Ascorbic acid is thought to interact with copper in the gastrointestinal tract of humans and decrease the absorption of the mineral. It is known experimentally hat copper deficient animals can have their lives shortened by adding 0.1 to 1% ascorbic acid to their diets, which worsens the copper deficiency symptoms in the animals. Ascorbic acid is thought to decrease copper absorption because it reduces copper from its cupric state (Cu2+) to its less absorbable cuprous state (Cu1+). Alternatively, ascorbic acid may inhibit the binding of copper to metallothionein and delay or prevent its absorption through the intestinal mucosa. However, the role of ascorbic acid on copper metabolism is not limited to the gastrointestinal tract, and there is evidence to suggest that ascorbic acid plays an important role in copper transport and cellular uptake.
Ceruoplasmin is a glycoprotein involved in the transport of copper in the blood, and is also found bound to receptors on the surface of cells. Ceruoplasmin is know to undergo reactions in response to reducing agents such as ascorbic acid, which may facilitate the exchange of copper from ceruoplasmin to cells. Cell studies have shown that ascorbic acid stimulates the uptake of copper from ceruoplasmin to cultured cells by approximately 10-fold, suggesting a role for ascorbic acid in cellular copper uptake. Copper absorbed to cells from ceruoplasmin appears to be the Cu1+ cuprous form. Once in the cell, copper may bind to glutathione, which facilitates its transport to either superoxide dismutase or to metallothionein. Copper can also be transported bound to albumin, and in this case histidine plays a role in the transfer of copper to certain cells.
Cell experiments suggest that less copper binds to superoxide dismutase when ascorbate levels are high in the culture medium. In high ascorbate conditions, only 33% of copper can be immunoprecipitated with antibodies to superoxide dismutase, but when ascorbic acid is absent, 94% of the copper is immunoprecipitable. Experimental data suggests that ascorbate inhibits the post translations step of inserting copper into the super oxide dismutase protein. Similarities between the symptoms of copper deficiency in animals and scurvy in humans would tend to suggest that there is a mutual synergism between ascorbic acid and copper. Bone and connective tissue defects, anaemia and subcutaneous haemorrhaging are seen in both deficiency states. Therefore ascorbate appears to play a dual role in cooper metabolism, inhibiting the absorption of copper from the gut, but stimulating uptake at the cellular level.
RdB
