Zinc metabolism in animals: Pathology, immunology and genetics

Abstract

Deficiency of dietary Zn rapidly reduces both appetite and growth, the latter effect being apparently caused by a failure of cell replication. Diagnosis of presymptomatic Zn deficiency depends largely on estimation of plasma Zn concentration but is complicated by reductions of it during a range of stressful conditions. In the latter cases, the decrease in plasma Zn concentration does not appear to be associated with inadequate Zn intake. Only two genetic defects of Zn metabolism are known in animals. One is associated with lethally inadequate concentrations of Zn in the milk of mice, the other with the A46 trait in Friesian cattle. A46 is a recessively inherited defect of Zn absorption which is lethal in the absence of major Zn supplementation of the diet. The characteristics of the disease are very similar to those of acrodermatitis enteropathica in man.

Expression pattern, genomic structure and evaluation of the human SLC30A4 gene as a candidate for acrodermatitis enteropathica

“…Now, the protein encoded by SLC30A4 is the last identified member of a mammalian family of zinc transporters which primary function would be the transport of zinc out of the cytoplasm, either out of the cell (Slc30a1 and Slc30a2) or into cellular compartments comprising endosomes (Slc30a2) and synaptic vesicles (Slc30a3; Huang and Gitschier 1997;McMahon and Cousins 1998;Palmiter and Findley 1995;Palmiter et al 1996a;Palmiter et al 1996b). This discovery is all the more interesting with respect to our study because, as with AE, lm is transmitted as an autosomal recessive trait, and is characterized by very similar symptoms of zinc deficiency including, more particularly, erythematous dermatitis, and alopecia (Chesters 1983;Huang and Gitschier 1997;Piletz and Ganschow 1978). Given all these similarities, we considered that the chance of finding, in the human SLC30A4 gene, an equivalent mutation causing AE was quite reasonable.…”

Zn2+-stimulated Endocytosis of the mZIP4 Zinc Transporter Regulates Its Location at the Plasma Membrane

“…AE is characterized by symptoms of zinc deficiency (10), such as dermatological lesions, changes in the small bowel mucosa, reduced weight gain, and immune and reproductive dysfunction (11)(12)(13)(14). The primary basis of AE is hypothesized to be the reduced uptake of dietary zinc by intestinal cells (15,16) because patients respond positively to dietary zinc supplements (11,12,17,18).…”

Some nutritional aspects of trace metals

“…The dependence of an element's biochemical function on its physico-chemical properties is described elsewhere in this symposium (Williams, 1983), as are the known functions and deficiency features of copper (Camakaris, 1983), zinc (Vallee, 1983;Chesters, 1983;Aggett, 1983), molybdenum (Coughlan, 1983;Wadman, 1983) and selenium (Lombeck, 1983) deprivation. We will comment therefore only on manganese and chromium.…”