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Zinc deficiency is associated with poor growth and development. It has been postulated that a deficiency of the various zinc metalloenzymes results from the lack of dietary zinc. From present study, an examination of some aspects of this postulate, we conclude the following about zinc deficiency in pigs: (1) Of the tissues studied, it results im diminished zinc content only in liver, kidney, and pancreas. (2) It is associated with tissue abnormalities of various trace elements other than zinc. (3) Histochemical enzyme assays are satisfactory for qualitative but not quantitative determination of zinc metalloenzymes. (4) Deficiency of various tissue zinc metalloenzymes is difficult to demonstrate, even in severe zinc deficiency. (5) It is associated with decreased activity of hepatic leucine aminopeptidase and ornithine transcarbamylase, and decreased serum cholesterol concentrations. Our findings are consistent with the postulate that alterations in a number of trace elements may occur in the entity called zinc deficiency.

Pigs received a diet containing 0.59 p.p.m. Mn. Control pigs received the samequantity of the same diet which was supplemented with 22 p.p.m. of Mn. At the end of6 weeks, pigs fed the low Mn diet had a diminution in tissue Mn levels as well as a diminution in tissue Se content. Tissue levels of Zn, Cu, Ca, and Mg were notaffected by the dietary regimen. Indicative of the fact that experimental animals were probably Mn-deficient was a statistically significant decrease in hepatic arginaseactivity that could be enhanced by the addition of Mn. These studies represent the first experimental evidence that there may be a specific interaction between tissue Se and Mn. Tissue Se levels were decreased to a statistically significant degree in all tissues studied except the kidney in the Mn-deficient animals.