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Metal Exposure and Toxic Responses
Published in Stephen K. Hall, Joana Chakraborty, Randall J. Ruch, Chemical Exposure and Toxic Responses, 2020
There are two genetically inherited inborn errors of copper metabolism that are in a sense a form of copper toxicity. Wilson’s disease is characterized by excessive accumulation of copper in liver, brain, kidneys, and cornea. Affected individuals fall largely into two broad categories: one with symptoms involving primarily the nervous system; the other involving the liver. When the accumulated copper is removed by effective chelation therapy, the symptoms of the disease regress. Wilson’s disease is apparently synonymous with copper toxicity. Menke’s disease, apparently an inability to absorb copper, is a copper deficiency. This disease is characterized by rapidly progressive cerebral degeneration and the presence of spirally twisted hair. It appears that in Menke’s disease, copper is available but it is not metabolized in the normal manner.
Toxicology
Published in Martin B., S.Z., of Industrial Hygiene, 2018
There are two genetically inherited inborn errors of copper metabolism that are, in a sense, a form of copper toxicity. Wilson’s disease is characterized by excessive accumulation of copper in liver, brain, kidneys, and cornea. Affected individuals fall largely into two broad categories: one with symptoms involving primarily the nervous system; the other involving the liver. When the accumulated copper is removed by effective chelation therapy, the symptoms of the disease regress. Wilson’s disease is apparently synonymous with copper toxicity. Menke’s disease, apparently an inability to absorb copper, is a copper deficiency. This disease is characterized by rapidly progressive cerebral degeneration and the presence of spirally twisted hair. It appears that in Menke’s disease, copper is available but it is not metabolized in the normal manner.
Clinical Toxicology of Copper
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Sonal Sekhar Miraj, Mahadev Rao
Wilson’s disease is a rare, progressive, autosomal recessive disorder characterized by impaired transport and excessive accumulation of Cu in the liver, brain, and other tissue (Popević et al. 2011). The condition is due to mutations in Wilson’s disease protein of ATP7B gene, by impaired Cu incorporation to ceruloplasmin and biliary Cu excretion. It is characterized by hepatic cirrhosis, neurological manifestations, psychiatric manifestations, renal diseases, and Cu deposition in the cornea (Kayser-Fleischer ring) (Strausak et al. 2001; Schaefer and Gitlin 1999). In a study of Cu toxicosis in humans, lipid peroxidation and Cu content were significantly increased in hepatic mitochondria from patients with Wilson’s disease. Modest elevation in lipid peroxidation was existed in microsomes of Wilson’s disease patients. Mitochondrial Cu concentrations correlated strongly with the severity of mitochondrial lipid peroxidation. These data suggest that the hepatic mitochondria are an important target in hepatic Cu toxicity and that oxidative damage to the liver may be involved in the pathogenesis of Cu-induced injury. A significant decrease (37%) in the vitamin E/lipid ratio was also detectable in patients with Wilson’s disease showing high free serum Cu (>10 mcg/dL). The data support a role for free radicals in the pathogenesis of active liver diseases (von Herbay et al. 1994). Another study revealed that impaired conversion of 25 (OH)D to 1.25 (OH)2D occurs in Cu intoxication and suggests that altered vitamin D metabolism is a potential factor in the development of bone and mineral abnormalities in Wilson’s disease (Carpenter et al. 1988).
Synthesis, characterization and antioxidant activity of EGCG complexes with copper and zinc ions
Published in Journal of Coordination Chemistry, 2019
Maysoon Alhafez, Fadi Kheder, Malak Aljoubbeh
Copper is an essential trace element present in our diet [1]. There are about 80 mg of copper in the human body [2]. Over-accumulation of copper in the liver and brain causes Wilson’s disease, which is caused by inability of the patients’ bodies to transport copper out of the affected tissues via the blood protein ceruloplasmin or biliary excretion [3]. On the other hand, copper deficiency may cause other disturbances in the human body, because it is associated with bone health, cardiovascular risk and immune function [4]. Copper is necessary as well for some enzymes such as superoxide dismutase and cytochrome oxidase [2]. Zinc is also an essential mineral nutrient that acts as a growth factor in humans [5]. Zinc deficiency can cause a number of illnesses, such as growth retardation, premature death and reproduction disorders in both male and female [4]. Zinc appears to have an oxidative-stress prevention ability, probably because it can displace the redox active metal ions from the reaction where damage occurs [2].
Efficacy of copper and silver as residual disinfectants in drinking water
Published in Journal of Environmental Science and Health, Part A, 2019
Enue E. Sicairos-Ruelas, Charles P. Gerba, Kelly R. Bright
At moderate levels, copper is considered safe to humans, as demonstrated by the widespread and prolonged use of copper intrauterine devices [17] and copper pipes/plumbing fixtures which leach copper ions into potable water[68,69]. However, copper toxicity has been documented in specific populations with altered copper metabolism, such as individuals with Wilson’s disease[49,70]. Because of this risk, the EPA has set a secondary non-enforceable standard of 1000 μg/L for copper [https://www.epa.gov/dwstandardsregulations/secondary-drinking-water-standards-guidance-nuisance-chemicals; accessed April 2018]. In addition, the EPA’s Lead and Copper Rule requires drinking water utilities to monitor water at customer taps. If greater than 10% of the taps sampled exceed 1300 μg/L Cu, the system must take actions to control corrosion [https://www.epa.gov/dwreginfo/lead-and-copper-rule#rule-summary; accessed April 2018].