Trace (micro) minerals, are required in small microgram amounts by humans. Trace minerals are essential nutrients and as such a failure to obtain an adequate intake causes specific deficiency diseases and ultimately death. Plants are a good source of many trace minerals, but the amounts they provide are dependent on the mineral content of the soil on which the plants are grown. Mineral deficient soils produce mineral deficient plants and when eaten, mineral deficient plants produce mineral deficient animals including humans. Some animal foods also contain high amounts of trace minerals, for example seafood such as fish can be rich in many trace minerals such as selenium. Consuming a high quality diet of mineral rich foods is therefore of primary importance at maintaining optimal mineral status. However, an often forgotten facet of mineral status is the way that minerals interact. In this regard, high intakes of one mineral may decrease the availability of another mineral and this may cause metabolic stress or disease.
Mineral interactions can occur in body tissues. However it is increasingly being recognised that interactions in the gut may significantly affect mineral status. For example, the gastrointestinal interaction between copper and zinc is well reported. Generally high intakes of copper interfere with zinc status and vice versa. The exact location of this interaction is not fully understood, but evidence suggests that zinc may share common transport routes with copper and inhibition may occur within the enterocytes. For example, in one study researchers investigated the effects of high intakes of copper on the absorption of zinc using an animal gut model1. Rats were fed either high or low zinc diets for a period of time and then the animals were sacrificed and sections of their guts were removed. The researchers then used these sections to investigate the transport of copper. The results showed that in the rats fed a low zinc diet, more copper was able to pass through the gut sections to be collected into a medium on the opposite side.
Therefore the high zinc diet affect the ability of the enterocytes to transport the copper. Further investigation revealed that more copper was retained in the mucosal sections of the rats fed low zinc diets. The researchers then analysed the copper in the intestinal sections and found it was bound to a protein of the same molecular weight as metallothionein. The authors speculated that zinc may induce mucosal cells to increase production of a thionein protein that is able to bind copper and sequester it from the normal transport routes and thus lower the absorption rates of copper. The authors did suggest that the actual uptake of copper was likely normal but it was the sequestration effect that had prevented the passage of the copper over the serosal membrane. Very high and very low levels of zinc have been shown previously to inhibit growth in rats, but in this study the growth rates remained normal. Examination of the livers and plasma of the rats however, did show that the zinc intake had an effect of hepatic and plasma levels of copper.
RdB
