INTRODUCTION — Zinc is an essential trace element. Zinc intake is closely related to protein intake; as a result, it is an important component of nutritionally related morbidity worldwide. Symptoms attributable to severe zinc depletion include growth failure, primary hypogonadism, skin disease, impaired taste and smell, and impaired immunity and resistance to infection. Zinc supplementation in populations likely at risk for zinc deficiency appears to have beneficial effects on the incidence and outcome of serious childhood infectious diseases.
ZINC METABOLISM — Approximately 10 to 40 percent of dietary zinc is absorbed in the small bowel; absorption is inhibited by the presence of phytates and fiber in the diet that bind to zinc, as well as dietary iron and cadmium [1]. Nonetheless, a randomized trial showed that standard iron supplements did not significantly interfere with zinc absorption or reduce zinc levels in healthy breastfed infants [2]. Approximately 0.5 to 1.0 mg/day is secreted in the biliary tract and excreted in the stool.
Zinc circulates at a concentration of 70 to 120 mcg/dL with 60 percent loosely bound to albumin and 30 percent tightly bound to macroglobulin. Urinary excretion typically ranges from 0.5 to 0.8 mg/day. The primary stores of zinc include the liver and kidney. Most of the body zinc stores are intracellular where zinc is bound to metalloproteins
ACTIONS — Zinc is the intrinsic metal component or activating cofactor for more than 70 important enzyme systems, including carbonic anhydrase, the alkaline phosphatases, dehydrogenases, and carboxypeptidases. It is involved in the regulation of nucleoproteins and the activity of various inflammatory cells and plays a role in growth, tissue repair and wound healing, carbohydrate tolerance, and synthesis of testicular hormones.
Zinc is involved in the immune response and the response to infection. Zinc deficiency is associated with impaired phagocytic function, lymphocyte depletion, decreased immunoglobulin production, a reduction in the T4+/T8+ ratio, and decreased interleukin (IL)-2 production [3-5].
Emerging evidence suggests that zinc may have specific inhibitory effects on some pathogens. As examples, zinc appears to block the secretory effects of cholera toxin and E. coli heat-labile enterotoxin [6], and has direct inhibitory effects on enteropathogenic E. coli [7]. Such effects appear to be due to local rather than systemic effects of the zinc