Summary
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. Chronic toxicity by copper is rare. 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. So low is the toxicity of copper that copper(II) sulfate is a routine reagent in undergraduate chemistry laboratories. 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. Individuals with glucose-6-phosphate dehydrogenase deficiency may be at increased risk of hematologic effects of copper. Hemolytic anemia resulting from the treatment of burns with copper compounds is infrequent. Chronic (long-term) copper exposure can damage the liver and kidneys. Mammals have efficient mechanisms to regulate copper stores such that they are generally protected from excess dietary copper levels. 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. Many of the substances that protect us from excess copper perform important functions in our 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.
About this result
This page is automatically generated and may contain information that is not correct, complete, up-to-date, or relevant to your search query. The same applies to every other page on this website. Please make sure to verify the information with EPFL's official sources.