Copper toxicity

Last updated

Copper toxicity
Other namesCopperiedus
Kayser-Fleischer ring.jpg
A Kayser–Fleischer ring, copper deposits found in the cornea, is an indication the body is not metabolizing copper properly.
Specialty Toxicology

Copper toxicity (or Copperiedus) is a type of metal poisoning caused by an excess of copper in the body. Copperiedus could occur from consuming excess copper salts, but most commonly it is the result of the genetic condition Wilson's disease and Menke's disease, which are associated with mismanaged transport and storage of copper ions. Copper is essential to human health as it is a component of many proteins, but hypercupremia (high copper level in the blood) can lead to copper toxicity if it persists and rises high enough.

Contents

Chronic toxicity by copper is rare. [1] The suggested safe level of copper in drinking water for humans varies depending on the source, but tends to be pegged at 1.3 mg/L. [2] So low is the toxicity of copper that copper(II) sulfate is a routine reagent in undergraduate chemistry laboratories. [3]

Signs and symptoms

Acute symptoms of copper poisoning by ingestion include vomiting, hematemesis (vomiting of blood), hypotension (low blood pressure), melena (black "tarry" feces), coma, jaundice (yellowish pigmentation of the skin), and gastrointestinal distress. [4] Individuals with glucose-6-phosphate dehydrogenase deficiency may be at increased risk of hematologic effects of copper. [4] Hemolytic anemia resulting from the treatment of burns with copper compounds is infrequent. [4]

Chronic (long-term) copper exposure can damage the liver and kidneys. [5] Mammals have efficient mechanisms to regulate copper stores such that they are generally protected from excess dietary copper levels. [5] [6] The biological half-life of copper in human is about 13–33 days, [7] [8] [9] with excess copper excreted primarily through the bile into feces, and small amounts can be excreted through urine, saliva, and perspiration. [10] [11] [12] [13]

Those same protection mechanisms can cause milder symptoms, which are often misdiagnosed as psychiatric disorders. There is a lot of research on the function of the Cu/Zn ratio in neurological, endocrinological, and psychological conditions. [14] [15] [16] Many of the substances that protect humans from excess copper perform important functions in the neurological and endocrine systems, leading to diagnostic difficulties. When they are used to bind copper in the plasma, to prevent it from being absorbed in the tissues, their own function may go unfulfilled. Such symptoms often include mood swings, irritability, depression, fatigue, excitation, difficulty focusing, and feeling out of control. To further complicate diagnosis, some symptoms of excess copper are similar to those of a copper deficit.

The U.S. Environmental Protection Agency's Maximum Contaminant Level (MCL) in drinking water is 1.3 milligrams per liter. [4] [17] The MCL for copper is based on the expectation that a lifetime of consuming copper in water at this level is without adverse effect (gastrointestinal). The US EPA lists copper as a micronutrient and a toxin. [18] Toxicity in mammals includes a wide range of animals and effects such as liver cirrhosis, necrosis in kidneys and the brain, gastrointestinal distress, lesions, low blood pressure, and fetal mortality. [19] [20] [21] The Occupational Safety and Health Administration (OSHA) has set a limit of 0.1 mg/m3 for copper fumes (vapor generated from heating copper) and 1 mg/m3 for copper dusts (fine metallic copper particles) and mists (aerosol of soluble copper) in workroom air during an eight-hour work shift, 40-hour work week. [22] Toxicity to other species of plants and animals is noted to varying levels. [18]

EPA cancer data

The EPA lists no evidence for human cancer incidence connected with copper, and lists animal evidence linking copper to cancer as "inadequate". Two studies in mice have shown no increased incidence of cancer. One of these used regular injections of copper compounds, including cupric oxide. One study of two strains of mice fed copper compounds found a varying increased incidence of reticulum cell sarcoma in males of one strain, but not the other (there was a slightly increased incidence in females of both strains). These results have not been repeated. [23]

Pathophysiology

Indian childhood cirrhosis

One manifestation of copper toxicity, cirrhosis of the liver in children (Indian childhood cirrhosis), has been linked to boiling milk in copper cookware. The Merck Manual states that recent studies suggest that a genetic defect is associated with this particular cirrhosis. [24]

Wilson's disease

An inherited condition called Wilson's disease causes the body to retain copper, since it is not excreted by the liver into the bile. This disease, if untreated, can lead to brain and liver damage, and bis-choline tetrathiomolybdate is under investigation as a therapy against Wilson's disease.

Menke's disease

An X-linked recessive trait that is inherited named Menke's disease causes disruption of connective tissue due to mutations in genes. If severely affected the approximate span of life is three years. One treatment used to correct the mutation is copper-histidine treatment. [25]

Alzheimer's disease

Elevated free copper levels exist in Alzheimer's disease, [26] which has been hypothesized to be linked to inorganic copper consumption. [27] Copper and zinc are known to bind to amyloid beta proteins in Alzheimer's disease. [28] This bound form is thought to mediate the production of reactive oxygen species in the brain. [29]

Diagnosis

ICD-9-CM

ICD-9-CM code 985.8 Toxic effect of other specified metals includes acute and chronic copper poisoning (or other toxic effect) whether intentional, accidental, industrial etc.

In addition, it includes poisoning and toxic effects of other metals including tin, selenium, nickel, iron, heavy metals, thallium, silver, lithium, cobalt, aluminum and bismuth. Some poisonings, e.g. zinc phosphide, would/could also be included as well as under 989.4 Poisoning due to other pesticides, etc.

Excluded are toxic effects of mercury, arsenic, manganese, beryllium, antimony, cadmium, and chromium.

ICD-10-CM

CodeTerm
T56.4X1DToxic effect of copper and its compounds, accidental (unintentional), subsequent encounter
T56.4X1SToxic effect of copper and its compounds, accidental (unintentional), sequela
T56.4X2DToxic effect of copper and its compounds, intentional self-harm, subsequent encounter
T56.4X2SToxic effect of copper and its compounds, intentional self-harm, sequela
T56.4X3DToxic effect of copper and its compounds, assault, subsequent encounter
T56.4X3SToxic effect of copper and its compounds, assault, sequela
T56.4X4DToxic effect of copper and its compounds, undetermined, subsequent encounter
T56.4X4SToxic effect of copper and its compounds, undetermined, sequela

SNOMED

Concept IDTerm
46655005Copper
43098002Copper fever
49443005Phytogenous chronic copper poisoning
50288007Chronic copper poisoning
73475009Hepatogenous chronic copper poisoning
875001Chalcosis of eye
90632001Acute copper poisoning

Treatment

In cases of suspected copper poisoning, penicillamine is the drug of choice, and dimercaprol, a heavy metal chelating agent, is often administered. Vinegar is not recommended to be given, as it assists in solubilizing insoluble copper salts. The inflammatory symptoms are to be treated on general principles, as are the nervous ones. [30] Treatment can also look like ozone oxidation for environmental toxicity problems, as well as removing sediment in water areas because sediment can be a home for toxicants to reside. [31]

There is some evidence that alpha-lipoic acid (ALA) may work as a milder chelator of tissue-bound copper. [32] Alpha lipoic acid is also being researched for chelating other heavy metals, such as mercury. [33]

Aquatic life

Too much copper in water may damage marine and freshwater organisms such as fish and molluscs. [34] Fish species vary in their sensitivity to copper, with the LD50 for 96-h exposure to copper sulphate reported to be in the order of 58 mg per litre for Tilapia ( Oreochromis niloticus ) and 70 mg per litre for catfish ( Clarias gariepinus ) [35] The chronic effect of sublethal concentrations of copper on fish and other creatures is damage to gills, liver, kidneys and the nervous system. It also interferes with the sense of smell in fish, thus preventing them from choosing good mates or finding their way to mating areas. [36]

Copper-based paint is a common marine antifouling agent. [37] In the United States, copper-based paint replaced tributyltin, which was banned due to its toxicity, as a way for boats to control organic growth on their hulls. In 2011, Washington state became the first U.S. state to ban the use of copper-based paint for boating, although it only applied to recreational boats. [38] California has also pursued initiatives to reduce the effect of copper leaching, with the U.S. EPA pursuing research. [39]

Copper is an essential elemental for metabolic processes in marine algae. It is required for electron transport in photosynthesis and by various enzyme systems. Too much copper can also affect phytoplankton or marine algae in both marine and freshwater ecosystems. It has been shown to inhibit photosynthesis, disrupt electron transport in photosystem 2, reduce pigment concentrations, restrict growth, reduce reproduction, etc. [40] The toxicity of copper is widely recognized and is used to help prevent algal blooms. The effect of copper is solely dependent on the free copper the water is receiving. It's determined by the relative solubility and the concentration of the copper binding ligands.

Studies have shown that copper concentrations are toxic when marine phytoplankton are confined to areas that are heavily impacted by anthropogenic emissions. [41] Some of the studies have used a marine amphipod to show how copper affects it. This particular study said that the juveniles were 4.5 more times sensitive to the toxins than the adults. [42] Another study used 7 different algal species. They found that one species was more sensitive than the others, which was Synechococcus, and that another species was more sensitive in seawater, which was Thalassiosira weissflogii. [43]

One study used cyanobacteria, diatoms, coccolithophores, and dinoflagellates. This study showed that cyanobacteria was the most sensitive, diatoms were the least sensitive, and the coccolithophores and dinoflagellates were intermediate. They used copper ion in a buffer system and controlled it at different levels. They found that cyanobacteria reproduction rates were reduced while other algae had maximum reproduction rates. They found that Copper may influence seasonal successions of species. [44]

Bacteria

Copper and copper alloys such as brass have been found to be toxic to bacteria via the oligodynamic effect. The exact mechanism of action is unknown, but common to other heavy metals. Viruses are less susceptible to this effect than bacteria. Associated applications include the use of brass doorknobs in hospitals, which have been found to self-disinfect after eight hours, and mineral sanitizers, in which copper can act as an algicide. Overuse of copper sulfate as an algicide has been speculated to have caused a copper poisoning epidemic on Great Palm Island in 1979. [45]

Related Research Articles

<span class="mw-page-title-main">Selenium</span> Chemical element with atomic number 34 (Se)

Selenium is a chemical element; it has the symbol Se and atomic number 34. It has various physical appearances, including a brick-red powder, a vitreous black solid, and a grey metallic-looking form. It seldom occurs in this elemental state or as pure ore compounds in Earth's crust. Selenium was discovered in 1817 by Jöns Jacob Berzelius, who noted the similarity of the new element to the previously discovered tellurium.

<span class="mw-page-title-main">Algal bloom</span> Spread of planktonic algae in water

An algal bloom or algae bloom is a rapid increase or accumulation in the population of algae in fresh water or marine water systems. It is often recognized by the discoloration in the water from the algae's pigments. The term algae encompasses many types of aquatic photosynthetic organisms, both macroscopic multicellular organisms like seaweed and microscopic unicellular organisms like cyanobacteria. Algal bloom commonly refers to the rapid growth of microscopic unicellular algae, not macroscopic algae. An example of a macroscopic algal bloom is a kelp forest.

<span class="mw-page-title-main">Poison</span> Substance that causes death, injury or harm to organs

A poison is any chemical substance that is harmful or lethal to living organisms. The term is used in a wide range of scientific fields and industries, where it is often specifically defined. It may also be applied colloquially or figuratively, with a broad sense.

<span class="mw-page-title-main">Wilson's disease</span> Genetic multisystem copper-transport disease

Wilson's disease is a genetic disorder characterized by the excess build-up of copper in the body. Symptoms are typically related to the brain and liver. Liver-related symptoms include vomiting, weakness, fluid build-up in the abdomen, swelling of the legs, yellowish skin, and itchiness. Brain-related symptoms include tremors, muscle stiffness, trouble in speaking, personality changes, anxiety, and psychosis.

<span class="mw-page-title-main">Arsenic poisoning</span> Illness from ingesting arsenic

Arsenic poisoning is a medical condition that occurs due to elevated levels of arsenic in the body. If arsenic poisoning occurs over a brief period of time, symptoms may include vomiting, abdominal pain, encephalopathy, and watery diarrhea that contains blood. Long-term exposure can result in thickening of the skin, darker skin, abdominal pain, diarrhea, heart disease, numbness, and cancer.

<span class="mw-page-title-main">Mercury poisoning</span> Poisoning caused by mercury chemicals

Mercury poisoning is a type of metal poisoning due to exposure to mercury. Symptoms depend upon the type, dose, method, and duration of exposure. They may include muscle weakness, poor coordination, numbness in the hands and feet, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing. High-level exposure to methylmercury is known as Minamata disease. Methylmercury exposure in children may result in acrodynia in which the skin becomes pink and peels. Long-term complications may include kidney problems and decreased intelligence. The effects of long-term low-dose exposure to methylmercury are unclear.

<span class="mw-page-title-main">Liver disease</span> Medical condition

Liver disease, or hepatic disease, is any of many diseases of the liver. If long-lasting it is termed chronic liver disease. Although the diseases differ in detail, liver diseases often have features in common.

<span class="mw-page-title-main">Cyanotoxin</span> Toxin produced by cyanobacteria

Cyanotoxins are toxins produced by cyanobacteria. Cyanobacteria are found almost everywhere, but particularly in lakes and in the ocean where, under high concentration of phosphorus conditions, they reproduce exponentially to form blooms. Blooming cyanobacteria can produce cyanotoxins in such concentrations that they can poison and even kill animals and humans. Cyanotoxins can also accumulate in other animals such as fish and shellfish, and cause poisonings such as shellfish poisoning.

<span class="mw-page-title-main">Cinchophen</span> Chemical compound

Cinchophen is an analgesic drug that was first produced by Doebner & Gieskel in 1887, it was commercially introduced in 1908 as a treatment for gout. This drug is still used, in combination with Prednisolone, by veterinarians to treat arthritis in animals. It can be prepared starting from anilin, benzaldehyde and pyruvic acid in absolute ethanol. Use of this drug in humans ceased in the 1930s due to the discovery that cinchophen can cause serious liver damage. There is some evidence that it stimulates C-Fos.

Manganism or manganese poisoning is a toxic condition resulting from chronic exposure to manganese. It was first identified in 1837 by James Couper.

Iodomethane, also called methyl iodide, and commonly abbreviated "MeI", is the chemical compound with the formula CH3I. It is a dense, colorless, volatile liquid. In terms of chemical structure, it is related to methane by replacement of one hydrogen atom by an atom of iodine. It is naturally emitted in small amounts by rice plantations. It is also produced in vast quantities estimated to be greater than 214,000 tons annually by algae and kelp in the world's temperate oceans, and in lesser amounts on land by terrestrial fungi and bacteria. It is used in organic synthesis as a source of methyl groups.

<span class="mw-page-title-main">Hypervitaminosis A</span> Toxic effects of ingesting too much vitamin A

Hypervitaminosis A refers to the toxic effects of ingesting too much preformed vitamin A. Symptoms arise as a result of altered bone metabolism and altered metabolism of other fat-soluble vitamins. Hypervitaminosis A is believed to have occurred in early humans, and the problem has persisted throughout human history. Toxicity results from ingesting too much preformed vitamin A from foods, supplements, or prescription medications and can be prevented by ingesting no more than the recommended daily amount.

Zinc toxicity is a medical condition involving an overdose on, or toxic overexposure to, zinc. Such toxicity levels have been seen to occur at ingestion of greater than 50 mg of zinc. Excessive absorption of zinc can suppress copper and iron absorption. The free zinc ion in solution is highly toxic to bacteria, plants, invertebrates, and even vertebrate fish. Zinc is an essential trace metal with very low toxicity in humans.

<span class="mw-page-title-main">Cylindrospermopsin</span> Chemical compound

Cylindrospermopsin is a cyanotoxin produced by a variety of freshwater cyanobacteria. CYN is a polycyclic uracil derivative containing guanidino and sulfate groups. It is also zwitterionic, making it highly water soluble. CYN is toxic to liver and kidney tissue and is thought to inhibit protein synthesis and to covalently modify DNA and/or RNA. It is not known whether cylindrospermopsin is a carcinogen, but it appears to have no tumour initiating activity in mice.

<span class="mw-page-title-main">Metal toxicity</span> Harmful effects of certain metals

Metal toxicity or metal poisoning is the toxic effect of certain metals in certain forms and doses on life. Some metals are toxic when they form poisonous soluble compounds. Certain metals have no biological role, i.e. are not essential minerals, or are toxic when in a certain form. In the case of lead, any measurable amount may have negative health effects. There is a popular misconception that only heavy metals can be toxic, but lighter metals such as beryllium and lithium can be toxic too. Not all heavy metals are particularly toxic, and some are essential, such as iron. The definition may also include trace elements when abnormally high doses may be toxic. An option for treatment of metal poisoning may be chelation therapy, a technique involving the administration of chelation agents to remove metals from the body.

<span class="mw-page-title-main">Environmental toxicology</span> Multidisciplinary field of science

Environmental toxicology is a multidisciplinary field of science concerned with the study of the harmful effects of various chemical, biological and physical agents on living organisms. Ecotoxicology is a subdiscipline of environmental toxicology concerned with studying the harmful effects of toxicants at the population and ecosystem levels.

<span class="mw-page-title-main">Cirrhosis</span> Chronic disease of the liver, characterized by fibrosis

Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, chronic liver failure or chronic hepatic failure and end-stage liver disease, is a condition of the liver in which the normal functioning tissue, or parenchyma, is replaced with scar tissue (fibrosis) and regenerative nodules as a result of chronic liver disease. Damage to the liver leads to repair of liver tissue and subsequent formation of scar tissue. Over time, scar tissue and nodules of regenerating hepatocytes can replace the parenchyma, causing increased resistance to blood flow in the liver's capillaries—the hepatic sinusoids—and consequently portal hypertension, as well as impairment in other aspects of liver function. The disease typically develops slowly over months or years.

<span class="mw-page-title-main">2,3,7,8-Tetrachlorodibenzodioxin</span> Polychlorinated dibenzo-p-dioxin, chemical compound

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a polychlorinated dibenzo-p-dioxin (sometimes shortened, though inaccurately, to simply 'dioxin') with the chemical formula C12H4Cl4O2. Pure TCDD is a colorless solid with no distinguishable odor at room temperature. It is usually formed as an unwanted product in burning processes of organic materials or as a side product in organic synthesis.

Animal lead poisoning is a veterinary condition and pathology caused by increased levels of the heavy metal lead in an animal's body.

<span class="mw-page-title-main">Copper in biology</span>

Copper is an essential trace element that is vital to the health of all living things. In humans, copper is essential to the proper functioning of organs and metabolic processes. Also, in humans, copper helps maintain the nervous system, immune system, brain development, and activates genes, as well as assisting in the production of connective tissues, blood vessels, and energy. The human body has complex homeostatic mechanisms which attempt to ensure a constant supply of available copper, while eliminating excess copper whenever this occurs. However, like all essential elements and nutrients, too much or too little nutritional ingestion of copper can result in a corresponding condition of copper excess or deficiency in the body, each of which has its own unique set of adverse health effects.

References

  1. ↑ Barceloux DG, Barceloux D (1999). "Copper". Journal of Toxicology: Clinical Toxicology. 37 (2): 217–230. doi:10.1081/CLT-100102421. PMID   10382557.
  2. ↑ "The Water Supply (Water Quality) Regulations 2000". Archived from the original on 2010-07-25. Retrieved 2008-11-23.
  3. ↑ Rodríguez E, Vicente MA (2002). "A Copper-Sulfate-Based Inorganic Chemistry Laboratory for First-Year University Students That Teaches Basic Operations and Concepts". Journal of Chemical Education. 79 (4): 486. Bibcode:2002JChEd..79..486R. doi:10.1021/ed079p486.
  4. 1 2 3 4 Casarett L, Casarett L, Amdur M, Doull J (1996). Casarett & Doull's Toxicology, The Basic Science of Poisons (5th ed.). McGraw-Hill. p. 715. ISBN   0071054766.
  5. 1 2 "Copper: Health Information Summary" (PDF). Environmental Fact Sheet. New Hampshire Department of Environmental Services. 2005. ARD-EHP-9. Archived from the original (PDF) on 20 January 2017.
  6. ↑ Lutsenko S, Barnes NL, Bartee MY, Dmitriev OY (2007). "Function and Regulation of Human Copper-Transporting ATPases". Physiological Reviews. 87 (3): 1011–46. doi:10.1152/physrev.00004.2006. PMID   17615395.
  7. ↑ "Office of Dietary Supplements - Copper". 13 November 2024. Archived from the original on 11 November 2024. Retrieved 13 November 2024.
  8. ↑ Charkiewicz AE (August 2024). "Is Copper Still Safe for Us? What Do We Know and What Are the Latest Literature Statements?". Curr Issues Mol Biol. 46 (8): 8441–8463. doi: 10.3390/cimb46080498 . PMC   11352522 . PMID   39194715.
  9. ↑ Pfeiffer CC, Braverman ER (10 February 2024). "Copper: An essential metal in biology". Current Biology. 44 (21): 28–50. doi:10.1016/j.cub.2011.09.040. PMC   3718004 . PMID   22075424.
  10. ↑ "Wilson disease - Symptoms, diagnosis and treatment | BMJ Best Practice US". Archived from the original on 2023-03-11. Retrieved 2024-11-13.
  11. ↑ Linder MC (July 2020). "Copper Homeostasis in Mammals, with Emphasis on Secretion and Excretion. A Review". Int J Mol Sci. 21 (14): 4932. doi: 10.3390/ijms21144932 . PMC   7403968 . PMID   32668621.
  12. ↑ Chen J, Jiang Y, Shi H, Peng Y, Fan X, Li C (2020). "The molecular mechanisms of copper metabolism and its roles in human diseases". Pflügers Archiv - European Journal of Physiology. 472 (10): 1415–1429. doi:10.1007/s00424-020-02412-2. PMID   32506322. Archived from the original on 2024-08-19. Retrieved 2024-11-13.
  13. ↑ Ban Xx, Wan H, Wan XX, Tan YT, Hu Xm, Ban Hx, Chen Xy, Huang K, Zhang Q, Xiong K (2024). "Copper Metabolism and Cuproptosis: Molecular Mechanisms and Therapeutic Perspectives in Neurodegenerative Diseases". Current Medical Science. 44 (1): 28–50. doi: 10.1007/s11596-024-2832-z . PMID   38336987. Archived from the original on 2024-05-19. Retrieved 2024-11-13.
  14. ↑ Desai V, Kaler SG (2008). "Role of copper in human neurological disorders". The American Journal of Clinical Nutrition. 88 (3): 855S–8S. doi: 10.1093/ajcn/88.3.855S . PMID   18779308. Archived from the original on 6 March 2016. Retrieved 20 December 2015.
  15. ↑ Kaplan BJ, Crawford SG, Gardner B, Farrelly G (2002). "Treatment of Mood Lability and Explosive Rage with Minerals and Vitamins: Two Case Studies in Children". Journal of Child and Adolescent Psychopharmacology. 12 (3): 205–219. doi:10.1089/104454602760386897. PMID   12427294.
  16. ↑ Faber S, Zinn GM, Kern Ii JC, Skip Kingston HM (2009). "The plasma zinc/serum copper ratio as a biomarker in children with autism spectrum disorders". Biomarkers. 14 (3): 171–180. doi:10.1080/13547500902783747. PMID   19280374. S2CID   205770002.
  17. ↑ Federal Register / Vol. 65, No. 8 / Wednesday, January 12, 2000 / Rules and Regulations. pp. 1976.
  18. 1 2 US EPA Region 5 (2011-12-28). "Ecological Toxicity Information". US EPA. Archived from the original on 2015-03-30. Retrieved 17 June 2015.{{cite web}}: CS1 maint: numeric names: authors list (link)
  19. ↑ "Toxicological Profile for Copper". Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services. Retrieved 17 June 2015.
  20. ↑ Kabata-Pendias A (2010). Trace Elements in Soils and Plants, Fourth Edition (4th ed.). Taylor & Francis. ISBN   9781420093681. Archived from the original on 16 July 2015. Retrieved 17 June 2015.
  21. ↑ Ware GW (1983). Pesticides: Theory and application. New York: W.H. Freeman. OCLC   669712126.
  22. ↑ Occupational Safety and Health Administration, U.S. Department of Labor, Copper, Available Online at: https://www.osha.gov/SLTC/metalsheavy/copper.html Archived 2017-09-27 at the Wayback Machine
  23. ↑ "EPA results for copper and cancer. Accessed March 11, 2011". Archived from the original on September 13, 2015. Retrieved March 11, 2011.
  24. ↑ "Copper". Merck Manuals — Online Medical Library. Merck. November 2005. Retrieved 2008-07-19.[ permanent dead link ]
  25. ↑ Tümer Z, Møller LB (May 2010). "Menkes disease". European Journal of Human Genetics. 18 (5): 511–518. doi:10.1038/ejhg.2009.187. ISSN   1476-5438. PMC   2987322 . PMID   19888294.
  26. ↑ Brewer GJ (Apr 2010). "Copper toxicity in the general population". Clin Neurophysiol. 121 (4): 459–60. doi:10.1016/j.clinph.2009.12.015. PMID   20071223. S2CID   43106197.
  27. ↑ Brewer GJ (June 2009). "The risk of copper toxicity contributing to cognitive decline in the aging population and to Alzheimer's disease". J. Am. Coll. Nutr. 28 (3): 238–42. doi:10.1080/07315724.2009.10719777. PMID   20150596. S2CID   21630019.
  28. ↑ Faller P (2009-12-14). "Copper and zinc binding to amyloid-beta: coordination, dynamics, aggregation, reactivity and metal-ion transfer". ChemBioChem . 10 (18): 2837–45. doi:10.1002/cbic.200900321. PMID   19877000. S2CID   35130040.
  29. ↑ Hureau C, Faller P (October 2009). "Abeta-mediated ROS production by Cu ions: structural insights, mechanisms and relevance to Alzheimer's disease". Biochimie . 91 (10): 1212–7. doi:10.1016/j.biochi.2009.03.013. PMID   19332103.
  30. ↑ Royer A, Sharman T (2022), "Copper Toxicity", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   32491388, archived from the original on 2022-08-02, retrieved 2022-09-27
  31. ↑ "Treatment of high toxicity and high concentration organic wastewater includes adding copper sulfate and sodium sulfate to high toxicity and high concentration organic wastewater and treating organic wastewater by biological denitrification". Web of Science. Archived from the original on 2022-09-30. Retrieved 2022-09-30.
  32. ↑ Marangon K, Devaraj S, Tirosh O, Packer L, Jialal I (November 1999). "Comparison of the effect of α-lipoic acid and α-tocopherol supplementation on measures of oxidative stress". Free Radical Biology and Medicine. 27 (9–10): 1114–1121. doi:10.1016/S0891-5849(99)00155-0. PMID   10569644.
  33. ↑ "Mercury toxicity and antioxidants: part I: role of glutathione and alpha-lipoic acid in the treatment of mercury toxicity. (Mercury Toxicity)". Thorne Research Inc. 2002. Archived from the original on 22 December 2015. Retrieved 20 December 2015.
  34. ↑ Van Genderen EJ, Ryan AC, Tomasso JR, Klaine SJ (February 2005). "Evaluation of acute copper toxicity to larval fathead minnows (Pimephales promelas) in soft surface waters". Environ. Toxicol. Chem. 24 (2): 408–14. doi:10.1897/03-494.1. PMID   15720002. S2CID   6612606.
  35. ↑ Ezeonyejiaku, CD, Obiakor, MO and Ezenwelu, CO (2011). "Toxicity of copper sulphate and behavioural locomotor response of tilapia (Oreochromis niloticus) and catfish (Clarias gariepinus) species". Online J. Anim. Feed Res. 1 (4): 130–134.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  36. ↑ C. A. Flemming, J. T. Trevors (1989). "Copper toxicity and chemistry in the environment: a review". Water, Air, & Soil Pollution. 44 (1–2): 143–158. Bibcode:1989WASP...44..143F. doi:10.1007/BF00228784. S2CID   98175996.
  37. ↑ Earley PJ, Swope BL, Barbeau K, Bundy R, McDonald JA, Rivera-Duarte I (2014-01-01). "Life cycle contributions of copper from vessel painting and maintenance activities". Biofouling. 30 (1): 51–68. Bibcode:2014Biofo..30...51E. doi:10.1080/08927014.2013.841891. ISSN   0892-7014. PMC   3919178 . PMID   24199998.
  38. ↑ "Is Copper Bottom Paint Sinking? - BoatUS Magazine". Archived from the original on 2020-08-01. Retrieved 2016-09-22.
  39. ↑ "Marine Coatings: Making Sense of U.S., State, and Local Mandates of Copper-Based Antifouling Regulations". American Coatings Association. Archived from the original on 2016-10-20. Retrieved 2016-09-22.
  40. ↑ Gledhill M, Nimmo M, Hill SJ, Brown MT (1997). "The Toxicity of Copper (II) Species to Marine Algae, with Particular Reference to Macroalgae". Journal of Phycology. 33 (1): 2–11. Bibcode:1997JPcgy..33....2G. doi:10.1111/j.0022-3646.1997.00002.x. S2CID   84128896.
  41. ↑ Lopez JS, Lee L, Mackey KR (2019-01-24). "The Toxicity of Copper to Crocosphaera watsonii and Other Marine Phytoplankton: A Systematic Review". Frontiers in Marine Science. 5: 511. doi: 10.3389/fmars.2018.00511 . ISSN   2296-7745.
  42. ↑ Ahsanullah M, Florence TM (1984-12-01). "Toxicity of copper to the marine amphipod Allorchestes compressa in the presence of water-and lipid-soluble ligands". Marine Biology. 84 (1): 41–45. Bibcode:1984MarBi..84...41A. doi:10.1007/BF00394525. ISSN   1432-1793. S2CID   84484414.
  43. ↑ Quigg A, Reinfelder JR, Fisher NS (2006). "Copper uptake kinetics in diverse marine phytoplankton". Limnology and Oceanography. 51 (2): 893–899. Bibcode:2006LimOc..51..893Q. doi: 10.4319/lo.2006.51.2.0893 . ISSN   1939-5590.
  44. ↑ Brand LE, Sunda WG, Guillard RR (1986-05-01). "Reduction of marine phytoplankton reproduction rates by copper and cadmium". Journal of Experimental Marine Biology and Ecology. 96 (3): 225–250. doi:10.1016/0022-0981(86)90205-4. ISSN   0022-0981.
  45. ↑ Prociv P (September 2004). "Algal toxins or copper poisoning—revisiting the Palm Island 'epidemic'". Med. J. Aust. 181 (6): 344. doi:10.5694/j.1326-5377.2004.tb06316.x. PMID   15377259. S2CID   22054004.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.