Copper sulfate

Intravenous
Nutritional deficiency

Intravenous
Copper deficiency

Oral
Nutritional deficiency

Young children. Pregnancy, lactation. Wilson's disease. Chronic liver/renal failure. Hepatic impairment: copper may accumulate if biliary obstruction or hepatic disease is present.

Excessive dose may cause abdominal pain or cramps, diarrhoea, nausea/vomiting & metallic taste.

Severe GI effects. In extreme or long term overdosage, symptoms may be similar to that of Wilson's disease. Treatment is symptomatic and may involve the use of a chelating agent (e.g. penicillamine, trientine and zinc) to remove any absorbed metal. Dialysis may be useful.

Ascorbic acid (large doses). Inhibit intestinal absorption by oral iron supplements, oral/parenteral Zn, D-Penicillamine or trientine chelate copper. Excessive amounts of molybdenum may produce copper deficiency.

Concomitant intake with foods rich in phytic acid (unleavened bread, raw beans, seeds, nuts & grains & soy isolates) may decrease absorption of copper. Diets high in fructose may decrease copper status.

Description:
Mechanism of Action: An essential trace element important for proper functioning of many metalloenzymes including ceruloplasmin, ferroxidase II, lysyl oxidase, monoamine oxidase, Zn-copper superoxide dismutase, tyrosinase, dopamine-β-hydroxylase & cytochrome-c-oxidase. It is involved in erythropoiesis & leukopoiesis, bone mineralisation, elastin & collagen cross-linking, oxidative phosphorylation, catecholamine metabolism, melanin formation & antioxidant protection of cells. May also play a role in iron turnover, ascorbic acid metabolism, phospholipid metabolism, myelin formation, glucose homeostasis & cellular immune defense.
Pharmacokinetics:
Absorption: Principally absorbed in the small intestine.
Excretion: 80% eliminated via the bile. Little excretion by the kidney.

Electrolytes