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PubMed1998

Effect of infections on plasma zinc concentration and implications for zinc status assessment in low-income countries.

The development of intervention programs to control zinc deficiency is hampered by the lack of sensitive, specific, low-cost indicators of zinc status. The mean plasma zinc concentration of groups of individuals has been suggested as a possible indicator of a population's zinc status because the plasma zinc concentration seems to predict whether growth will increase in response to zinc supplementation. However, experimental studies in both animal models and adult human volunteers as well as clinical studies of infected and noninfected adults indicate that systemic infections that produce an acute phase response also cause the plasma zinc concentration to fall. Therefore, concerns have been raised about the usefulness of plasma zinc concentration as an indicator of zinc status in populations with high prevalences of infections. By contrast with the aforementioned studies in adults, cross-sectional, community-based surveys of children with and without common infections have not found any association between the presence of infection and plasma zinc concentration, possibly because the severity of those infections observed in children in field settings was less than that of the infections studied in adults. Thus, it appears that the mean plasma zinc concentration may be a useful indicator of population zinc status for children in low-income countries despite the high prevalence of common childhood infections encountered in these settings.

Adolescent↗

PubMed2002

Effect of supplemental zinc on the growth and serum zinc concentrations of prepubertal children: a meta-analysis of randomized controlled trials.

BACKGROUND: Multiple studies have been carried out to assess the effect of zinc supplementation on children's growth. The results of these studies are inconsistent, and the factors responsible for these varied outcomes are unknown. OBJECTIVE: Meta-analyses of randomized controlled intervention trials were therefore completed to assess the effect of zinc supplementation on the physical growth and serum zinc concentrations of prepubertal children. DESIGN: A total of 33 acceptable studies with appropriate data were identified by MEDLINE (National Library of Medicine, Bethesda, MD) searches and other methods. Weighted mean effect sizes (expressed in SD units) were calculated for changes in height, weight, weight-for-height, and serum zinc concentration by using random-effects models; factors associated with effect sizes were explored by meta-regression techniques. RESULTS: Zinc supplementation produced highly significant, positive responses in height and weight increments, with effect sizes of 0.350 (95% CI: 0.189, 0.511) and 0.309 (0.178, 0.439), respectively. There was no significant effect of zinc on weight-for-height indexes [weighted mean effect size: -0.018 (-0.132, 0.097)]. Zinc supplementation caused a large increase in the children's serum zinc concentrations, with an effect size of 0.820 (0.499, 1.14). Growth responses were greater in children with low initial weight-for-age z scores and in those aged >6 mo with low initial height-for-age z scores. CONCLUSIONS: Interventions to improve children's zinc nutriture should be considered in populations at risk of zinc deficiency, especially where there are elevated rates of underweight or stunting. The population mean serum zinc concentration is a useful indicator of the successful delivery and absorption of zinc supplements in children.

Adolescent↗

PubMed1975

Protection against zinc deficiency by prior excess dietary zinc in young Japanese quail.

Three experiments were designed to determine whether an excess of zinc during the first week of life would afford any protection to young Japanese quail during a subsequent period of zinc deprivation. Day-old birds of both sexes were fed an adequate purified diet containing soybean protein with requirement (25-30 mg/kg of diet) or higher levels of zinc for 1 week. The zinc level was reduced during the second week to the deficient level of 1mg/kg of diet, except for the controls which continued to receive an adequate or higher level of zinc (25, 30 or 75 mg/kg of diet). With this low zinc intake, birds that received an initial level of zinc in excess of requirement grew significantly better (body weight and length of primary wing feathers) than those that initially received the required amount of zinc. Data on zinc content of liver, breast muscle, tibia and whole body retention suggest that bone may store zinc consumed in excess of requirement and that this zinc may be available for utilization during a subsequent period of zinc deprivation in a growing animal that has rapidly remodeling bones.

Animals↗

PubMed1978

Zinc, nitrogen, copper, iron, and manganese balance in adolescent females fed two levels of zinc.

The effect of feeding two different levels of zinc (Diet Z11.5 and Diet Z14.7) on zinc, nitrogen, copper, iron, and manganese balances was determined in 11 girls, 12.5 to 14.2 years, during a 30-day period. Diet Z11.5 provided 11.32 or 11.64 mg zinc daily, levels similar to that determined previously to be consumed by average adolescent females. Diet Z14.7 provided 14.52 or 14.84 mg zinc daily. These levels were just slightly less than the Recommended Dietary Allowance for zinc. When fed Diet Z14.7, subjects lost significantly more zinc in their feces than when fed Diet Z11.5. Regression analyses were applied to the zinc balance data from this study and a previous study with adolescent females. By extrapolation, a dietary intake of 11 mg zinc daily was estimated to compensate for fecal and urinary zinc losses of the average girl in these studies. The standard error of the estimate was 2.18 mg zinc daily. Nitrogen excretion and retention were unaffected by the variations in zinc intake. Copper excretion in the feces was significantly increased when subjects were fed Diet Z14.7 rather than Diet Z11.5. Manganese and iron fecal losses were also significantly correlated to zinc fecal losses.

Adolescent↗

PubMed1983

Effect of dietary zinc and protein levels on the utilization of zinc and copper by adult females.

Zinc and copper utilization were examined in twenty-three young adult females fed either a moderate protein, low zinc diet, a high protein, low zinc diet, a moderate protein, high zinc diet, or a high protein, high zinc diet during a 24-day metabolic balance study. The moderate and high protein diets contained 7.9 g and 15.2 g nitrogen per day, respectively. The low and high levels of zinc were 9.5 or 10.1 and 18.4 or 19.9 mg daily. Copper intake was constant at approximately 2.0 mg/day. Urinary zinc excretion was significantly greater (P less than 0.05) in subjects consuming the high protein diets. Fecal zinc paralleled zinc intake but was not affected by protein intake. Apparent retention of zinc was not significantly different among dietary treatments ranging from -0.29 to 1.58 mg/day. Fecal excretion and apparent retention of copper were not affected by protein intake. Mean copper retentions ranged from 0.12 to 0.30 mg/day. Dietary zinc did not affect copper excretion or retention. Dietary protein, at levels commonly consumed by a substantial portion of the American adult female population, did not affect zinc and copper utilization. Individuals were not consistently in positive balance although average retentions were generally positive.

Adolescent↗

PubMed1984

A model to produce pure zinc deficiency in rats and its use to demonstrate that dietary phytate increases the excretion of endogenous zinc.

An early effect of zinc deficiency in rats is loss of appetite with consequent malnourishment. To obviate the need for pair-feeding, rats were fed liquid semipurified diets by gastric tube feeding. Rats tube fed a zinc-deficient diet at a daily rate of 90-110 g/kg thrived for 6-7 days and then rapidly became seriously ill. In contrast rats fed the deficient diet ad libitum stopped growing after 3 days but remained relatively healthy. Animals tube fed a zinc-replete diet or the deficient diet with subcutaneous injections of zinc grew normally and suffered no ill effects. Rats tube fed the deficient diet and supplemented parenterally with zinc excreted significantly more endogenous zinc into small intestinal luminal washings and into feces than unsupplemented rats. Sodium phytate, added to the tube feed in three groups of rats fed the deficient diet and supplemented daily with 0, 0.33 and 3.3 mg Zn/kg, significantly increased the zinc content of luminal washings in all three groups, increased fecal zinc excretion in two groups and lowered body zinc levels, estimated by femur zinc, in two groups. Tube feeding provides a means to study: 1) pure zinc deficiency without malnourishment of other nutrients; and 2) the excretion of endogenous zinc into the gastrointestinal tract.

Animals↗

PubMed1984

Zinc-copper interactions in the pregnant rat: fetal outcome and maternal and fetal zinc, copper and iron.

The interaction between zinc and copper in the pregnant rat was investigated by feeding Sprague-Dawley rats, from mating to term, diets that varied in zinc and copper concentrations. A factorial design was used with diets containing 1, 10, 100 or 1000 micrograms zinc/gram and 0.5, 5, 10 or 100 micrograms copper/gram. Malformations were found only in fetuses from rats fed the zinc-deficient diets (1 microgram/g), and the frequency of malformed fetuses increased as concentration of dietary copper increased. Maternal and fetal tissues of rats fed diets deficient in either zinc or copper were significantly lower in these elements than were those of rats fed a control diet. An antagonistic effect of dietary zinc on maternal and fetal tissue copper concentration was observed. The concentration of fetal liver zinc from rats fed a copper-deficient diet was significantly higher than controls. The concentration of iron in maternal and fetal tissues was significantly affected by the level of dietary zinc, with values highest in the zinc-deficient groups. Maternal plasma cholesterol and triglyceride levels were significantly lower than normal in the zinc-deficient animals. These data show that when the concentration of zinc in the diet is deficient an interaction can occur between dietary zinc and copper such that high levels of copper potentiate the teratogenicity of zinc deficiency.

Animals↗

PubMed1985

Zinc content of blood cellular components and lymph node and spleen lymphocytes in severely zinc-deficient rats.

Several investigators have suggested that the measurement of leukocyte zinc may be useful for the assessment of zinc nutriture. However, in an earlier study, we found that the methods used did not adequately separate platelets from the different leukocyte populations. We subsequently developed a method which does adequately separate platelets, mononucleated cells (MNC), polymorphonucleated cells (PMN), and erythrocytes (RBC) from a single blood sample. This method was applied to a study of severe zinc deficiency in adult male rats. Significant reductions in plasma and femur zinc indicated severe zinc deficiency in the zinc-deficient animals compared with pair-fed or ad libitum-fed control rats in two separate experiments. However, we noted no differences in the zinc content of the MNC, PMN, RBC or lymph node lymphocytes, on a per cell basis, between the zinc-deficient and ad libitum- or pair-fed control groups of rats. A minor, but not significant (P greater than 0.05) reduction of platelet zinc was noted in zinc-deficient rats in two separate studies. These data indicate that the zinc contents of blood cellular components are not sensitive indicators of zinc deficiency in rats.

Animals↗

PubMed1993

Bone zinc is poorly released in young, growing rats fed marginally zinc-restricted diet.

The effect of marginal zinc restriction on bone zinc release was studied. Male weanling rats were fed zinc-adequate diet (12 mg zinc/kg diet) for 1 wk, intubated with 65Zn, refed the zinc-adequate diet for an additional week, and divided into one baseline group and five marginally zinc-restricted groups (6 mg/kg) and five corresponding zinc-adequate pair-fed groups. Significantly lower (P < 0.05) 65Zn radioactivity (10-20%) in the first week was observed in femurs of rats fed the marginally zinc-restricted diet without further change in the following weeks. Pair-fed rats showed higher 65Zn radioactivity in femurs in the second week, and the level was maintained. Similar results were found in tibia 65Zn radioactivity. Muscle zinc concentration was higher in the first week (P < 0.05) but subsequently returned to baseline levels in the second week through the fifth week. The results support the existence of two zinc pools in the skeleton, one a small, rapidly turning-over pool (10-20% in size), and the other a slowly turning-over pool. When rats suffer marginal zinc restriction, zinc from the readily turning-over bone pool is utilized for soft tissue needs, followed by decreased growth rate to maintain zinc homeostasis.

Animals↗

PubMed1998

Identification of a zinc-specific metalloregulatory protein, Zur, controlling zinc transport operons in Bacillus subtilis.

Zinc is an essential nutrient for all cells, but remarkably little is known regarding bacterial zinc transport and its regulation. We have identified three of the key components acting to maintain zinc homeostasis in Bacillus subtilis. Zur is a metalloregulatory protein related to the ferric uptake repressor (Fur) family of regulators and is required for the zinc-specific repression of two operons implicated in zinc uptake, yciC and ycdHIyceA. A zur mutant overexpresses the 45-kDa YciC membrane protein, and purified Zur binds specifically, and in a zinc-responsive manner, to an operator site overlapping the yciC control region. A similar operator precedes the ycdH-containing operon, which encodes an ABC transporter. Two lines of evidence suggest that the ycdH operon encodes a high-affinity zinc transporter whereas YciC may function as part of a lower-affinity pathway. First, a ycdH mutant is impaired in growth in low-zinc medium, and this growth defect is exacerbated by the additional presence of a yciC mutation. Second, mutation of ycdH, but not yciC, alters the regulation of both the yciC and ycdH operons such that much higher levels of exogenous zinc are required for repression. We conclude that Zur is a Fur-like repressor that controls the expression of two zinc homeostasis operons in response to zinc. Thus, Fur-like regulators control zinc homeostasis in addition to their previously characterized roles in regulating iron homeostasis, acid tolerance responses, and oxidative stress functions.

ATP-Binding Cassette Transporters↗

PubMed1992

Symptomatic zinc deficiency in experimental zinc deprivation.

An evaluation of indices of poor zinc status was undertaken in five male subjects in whom dietary zinc intake was reduced from 85 mumol d-1 in an initial phase of the study to 14 mumol d-1. One of the subjects developed features consistent with zinc deficiency after receiving the low zinc diet for 12 days. These features included retroauricular acneform macullo-papular lesions on the face, neck, and shoulders and reductions in plasma zinc, red blood cell zinc, neutrophil zinc and plasma alkaline phosphatase activity. Alcohol induced hepatitis, which was suspected in this subject, may have caused a predisposition to altered zinc metabolism and possible zinc deficiency which was exacerbated by subsequent zinc deprivation. The report supports the value of neutrophil zinc concentration as an indicator of poor zinc status.

Adult↗

PubMed2005

hZIP1 zinc uptake transporter down regulation and zinc depletion in prostate cancer.

BACKGROUND: The genetic and molecular mechanisms responsible for and associated with the development and progression of prostate malignancy are largely unidentified. The peripheral zone is the major region of the human prostate gland where malignancy develops. The normal peripheral zone glandular epithelium has the unique function of accumulating high levels of zinc. In contrast, the ability to accumulate zinc is lost in the malignant cells. The lost ability of the neoplastic epithelial cells to accumulate zinc is a consistent factor in their development of malignancy. Recent studies identified ZIP1 (SLC39A1) as an important zinc transporter involved in zinc accumulation in prostate cells. Therefore, we investigated the possibility that down-regulation of hZIP1 gene expression might be involved in the inability of malignant prostate cells to accumulate zinc. To address this issue, the expression of hZIP1 and the depletion of zinc in malignant versus non-malignant prostate glands of prostate cancer tissue sections were analyzed. hZIP1 expression was also determined in malignant prostate cell lines. RESULTS: hZIP1 gene expression, ZIP1 transporter protein, and cellular zinc were prominent in normal peripheral zone glandular epithelium and in benign hyperplastic glands (also zinc accumulating glands). In contrast, hZIP1 gene expression and transporter protein were markedly down-regulated and zinc was depleted in adenocarcinomatous glands and in prostate intra-epithelial neoplastic foci (PIN). These changes occur early in malignancy and are sustained during its progression in the peripheral zone. hZIP1 is also expressed in the malignant cell lines LNCaP, PC-3, DU-145; and in the nonmalignant cell lines HPr-1 and BPH-1. CONCLUSION: The studies clearly establish that hZIP1 gene expression is down regulated and zinc is depleted in adenocarcinomatous glands. The fact that all the malignant cell lines express hZIP1 indicates that the down-regulation in adenocarcinomatous glands is likely due to in situ gene silencing. These observations, coupled with the numerous and consistent reports of loss of zinc accumulation in malignant cells in prostate cancer, lead to the plausible proposal that down regulation of hZIP1 is a critical early event in the development prostate cancer.

Cation Transport Proteins↗

PubMed2000

Zinc concentration of selected ocular tissues in zinc-deficient rats.

A study was performed to determine the effect of zinc deficiency on the zinc concentration of the retina, lens, and the retinal pigment epithelium and choroid. Weanling, male Sprague-Dawley rats were fed ad libitum modified AIN-93 diets containing 3 mg zinc/kg diet (-Zn; n = 10) for 6 wk. Control animals were pair-fed (+ZnPF; n = 10) or fed ad libitum (+ZnAL; n = 10) diets containing 100 mg zinc/kg diet. At 6 wk, plasma and tibia zinc were measured by flame atomic absorption spectrophotometry to confirm zinc deficiency. The zinc concentration of ocular tissues was measured by inductively coupled plasma-mass spectrometry. Mean (+/- SEM) lens zinc concentration was significantly depressed in the zinc-deficient group as compared to that of pair-fed or ad libitum-fed controls, suggesting that the role of zinc in cataract formation should be investigated. The zinc concentration of total neural retina was preserved in zinc deficiency. Previously reported deterioration of retinal function in zinc deficiency may be the result of a decline in the zinc concentration of a specific cell layer of the retina that cannot be detected on gross analysis of the entire retina.

Animals↗

PubMed2004

Effect of dietary protein, zinc, and carbon monoxide on fetal zinc concentration in mice.

Dietary protein and zinc deficiencies known to be detrimental to the developing fetus are common in pregnant women in developing countries. Everyone in modern society is at risk of exposure to carbon monoxide (CO). This study was conducted to observe the effect of dietary protein, zinc, and exposure to CO on the fetal zinc concentrations by factorial experimentation. Pregnant mice of CD-1 strain were maintained on 17% (control) or 9% (deficient) protein diets mixed with deficient, normal (control), or supplemental zinc throughout gestation. The dams in each dietary group were exposed to air (control) or 500 ppm CO in air in environmental chambers from gestation day 8 to gestational day 18. The dams were sacrificed on d 18 and fetal zinc levels were measured by atomic absorption spectrophotometry. Carbon monoxide levels used in this study had no significant effect on fetal zinc concentration in any treatment group. When both dietary protein and zinc levels were normal, the mean fetal zinc concentrations were higher than all other dietary protein/zinc combinations (15.2 +/-6.0 and 14.2 +/- 4.1 microg Zn/g of tissue for 0 and 500 ppm CO levels). However, when dietary protein levels were deficient, supplemental zinc increased the fetal zinc concentrations significantly (12.7+/-3.8 and 13.1+/-0.3.6 microg Zn/g of tissue, in 0 and 500 ppm CO groups) as compared to zinc-deficient groups (8.7 +/- 3.0 and 10.0 +/- 3.3 microg Zn/g of tissue in 0 and 500 ppm CO groups). The results of this study may be relevant to populations that experience both marginal zinc and protein diets during gestation.

Animals↗

PubMed1976

Effect of high dietary zinc upon zinc metabolism and intracellular distribution in cows and calves.

Changes in the metabolism of zinc were investigated in mature nonlactating Holstein cows and 4-mo old calves fed high but nontoxic amounts of dietary zinc. Increasing dietary zinc of calves from 42 to 642 ppm elevated the zinc content of liver and pancreas 600% and 1400%, respectively. The elevated zinc in liver and pancreas involved a substantial increase in all intracellular fractions, with by far the largest amount associated with a 10,000 molecular-weight protein in the soluble cell fraction. This zinc-binding protein may protect the cell against damage from increased zinc. A comparable increase in dietary zinc of mature cows did not affect zinc content of liver or kidney nor alter the intracellular distribution of zinc in the liver. In mature cows, homeostatic control mechanisms which regulate the zinc content of tissue are much more effective than in calves. Accordingly, mature cows probably are able to tolerate higher concentrations of dietary zinc.

Age Factors↗

PubMed1990

Influence of dietary zinc and iron on zinc retention in pregnant rhesus monkeys and their infants.

To test the idea that zinc uptake may be enhanced in conditions of zinc deficiency, we fed rhesus monkeys diets containing either 4 micrograms zinc (low-zinc group) or 100 micrograms zinc (controls) throughout pregnancy and lactation. Each group was divided into two subgroups, one of which received an iron supplement (4 mg ferrous sulfate/kg/day). We investigated iron supplements because excess dietary iron has been suggested to inhibit zinc absorption. 65Zn retention from labeled meals was studied in the dams during pregnancy and lactation and in their 10-day-old infants. In both the mothers and the infants, zinc absorption/retention, as measured by whole-body counting, was more than 25% higher in the low-zinc group than in the controls. Iron supplementation had no effect on initial dietary zinc retention, but resulted in a reduction in whole-body 65Zn turnover. Thus, changes in zinc status and dietary factors such as iron can affect net retention and turnover of zinc in pregnant and lactating primates fed low-zinc diets.

Animals↗

PubMed1989

Zinc requirement for macrophage function: effect of zinc deficiency on uptake and killing of a protozoan parasite.

The effects of suboptimal levels of zinc, an essential trace element, on the ability of murine macrophages to associate with and destroy a pathogenic parasite, Trypanosoma cruzi, were evaluated. Young adult A/J mice were fed zinc-deficient, zinc-adequate or restricted amounts of a zinc-adequate diet for 28 days. On the basis of weight loss and parakeratosis, the zinc-deficient mice were further divided into moderately and severely zinc-deficient on Day 28. Both the percentage of mouse peritoneal macrophages (MPM) with associated parasites and the number of parasites per 100 macrophages were significantly lower for macrophages from moderately and severely deficient mice compared to MPM from mice fed restricted or zinc-adequate diet. Furthermore, MPM from both zinc-deficient groups of mice killed fewer internalized parasites than did MPM from restricted or zinc-adequate mice. Pretreatment of MPM from zinc-deficient mice with 5 micrograms zinc/ml for 30 min completely restored both their capacity to take up and kill the parasites. Other trace metals tested, including copper, manganese and nickel, failed to reverse the effects of zinc deficiency. These results point to an important role for zinc in the biochemical events associated with macrophage uptake and killing of the parasite.

Animals↗

PubMedDate not supplied

Zinc absorption and its correlation with results of oral zinc tolerance testing in nonalcoholic liver cirrhosis; kinetic study.

BACKGROUND/AIMS: Liver cirrhosis is often complicated by symptoms of zinc deficiency, i.e., disturbances of taste and smell, skin eruptions, and other symptoms. We evaluated zinc absorption in patients with nonalcoholic liver cirrhosis to clarify the cause of zinc deficiency. METHODS AND MATERIALS: The absorption of zinc was calculated from the results of both the oral and intravenous zinc loading tests. RESULTS: Absorption was significantly reduced the cirrhotic patients, 20.4 +/- 10.7% as compared with the controls, 38.3 +/- 11.0%. In the cirrhotic patients with hepatocellular carcinoma, it was 17.8 +/- 9.3%, not significantly different from that of cirrhotics without hepatocellular carcinoma, 24.1 +/- 10.7%. CONCLUSIONS: Therefore, the development of hepatocellular carcinoma in patients with nonalcoholic liver cirrhosis had no influence on zinc absorption. Because a lower correlation between zinc absorption and the results of oral zinc tolerance testing was observed, the oral zinc tolerance test alone cannot be used as an accurate procedure for evaluating zinc absorption in liver cirrhosis. One should thus use both the intravenous as well as the oral zinc loading test when evaluating zinc absorption.

Absorption↗