Zinc deficiency severe

In addition to their endocrine disrupting properties, it must be appreciated that many of the chemicals in question possess more general toxic properties, which may be potentiated by metabolism by the organism. Several PAHs, PCBs and PCDDs are carcinogenic, while certain phthalate esters can enhance the excretion of zinc, potentially leading to zinc deficiency. Zinc, an essential element, plays a vital role in spermatogenesis and mature T-cell production. Deficiency may result in abnormalities of the male reproductive system, depletion of spermatogenesis and suppression of the immune system. 

Zinc deficiency in domestic pig (Sus spp.) is associated with a condition known as porcine parakeratosis, characterized by dermatitis, diarrhea, vomiting, anorexia, severe weight loss, and eventually death. The condition is exacerbated by high calcium levels (Vallee 1959). 

The balance between excess and insufficient zinc is important. Zinc deficiency occurs in many species of plants and animals, with severe adverse effects on all stages of growth, development, reproduction, and survival. In humans, zinc deficiency is associated with delayed sexual maturation in adolescent males poor growth in children impaired growth of hair, skin, and bones disrupted Vitamin A metabolism and abnormal taste acuity, hormone metabolism, and immune function. Severe zinc deficiency effects in mammals are usually prevented by diets containing >30 mg Zn/kg DW ration. Zinc deficiency effects are reported in aquatic organisms at nominal concentrations between 0.65 and 6.5 pg Zn/L of medium, and in piscine diets at <15 mg Zn/kg FW ration. Avian diets should contain >25 mg Zn/kg DW ration for prevention of zinc deficiency effects, and <178 mg Zn/kg DW for prevention of marginal sublethal effects. 

Human food, both plant and animal, usually contains satisfactory amounts of zinc to cover the requirement for this metal, which is present within the range of few to several pg per g of product. Zinc deficiencies are usually caused by a reduction of its absorption in the gastrointestinal tract rather than by its lack. Reduction in absorption may be caused by antagonistic activity of cadmium, calcium or phytates. A decrease in assimilation of zinc is also observed among alcoholics. 

Zinc (Zn) deficiency is teratogenic in rats, and fetal skeletal defects are prominent. Embryofetal zinc deficiency secondary to changes induced by substances in maternal Zn metabolism is a well-established mechanism for developmental toxicity (29-31). Several substances, including urethane and alpha-hederin cause similar malformations as Zn deficiency in rodents. A number of mechanistic studies have shown that these substances act via an acute-phase reaction induction of metallothionein in the maternal liver which binds systemically available Zn in the pregnant animal. This results in a systemic redistribution of Zn. As a consequence the substances produce a transient but developmentally adverse Zn deficiency in the... 

In addition to the classical symptoms of zinc deficiency mentioned above, the following unusual conditions have been reported liver and spleen enlargement, abnormal dark adaptation and abnormalities of taste. Several laboratory procedures for diagnosing zinc deficiency are available. Measurement of zinc levels in plasma is useful in certain cases. Levels of zinc in the red cells and hair may be used for assessment of body zinc status. More accurate and useful parameters are neutrophil zinc determination and quantitative assay of alkaline phosphatase activity in neutrophils. Determination of zinc in 24 h urine may help diagnose deficiency if sickle cell disease, chronic renal disease and liver cirrhosis are ruled out. A metabolic balance study may clearly distinguish zinc-deficient subjects. 

Although the role of zinc in human subjects has been now defined and its deficiency recognized in several clinical conditions, these examples are not representative of a pure zinc deficient state in man. It was, therefore, considered desirable to develop a human model which would allow a study of the effects of a mild zinc deficient state in man. Recently such a model has been established successfully in human volunteers with the use of a semi-purified diet based on texturized soy protein. 

Definitions of Zinc Deficiency. It is clear that zinc deficiency can be defined only with difficulty since the zinc content of a single body fluid or tissue level cannot provide a definitive estimate of body zinc status (If3 ) It is also not possible to rely on the concentration of zinc in several body tissues to estimate body zinc status since differing concentrations in different tissues lead to non-definitive conclusions. 

Zinc is a required mineral nutrient in the diet of animals and the signs and effects of a dietary deficiency have been described in several species ( ). Nutritional zinc deficiency has also been described in humans (2). Signs of nutritional zinc deficiency may be manifest even though the individual is consuming an amount of dietary zinc that exceeds the usually designated requirement (2). Thus, bloavailabillty of dietary zinc is a factor that must be evaluated in considering adequacy of dietary intake (jl). 

Zinc and Immunity. Zinc is required for Immunocompetence. Recently published reviews have detailed the role of zinc (92-95). Early clinical descriptions of zinc deficiency and impaired Immune function were first reported by Brummerstedt et al.(96) who reported that calves with a genetically acquired inability to absorb zinc suffered from stunted growth, several skin disorders, viral and fungal infections, and atrophied thymus glands. These symptoms could be reversed by the administration of large amounts of dietary zinc. 

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