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PHARMACOLOGICAL ACTIVITIES - TOXICOLOGY - DRUG INTERACTIONS

Copper (Gluconate)

Copper is an essential trace element for humans and animals. In the body, copper shifts between
the cuprous (Cu ) and cupric (Cu ) forms, though the majority of the body’s copper is in the
1+
2+
Cu form. Copper is a critical functional component of a number of essential enzymes known as
2+
cuproenzymes. Some of the physiologic functions known to be copper-dependent include energy
production, regulation of gene expression (Uauy et al., 1998), formation of connective tissue,
the pigment melanin and maintenance of myelin sheath (Shils et al., 2006), iron metabolism,
synthesis of the neurotransmitter norepinephrine (O’Dell & Sunde, 1997), metabolism of
neurotransmitters norepinephrine, epinephrine, dopamine and serotonin (FNB & IOB, 2001),
antioxidant functions such as copper dependent superoxide dismutase and ceruloplasmin
(Johnson et al., 1992). In dogs copper deficiency can cause lameness and bone fragility, loss of hair
pigmentation, and hyperextension in the distal phalanges (Ettinger & Feldman, 2000b; NRC,
2006).

Toxicity for copper gluconate has not been documented in dogs and cats when administered orally in
TOXICOLOGY copper toxicosis similar to Wilson’s disease in humans has been identified. Acute poisoning is usually seen after
therapeutic doses. However, in various breeds of dogs, especially Bedlington Terriers, an inherited sensitivity to

accidental administration of excessive amounts of soluble copper salts (Kahn & Line, 2010). Intradermal LD
50
for copper salts is >1124 mg/kg of body weight in rats (EVM, 2000).

DRUG Validated interactions studies do not exist for copper preparations. However, penicillamine
INTERACTIONS dramatically increases the urinary excretion of copper; individuals taking the medication for
reasons other than copper overload may have an increased copper requirement. Additionally,
antacids may interfere with copper absorption when used in very high amounts (Shils et al., 2006).

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