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home - Nutrition - Minerals - Copper Written by Dr Sebastian Zeki


Acute: GI upset If severe: Cardiac and renal failure, hepatic necrosis, encephalopa-thy, and ultimately death. Albumin amino acids Copper Proximal small intestine Ferroportin Hephaestin Metalloreductase Cu2+ Cu1+ Ctr1 ATP7A (active removal) Cu1+ Secretory path Copper is incorporated into caeruloplasmin (also an acute phase reactant and transported to the peripheriesMetallothionein may be used for copper storage. 50% excreted in bile Dietary sources:Vegetables -20%.Grains -20%.Pulses (leguminous seeds such as beans, peas, and lentils)-20 %.Meat (esp liver), fish, and poultry- 20%. Enzymes:Zinc-copper superoxide dismutase (antioxidant defense)Dopamine mono-oxygenase (neurotransmitter synthesis)Lysyl oxidase (collagen cross-linking, bone formation)Ceruloplasmin (copper transporter and ferroxidase)Cytochrome c oxidase (electron transport)Factor V (thrombosis) Tyrosinase (melatonin production) Neurological abnormali-ties (ataxia, neuropathy and cognitive deficits- similar to B12 deficiency)Fragile, abnormally-formed hairDepigmentation of the skinMuscle weaknessHepatosplenomegalyHematological findings: Microcytic anemia Neutropenia ThrombocytopeniaOsteoporosisOedema ? Acquired Deficiency Risk factors:Premature infants receiving milk formulas.Chronic diarrhoea.Chronic peritoneal dialysis.Zinc supplements.Prior foregut surgery, including gastrectomy. ATP7A gene mutation X-linked Copper deficiency with progressive neurologic deterioration and death during early childhood. "Kinky" hair, Growth retardation, Hypopigmentation of the skin, Bony abnormalities (osteoporosis and spur) Treatment: iv copper-histidine complex. Copper Congenital Deficiency Menke’s kinky hair disease Toxicity Biological role Written by Dr Sebastian Zeki

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