultimately results in excessive oxidative stress and tissue damage. Similar to copper deficiency, copper toxicity can result in significant oxidative stress and subsequent tissue damage. The oxidative stress associated with copper toxicity is in part a consequence of its redox reactivity, the ability of free copper or low molecular weight copper complexes to catalyze the reaction between superoxide anion and H2O2 producing the hydroxyl radical. In addition, copper can bind directly to free thiols of cysteines which can result in oxidation and subsequent crosslinks between proteins leading to impaired activity (65). Moreover, combining low plasma levels of copper and mixed normal plasma levels of Zinc in patients may be associated with an increased risk of preeclampsia (66). However, these micronutrients are essential trace elements needed to strengthen the immune system and also useful in the fight against tuberculosis (67).
4-Formylphenyl boronic acid grafted amino MCM-41 for efficient adsorption of Cu(II) ions in aqueous medium: isotherm, kinetic and optimization studies
Published in Toxin Reviews, 2022
Inderpreet Kaur, Navjot Kaur, Bhupinder Pal Singh, Rajeev Kumar, Jyoti Chawla
Copper and its compounds have been widely used in a variety of applications and ubiquitous in the environment. Copper is the major constituent in various metal alloys used in jewellery, marine hardware, coins and strain gauges. Copper is also present in different bacteriostatic agents, fungicides and wood preservatives. Copper bearing acid mine drainage and mining wastes are accountable for discharging considerable dose of dissolved copper in wastewater. Additional potential anthropogenic sources of copper containing waste include plating baths, industries of fertilizers, paints and pigments; municipal, agricultural and storm water runoffs which increases the levels of copper in environment and pose a serious threat to living resources including both humans and aquatic organisms along with ecological systems as they are non-biodegradable and toxic when present above the permissible limits. WHO prescribed the permissible limit of 1.0 ppm in drinking water (WHO 2011). Although copper is essential for smooth functioning of biological systems but its high concentration can cause metal poisoning called copperiedus associated with acute symptoms such as vomiting, hematemesis, hypotension, melena, coma, jaundice and gastrointestinal distress (Seiler et al. 1987). Disorders like Menkes syndrome and Wilson disease are caused by excess of copper in human body which leads to liver and brain damage (Brewer 2012). Copper toxicity in mammals also include health hazards such as liver cirrhosis, necrosis in kidneys and brain, skin lesions, low blood pressure and fetal mortality (Gaggelli et al. 2006, Kapoor et al. 2014). Excess of copper in water may harm marine and freshwater organisms such as fishes and mollusks. Increased concentration of copper in fishes and other aquatic creatures cause damage to gills, liver, kidneys, sense of smell (in fish) and the nervous system (McIntyre et al. 2008).