Abstract
The suggestion that the "meat anemia" of mice is due to a dietary lack of copper accompanied by an excess of zinc in meat was investigated.
Muscle meat contains small amounts of copper and much more zinc whereas liver which protects against "meat anemia" contains more copper and less zinc than muscle. Supplementation of meat with copper or liver, which reduce the zinc-copper ratio of the diet, prevents anemia. Addition of zinc, which increases the zinc-copper ratio, leads to anemia.
Calcium prevents anemia even when the zinc-copper ratio is high. Treatment with vitamin D does not protect against anemia. It is concluded that calcium acts before its absorption in the intestinal tract, probably by interfering with the absorption of zinc.
Anemia also develops in mice which are maintained on a semisynthetic low-calcium diet with a higher content of zinc than of copper. Supplementation of this diet with calcium likewise alleviates the anemia.
Rats, which are resistant to "meat anemia," are less susceptible to the toxic effects of zinc than mice.
"Meat anemia" of mice seems, therefore, to result mainly from the presence in meat of insufficient amounts of copper accompanied by an excess of zinc, the effects of which are accentuated by a concomitant lack of calcium. Genetic factors determining the particular sensitivity to zinc seem to play an important role as well.
