Copper as Mineral – Rich Food Sources, Functions, Deficiency & Daily Requirements for Children, Men & Women

Presentation Notes on Copper (Cu) Vegetarian & Non Vegetarian Food Sources, Recommended Dietary allowance, Copper deficiency disorders, Role in Human Body with Treatment & Toxicity in word / .doc / ppt format

Copper :

The normal concentration of copper in serum is 90mg/dl. Copper is transported in the bound form as ceruloplasmin. It is stored in liver, muscles and bones of the body. Copper is present in a number of metalloenymes.

Daily requirement:

  • Adults : 2mg.Serum level 11-20umol/L

  • Nuts, dried fruits, pulses, meats, fruits’ oysters and fish.

  • Copper is present in oxidases. Eleven such enzymes are identified, e.g., cytochrome oxidases, superoxide dismutase.
  • Required for biosynthesis of haemoglobin. Utilization of iron for haemoglobin synthesis is enhanced by ceruloplasmin which is a blue copper protein complex that catalyzes Fe2+®Fe3+.
  • Deficiency of copper leads to microcytic anaemia.
  • Required for bone formation and maintenance of myelin.
  • Plays role in lipid and amino acid metabolism.
  • Copper-containing proteins are:
-          Ceruloplasmin.
-          Erythrocuprin.
-          Cytochrome oxidase.
-          Monoamine oxidase.
-          Melanin.


  • Cu2+ is insoluble at intestinal pH.
  • It gets bound to a protein (metallothionein) and gets absorbed from intestional mucosal cells and stomach.
  • Leucine enhances absorption of copper.
  • Once absorbed, copper gets bound to albumin.

  • It is excreted in bile, urine and sweat.

Clinical manifestations:

Wilson’s disease or hepatocellular degeneration:

-          Caused by a defect in transporting the absorbed copper across the serosal membrane of intestinal mucosal cells.
-          Pathological changes include demyelination, degeneration and cavitation of the basal ganglion in the brain and cirrhosis of the liver. Personality changes, tremors and hepatic failure occur.
-          Low plasma and high urinary levels, high deposition of copper and low ceruloplasmin.
-          Abnormal muscular movements, diabetes mellitus, renal tubular damage, visible brown rings (Kayser-Fleischer ring) at the margin of cornea, dementia and jaundice.
-          The patient dies of hepatic failure.
-          Copper-chelating agents are used to treat the disease, e.g., pencillamine.

Menke’s kinky hair syndrome:

-          It is a genetic disorder.
-          Occurs due to deficiency in copper absorption.
-          Symptoms are kinky hair, pale skin, depigmented hair, low body temperature and demineralization of the bone. Mental retardation occurs.


-          Toxicity of copper results in nausea, vomiting, headache, dizziness, hypertension and death. Copper toxicity also hepatic cirrhosis, tremor, mental deterioration, Kayser-Fleischer rings, heaemolytic anaemia and renal dysfunction (Fanconi-like syndrome).

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