Zinc Deficiency in Animals

Acute zinc deficiency in adults is usually associated with specific signs and symptoms associated with the rapid and progressive loss of body zinc. The initial symptoms of this condition is almost uniformly anorexia (6,JJ), a symptom also seen early in experimental zinc deficiency in animals made deficient by limitation of dietary zinc (14,15). Anorexia is commonly followed by taste and smell dysfunction, then hypogeusia and hy-posmia (loss of taste and smell acuity, respectively), followed by dysosmia and dysgeusia. 

While many a jogger has suggested that exercise can improve his/ her resistance to infectious diseases, conclusive scientific evidence that exercise enhances immune response has yet to be presented. Experimental zinc deficiency in animals may provide a workable model for such investigations. It is well known that exercise induces hypertrophy of adrenal glands with a concomitant increase in the serum concentration of glucocorticoids. Zinc deficiency decreases T cell helper activity and thymic involution followed by a rise in glucocorticoids (98). The observations cited above suggest that it is possible to delineate experimentally the roles of zinc and exercise in immune response. 

Anorexia is another prominent and early feature of zinc deficiency in animals, and most of the children with low hair zinc levels in the original Denver study also had a history of poor appetite. In particular, the consumption of meats was very limited despite access to larger quantities. As animal products are the best source of available zinc, it is quite possible that the dietary zinc intake of these children was inadequate. 

It was appreciated later that zinc might be fundamental to the pathogenesis of this rare inherited disorder and that the clinical improvement reflected improvement in zinc status. Support for zinc deficiency hypothesis came from the observation that a close resemblance between the symptoms of zinc deficiency in animals and man as reported earlier (85) and... 

A deficiency of zinc in . gracilis has been shown to affect adversely all the phases of cell cycle (Gi, S, G2, and mitosis), thus indicating that zinc is required for biochemical processes essential for cells to pass from G2 to mitosis, from S to G2, and from Gi to S (13). The effect of zinc on cell cycle is undoubtedly attributable to its vital role in DNA synthesis (90,9i). Many studies have shown that zinc deficiency in animals im-... 

Zinc Deficiency in Animals Only small amounts of the zinc stored in the body of animals are available and, therefore, the metal must be supplied continuously via the diet. The required amounts of zinc depend on the species, age, pregnancy stage, health condition, the type of diet, and its zinc content as well as on any local industrial emissions, and the burden of different antagonists of zinc. 

Behavioral Changes Accompanying Zinc Deficiency in Animals, Edward S. Halas... 

Khandaker, Z.H. and S.B. Telfer. 1990. Treatment of zinc deficiency in sheep by zinc containing boluses. Asian-Australasian Jour. Anim. Sci. 3 53-59. 

Interesting research assessing the influence of select nutrients on apo A-I expression has been published (reviewed in Mooradian et al.36). Among some of the nutrients associated with decreased expression of the apo A-I gene in cell culture or animal models are polyunsaturated fatty acids, trans-fatty acids, omega-3 fatty acids, glucose, antioxidant vitamins, and zinc deficiency. In contrast, monounsaturated fatty acids, soy proteins, alcohol, and copper deficiency are associated with increased expression of the human apo A-I gene. 

In the first report of clinical zinc deficiency in humans (31, 32) the significant dietary consideration, not fully appreciated at that time, was that the village population subsisted primarily on unleavened whole wheat bread or bread and beans and very little animal protein was consumed by this population. 

The relative vulnerability of the secreted zinc to phytate complexatlon has only recently been demonstrated. The injection p zinc deficient rats intraperitoneally with a tracer dose of zlnc allows a portion of this zinc to be in equilibrium with the endogenous metabolic pool. This zinc then is secreted thru the saliva, pancreatic fluid, and bile. Those animals maintained on the phytate containing soy protein contained 2-4 times the radioactivity of the animals fed a casein protein diet (Table II). Therefore, not only does phytate affect the bioavailability of dietary zinc but also the reabsorption of endogenous zinc and thus has a net effect on zinc homeostasis. Since this total phytate effect cannot be measured ly labeling only the dietary pool, the expression of the net effect as the phytateizinc molar ratio is the most sensitive and accurate method of estimating the relative risk of zinc deficiency in any individual or population. 

Almost all the evidence showing that phytate decreases zinc absorption in man and animals is based on pure phytate added to the diet. The effect of natural phytate is variable (18). It has, however, been reported that phytate in bran affected zinc bioavailability in the same way as sodium phytate (19). Dietary fibre in the rural Iranian diet was considered to be the main cause of zinc deficiency in Iran (20). However, the addition of 26 g of fibre from various sources to the American diet did not have any significant effect on the zinc requirements of male adults (21). Similarly, Indian men consuming a diet containing only 10.8 mg of zinc were reported to be in balance in spite of a dietary fibre intake of 50 g per day (22). Moreover, the presence of fibre and phytate in soy flour did not affect the bioavailability of zinc added as zinc carbonate, to the diet of rats (17), although others (23) have reported that the bioavailability of zinc in breakfast cereals depends mainly on their phytate-zinc molar ratio. Our results indicate that there is some, as yet, undetermined difference in the phytate or the fibre of cereals which affects the bioavailability of zinc. It may be some component of dietary fibre (24) or the intrinsic differences in the protein-phytate-mineral complex (10). 

ALTHOUGH ZINC WAS KNOWN as a required mineral nutrient for the diets of animals, zinc deficiency in humans diets was not recognized until the early 1960s. Individuals consuming an amount of dietary zinc exceeding the usual designated requirement still may show signs of nutritional zinc deficiency. Thus, the adequacy of zinc in humans diets must be evaluated based on the bioavailability of dietary zinc. 

Interactions Overabundance of one trace element can interfere with the metabolic use of another element available at normal levels. For example, addition of large amounts of zinc to a diet interferes with (antagonizes) intestinal copper absorption, resulting in copper deficiency from a diet with adequate copper content. Copper deficiency can provoke iron deficiency and anaemia. Molybdenum deficiency in animals can be induced by co-administration of large amounts of the similar element tungsten. Iron deficiency can also increase retention of cadmium and lead, and selenium has been proposed to protect against cadmium and mercury toxicity. 

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