Zinc deficiency control

Hotz, C. and Brown, K. (2004). International Zinc Nutrition Consultative Group (IZiNCG) technical document 1. Assessment of the risk of zinc deficiency in populations and options for its control. Food Nutr. Bull. 25(1, Suppl 2), S94-S203. 

Although a-D-mannosidase appears to be under endocrine control,28,28 its natural function remains obscure. It is probable that the enzyme is important in the catabolism of D-mannose-containing glycoproteins,12,16,88 and, therefore, that the important trace element zinc could be indirectly implicated in this process. It is well known that zinc deficiency has an adverse effect on fertility in the male,89,90 and it could be argued that the changes observed in a-D-mannosidase activity in uterus and epididymis indicate that this enzyme is important in reproduction. It is scarcely justifiable to ascribe a cause-and-effect relationship to the correlations observed between the zinc content and the a-D-mannosidase activity in epididymis. All that can be said with any certainty is that, under certain circumstances, the two variables respond together to a common stimulus. 

Table III. Esophageal Tumor Incidence in Control and Zinc Deficient...

We have fed control and zinc-deficient rats their respective diets and administered N-nitrosodimethylamine (DMN) at a dose level of 2 mg/kg twice weekly for 3 weeks followed by 4 mg/kg of the same carcinogen for another 5 weeks, a total of 52 mg/kg. After 45 weeks none of the control rats had developed esophageal or forestomach lesions but, as shown in Table VIII, most of the zinc-deficient rats developed forestomach lesions or tumors (28). Mechanisms for this interesting observation are unclear but the underlying toxicology probably resides in metabolism affecting the site of tumor occurrence and type of activation of DMN. 

Changes in the erythrocyte zinc concentration were slow to appear as expected on the other hand, changes In the leukocyte zinc concentration appeared more sensitive to changes In zinc intake. Urinary excretion of zinc decreased as a result of dietary zinc restriction, suggesting that renal conservation of zinc may be Important for the homeostatic control mechanism in man. Thus, measuring zinc concentration in a 24-h urine test may be of additional help in diagnosing zinc deficiency provided cirrhosis of the liver, sickle cell disease, and chronic renal diseases are ruled out. These conditions are known to have hyperzlncuria and associated zinc deficiency. 

Figure 4. Eadie-Hofstee plot of I min zinc uptake by brush border membrane vesicles from control (- Zn) and 4-day zinc deficient ( Zn) rats.

Zinc deficiency is relatively uncommon in the United States, but may occur in adults with alcoholism or intestinal malabsorption problems. Low plasma zinc has been found in patients with alcoholic cirrhosis, Crohn s disease, and coeliac disease, Zinc deficiency, as well as deficiencies in a variety of other trace minerals, has occurred in hurnans fed for prolonged periods w lth intravenous diets from which the mineral had been inadvertently omitted. Controlled studies with humans have shown that the signs of zinc deficiency present after 2 to 5 weeks of consumption of a zinc-free diet- The signs include a facial rash, diarrhea, and alopecia. The rash occurs on the face, groins, hands, and feet. The symptoms can be reversed by administering zinc. 

The adverse effects on the brain of the suckling rats are apparently not readily reversible, as behavioral testing of nutritionally rehabilitated 60-80-day-old male rats has shown that they performed poorly on a Tolman-Honzik Maze (70) when compared with pair-fed and ad libi-tum-fed control rats. These findings suggested that zinc deficiency during the critical developmental period of the rat brain induces poorly reversible abnormalities which are manifested by impaired behavioral development. 

Prasad and Oberleas (90) provided evidence that decreased activity of deoxythymidine kinase may be responsible for this early reduction in DNA synthesis. As early as six days after the animals were placed on the dietary treatment, the activity of deoxythymidine kinase was reduced in rapidly regenerating connective tissue of zinc-deficient rats, compared with pair-fed controls. These results recently have been confirmed by Dreosti and Hurley (94), The activity of deoxythymidine kinase in 12-day-old fetuses taken from females exposed to a dietary zinc deficiency during pregnancy was significantly lower than in adlibitum and restricted-fed controls. Activity of the enzyme was not restored by in vitro addition of zinc, whereas addition of copper severely aflFected the enzyme activity adversely. Recently zinc has been shown to be an essential constituent for the DNA polymerase of E. coli (95). Whether or not this enzyme is affected adversely in animal model, because of deficiency of zinc, is not known. 

Livers from zinc-deficient rats incorporated less phosphorus-32 into the nucleotides of RNA than livers from pair-fed controls, and DNA-dependent RNA polymerase has been shown to be a zinc-dependent enzyme (96,97). The activity of RNase is increased in zinc deficient tissues (98). This suggests that the catabolism of RNA can be regulated by zinc. 

Enzyme Changes in Zinc Deficiency. Since zinc is required for many enzymes, it is reasonable to speculate that the level of zinc in cells controls the physiological processes through the formation and/or regulation of activity of zinc-dependent enzymes. Until 1965, there was no evidence in the literature to support this concept. During the past decade it has been shown that the activity of various zinc-dependent enzymes was reduced in the testes, bones, esophagus, and kidneys of zinc-deficient rats in comparison with their pair-fed controls (90,91,100,101), These results correlated with the decreased zinc content in the above tissues... 

Prevention and Control Similar symptoms are caused by a zinc deficiency. Try spraying the leaves with kelp extract. If the infected plant shows no response, remove and destroy it. 

Zinc deficiency is common in patients with cirrhosis and has been reported to cause overt HE. Zinc is a required cofactor for ammonia metabohsm two of the five metabolic pathways are zinc dependent. Both supportive and nonsupportive studies evaluating the efficacy of zinc replacement have been published. In a controlled trial in cirrhotic patients with mild HE, the administration of zinc sulfate 600 mg/day for 3 months resulted in increased urea formation and lower ammonia levels, along with improvement in psychological test scores. Zinc supplementation is recommended for long-term management in patients with cirrhosis who are zinc deficient. ... 

The body s natural homeostatic mechanisms control zinc absorption from the gastrointestinal tract (Davies 1980). Persons with adequate nutritional levels of zinc absorb approximately 20-30% of all ingested zinc. Those who are zinc-deficient absorb greater proportions of administered zinc (Johnson etal. 1988 Spencer etal. 1985). 

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