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PubMed2006

The zinc-sensing mechanism of mouse MTF-1 involves linker peptides between the zinc fingers.

Mouse metal response element-binding transcription factor-1 (MTF-1) regulates the transcription of genes in response to a variety of stimuli, including exposure to zinc or cadmium, hypoxia, and oxidative stress. Each of these stresses may increase labile cellular zinc, leading to nuclear translocation, DNA binding, and transcriptional activation of metallothionein genes (MT genes) by MTF-1. Several lines of evidence suggest that the highly conserved six-zinc finger DNA-binding domain of MTF-1 also functions as a zinc-sensing domain. In this study, we investigated the potential role of the peptide linkers connecting the four N-terminal zinc fingers of MTF-1 in their zinc-sensing function. Each of these three linkers is unique, completely conserved among all known vertebrate MTF-1 orthologs, and different from the canonical Cys2His2 zinc finger TGEKP linker sequence. Replacing the RGEYT linker between zinc fingers 1 and 2 with TGEKP abolished the zinc-sensing function of MTF-1, resulting in constitutive DNA binding, nuclear translocation, and transcriptional activation of the MT-I gene. In contrast, swapping the TKEKP linker between fingers 2 and 3 with TGEKP had little effect on the metal-sensing functions of MTF-1, whereas swapping the canonical linker for the shorter TGKT linker between fingers 3 and 4 rendered MTF-1 less sensitive to zinc-dependent activation both in vivo and in vitro. These observations suggest a mechanism by which physiological concentrations of accessible cellular zinc affect MTF-1 activity. Zinc may modulate highly specific, linker-mediated zinc finger interactions in MTF-1, thus affecting its zinc- and DNA-binding activities, resulting in translocation to the nucleus and binding to the MT-I gene promoter.

Amino Acid Sequence↗

PubMed2000

Zinc uptake by human placental microvillous membrane vesicles: effects of gestational age and maternal serum zinc levels.

Zinc uptake by syncytiotrophoblast microvillous membrane vesicles (SMMV) from human placentas was characterized and the effects of maternal serum zinc levels at term and of gestational age on kinetic parameters were evaluated. Zinc uptake at pH 7.2 was rapid for the first 2 min, followed by a slower increase, approaching equilibrium after 30 min. Uptake was saturable at a zinc concentration of 30 micromol/L, higher than the upper range of the physiological serum zinc level. Kinetic analysis of uptake at 1 min in SMMV from term placenta showed similar Km values (mean: 6.9+/-0.6 micromol/L) for different levels of maternal serum zinc. However, Vmax was higher (p < 0.05) in SMMV from mothers with serum zinc lower than 7.6 micromol/L compared to those with higher serum zinc levels (35.8+/-1.6 and 26.6+/-1.6 nmol 65Zn/mg protein/min, respectively). Km values were similar in term (>37 wk of gestation) and preterm (20-25 wk of gestation) placentas, whereas Vmax was higher (p < 0.05) in the preterm (34.3+/-1.6 nmol Zn/mg protein/min) compared to term placentas from mothers with serum zinc levels above 7.6 micromol/L. These results suggest that whereas afffinity for zinc was not altered with gestational age or maternal serum zinc levels, zinc-uptake capacity in human placenta is influenced both by gestational age and by low levels of maternal serum zinc in order to ensure an adequate maternal-fetal zinc transfer.

Adult↗

PubMed1984

Forced resting by high dietary zinc: tissue zinc accumulation and reproductive organ weight changes.

An experiment was conducted to investigate the effects of high dietary zinc, as a means of inducing a forced-rest, on selected organ accumulation of zinc and reproductive function in terms of ovary and oviduct weight in the laying hen. Single Comb White Leghorn hens laying approximately at 60% production were fed either 10,000 ppm zinc as zinc oxide (10 Zn) or 20,000 ppm zinc (20 Zn) for a period of 4 days. At the initiation of the experiment (Day 0), five hens were killed and organs obtained for analysis. On 4, 10, 16, and 22 days afterward, similar samples were obtained from 5 hens per treatment. Ovary and oviduct weights were determined and zinc analysis performed on the latter as well as liver, kidney, and pancreas. The brief 4-day feeding of either high zinc diet caused a marked 80% reduction in ovary weight by Day 10. The oviduct, although less affected, was still reduced approximately 60% in weight after feeding either 10 Zn or 20 Zn for 4 days. The oviduct exhibited a statistically significant elevation in zinc concentration on Day 4 but was normal by Day 10 (6 days following the refeeding of a normal diet) and not different between treatments. There was extensive accumulation of zinc in kidney, liver, and especially pancreas after 4 days of feeding either 10 Zn or 20 Zn. The level of dietary zinc had no effect on the extent of accumulation in any tissue. The depletion of tissue zinc roughly corresponded to the magnitude of increase in the concentration of zinc observed at Day 4. Possible ramifications of the dramatic increase observed in pancreatic zinc were discussed. We concluded that feeding either 10 Zn or 20 Zn as a means of inducing a forced rest effects a marked and rapid reduction in ovary and oviduct weight as well as an extensive increase in renal, hepatic, and especially pancreatic zinc.

Animals↗

PubMed1989

Abnormal zinc content in human milk. Risk for development of nutritional zinc deficiency in infants.

An abnormally low concentration of zinc in mother's milk has been associated with clinical nutritional zinc deficiency in premature and term newborns. Defective mammary gland secretion of zinc was suggested as the causative factor. We investigated whether low milk zinc concentration might be reflected in an abnormality of the distribution of zinc between casein, whey, and fat components of the milk, in a reduction in the levels of milk citrate, a zinc-binding ligand, or in abnormal levels of copper and iron. Milk from mothers of four low-birth-weight infants was identified as being deficient in zinc content for the lactational stage. One infant had clinical signs of nutritional zinc deficiency. For two of the three infants with subclinical deficiencies in whom balance study data were available, the apparent zinc balance was negative (-5.7 and -6.0 mumol/kg per day). These milks were examined for content and distribution of zinc, copper, and iron, and citrate concentration. Although total zinc concentration (4.5 to 17.2 mumol/L) was below the 95% prediction interval (15.2 to 59.7 mumol/L) for the lactational stage, the distribution of zinc was normal between milk components. Levels of citrate (1.46 to 5.13 mmol/L) were also within normal limits, as were levels of copper (0.27 to 0.85 mumol/L and iron (0.41 to 1.13 mumol/L). We concluded that there was no indirect evidence of a secretory abnormality in milk zinc deficiency, but speculated that there might instead be an abnormality of zinc uptake by the mammary gland from the plasma.

Breast Feeding↗

PubMed1979

[Zinc deficiency syndrome during long-term parenteral nutrition in a patient with Crohn's disease and cirrhosis of the liver. Casuistry and zinc-pharmacokinetic (author's transl)].

A 29 year old patient with Crohn's disease and posthepatitic HBsAg-positive cirrhosis developed zinc deficiency in the course of complete parenteral nutrition. Zinc deficiency was proven by a low plasma zinc level of 12 microgram/dl. The daily input of zinc was 0.5 mg as calculated from the zinc concentration of infusion solutions used in parenteral nutrition during 3 1/2 months of treatment. The clinical picutre was that of acrodermatitis enteropathica. Cirrhosis of the liver and Crohn's disease were contributory causes of zinc deficiency. 6 bolus injections of 12-36 mg of zinc (total amount 144 mg) were given during 13 days. The plasma zinc level increased to 60-80 microgram/dl. 52% of the total amount of zinc injected were excreted by urine. The plasma half-life times of zinc were independent from basic zinc concentrations and averaged 1.55 +/- 0.22 h. It is concluded that severe signs of zinc deficiency will develop during parenteral nutrition in the presence of conditions leading to a negative zinc balance. In the case of long-term complete parenteral nutrition zinc should be substituted from the beginning of the treatment on.

Acrodermatitis↗

PubMed2006

Oral zinc augmentation with vitamins A and D increases plasma zinc concentration: implications for burden of disease.

A study evaluating zinc supplementation in patients with Alzheimer's disease yielded variable zinc plasma levels in spite of positive cognitive and physiological results. In an attempt to raise and sustain plasma zinc levels, a single patient was given 15 mg zinc/day with various combinations of vitamins. A sustained raise in plasma zinc concentration (and therefore its potential bioavailability) was obtained only when the zinc was augmented with both vitamins A and D (in RDA concentrations). In order to verify these results, a follow-up study was conducted in 70 volunteers. Seven groups of 10 healthy subjects received various combinations of zinc and the two vitamins A and D, namely: zinc, vitamin A, vitamin D, zinc plus vitamin A, zinc plus vitamin D, vitamins A and D, and zinc plus vitamins A and D. Plasma zinc levels were determined at baseline, 3 weeks and 6 weeks. Plasma zinc levels increased significantly (p < 0.02) from 11.82 (+/-2.60) to 13.32 (+/-3.04) mum/L only in the group receiving the combination of zinc and vitamins A and D. This novel method of increasing plasma zinc levels by the augmentation of vitamins A and D may have implications for the reduction of burden of disease.

Alzheimer Disease↗

PubMed2006

Region-specific loss of zinc in the brain in pentylentetrazole-induced seizures and seizure susceptibility in zinc deficiency.

The hippocampus is thought to be an epileptic focus in human temporal lobe epilepsy. Kainate-induced seizures decrease zinc concentrations in the hippocampus, which is also decreased in young mice fed a zinc-deficient diet for 4 weeks, and is enhanced by zinc deficiency. To understand zinc movement in the brain in epileptic seizures, zinc concentrations in the brain were measured in young mice after administration of pentylentetrazole, a GABAA receptor antagonist. Zinc concentration in the hippocampus and Timm's stain, with which histochemically reactive zinc in the presynaptic vesicle is detected, were decreased after the administration, suggesting that excessive excitation of zinc-containing glutamatergic neurons is induced in the hippocampus with pentylentetrazole. To clarify whether the decrease in zinc concentration in the hippocampus in zinc deficiency alter seizure susceptibility, furthermore, susceptibility to pentylentetrazole-induced seizures was examined in young mice fed the zinc-deficient diet for 4 weeks. The susceptibility, unlike susceptibility to kainate-induced seizures, was not appreciably enhanced by zinc deficiency. These results suggest that the decrease in zinc concentration in the hippocampus in zinc deficiency does not influence susceptibility to pentylentetrazole-induced seizures.

Animals↗

PubMed2005

Longitudinal measurements of zinc absorption in Peruvian children consuming wheat products fortified with iron only or iron and 1 of 2 amounts of zinc.

BACKGROUND: Information is needed on the fractional absorption of zinc (FAZ) and absorbed zinc (AZ) during prolonged exposure to zinc-fortified foods. OBJECTIVE: The objective was to measure FAZ and AZ from diets fortified with different amounts of zinc and to determine whether zinc absorption changes over approximately 7 wk. DESIGN: Forty-one stunted, moderately anemic children received daily, at breakfast and lunch, 100 g wheat products fortified with 3 mg Fe (ferrous sulfate) and 0 (group Zn-0), 3 (group Zn-3), or 9 (group Zn-9) mg Zn (zinc sulfate) per 100 g flour. FAZ was measured on days 2-3 and 51-52; meal-specific AZs were calculated as the product of FAZ and zinc intake. RESULTS: For the breakfast and lunch meals combined, mean total zinc intakes were 2.14, 4.72, and 10.04 mg/d in groups Zn-0, Zn-3, and Zn-9, respectively, during the initial absorption studies; mean (+/-SD) FAZ values were 0.341 +/- 0.111, 0.237 +/- 0.052, and 0.133 +/- 0.041, respectively, on days 2-3 (P < 0.001) and did not change significantly on days 51-52 in the subset of 31 children studied twice. Mean initial AZ was positively related to zinc intake (0.71 +/- 0.18, 1.11 +/- 0.21, and 1.34 +/- 0.47 mg/d, respectively; P < 0.001); final values did not differ significantly from the initial values. CONCLUSIONS: AZ from meals containing zinc-fortified wheat products increases in young children relative to the level of fortification and changes only slightly during approximately 7-wk periods of consumption. Although consumption of zinc-fortified foods may reduce FAZ, zinc fortification at the levels studied positively affects total daily zinc absorption, even after nearly 2 mo of exposure to zinc-fortified diets.

Biological Availability↗

PubMed1987

Iron and zinc concentrations and 59Fe retention in developing fetuses of zinc-deficient rats.

Because disturbances in iron metabolism might contribute to the teratogenicity of zinc deficiency, we examined the effect of zinc deficiency on fetal iron accumulation and maternal and fetal retention of 59Fe. Pregnant rats were fed from mating a purified diet containing 0.5, 4.5 or 100 micrograms Zn/g. Laparotomies were performed on d 12, 16, 19 and 21 of gestation. Maternal blood and concepti were analyzed for zinc and iron. Additional groups of dams fed 0.5 or 100 micrograms Zn/g diet were gavaged on d 19 with a diet containing 59Fe. Six hours later maternal blood and tissues, fetuses and placentas were counted for 59Fe. Maternal plasma zinc, but not iron, concentration was affected by zinc deficiency on d 12. Embryo zinc concentration on d 12 increased with increasing maternal dietary zinc, whereas iron concentration was not different among groups. On d 16-21 plasma iron was higher in dams fed 0.5 micrograms Zn/g diet than in those fed 4.5 or 100 micrograms/g, whereas plasma zinc was lower in dams fed 0.5 or 4.5 micrograms Zn/g than in those fed 100 micrograms Zn/g diet. On d 19 zinc concentration in fetuses from dams fed 0.5 micrograms/g zinc was not different from that of those fed 4.5 micrograms/g zinc, and iron concentration was higher in the 0.5 microgram Zn/g diet group. The increase in iron concentration in zinc-deficient fetuses thus occurs too late to be involved in major structural teratogenesis. Although whole blood concentration of 59Fe was not different in zinc-deficient and control dams, zinc-deficient dams had more 59Fe in the plasma fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

PubMed1989

Studies of iron:zinc interactions in adult rats and the effect of iron fortification of two commercial infant weaning products on iron and zinc status of weanling rats.

The effect of iron on zinc absorption in the rat, and vice versa, was investigated from single starch:sucrose test meals (containing 65Zn or 59Fe) by whole body counting. Zinc had no effect on iron absorption, but iron reduced zinc absorption when the total ionic species in the meal (iron plus zinc) reached 1.36 mg. Below this level, high iron:zinc molar ratios (10:1) had no effect on zinc absorption, presumably because the transport mechanism for zinc had not reached full capacity. Previous iron intake had no effect on zinc absorption. The relevance of these findings to infant foods was explored by feeding rats exclusively a vegetable or cereal weaning product, with or without additional iron, for 12 d and measuring zinc and iron status. The added iron raised body iron stores and caused a small reduction in zinc status in animals fed the oat, but not the vegetable, diet as measured by plasma and femur zinc concentrations. Since the threshold level of 1.36 mg ionic species would be exceeded when the animal ate 3-4 g of the iron-fortified weaning food at any one time, it appears that the iron:zinc interactive effect was absent in the vegetable and less potent in the oat formulation than in a carbohydrate test meal. Alternatively, it may be the case that the animals had responded over time to reduced zinc availability by increasing whole body zinc retention.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

PubMed2000

Importance of zinc in the central nervous system: the zinc-containing neuron.

Zinc is essential to the structure and function of myriad proteins, including regulatory, structural and enzymatic. It is estimated that up to 1% of the human genome codes for zinc finger proteins. In the central nervous system, zinc has an additional role as a neurosecretory product or cofactor. In this role, zinc is highly concentrated in the synaptic vesicles of a specific contingent of neurons, called "zinc-containing" neurons. Zinc-containing neurons are a subset of glutamatergic neurons. The zinc in the vesicles probably exceeds 1 mmol/L in concentration and is only weakly coordinated with any endogenous ligand. Zinc-containing neurons are found almost exclusively in the forebrain, where in mammals they have evolved into a complex and elaborate associational network that interconnects most of the cerebral cortices and limbic structures. Indeed, one of the intriguing aspects of these neurons is that they compose somewhat of a chemospecific "private line" of the mammalian cerebral cortex. The present review outlines (1) the methods used to discover, define and describe zinc-containing neurons; (2) the neuroarchitecture and synaptology of zinc-containing neural circuits; (3) the physiology of regulated vesicular zinc release; (4) the "life cycle" and molecular biology of vesicular zinc; (5) the importance of synaptically released zinc in the normal and pathological processes of the cerebral cortex; and (6) the role of specific and nonspecific stressors in the release of zinc.

Alzheimer Disease↗

PubMed2001

Exchangeable zinc pool masses and turnover are maintained in healthy men with low zinc intakes.

Previous studies suggest that rapidly exchanging zinc pools (EZP), thought to supply the zinc required by tissues, are smaller and turn over more rapidly in individuals with lower zinc intakes. We studied the effects of low dietary zinc (4.6 mg/d) on EZP mass and turnover in seven healthy men confined during a 20-wk clinical study. Supplements of 9.1 mg zinc were given during the 5-wk baseline and repletion periods, and placebos were given during a 10-wk zinc-restriction period. Stable 70Zn tracers were administered intravenously at the end of baseline, 3 and 10 wk after the start of zinc restriction and at the end of repletion. Multiple plasma samples were collected over an 8-d period after tracer administration. 70Zn:66Zn ratios were measured using inductively coupled plasma mass spectrometry, and tracer-tracee data were analyzed by compartmental modeling. Activities of the zinc-dependent enzymes, alkaline phosphatase and 5'nucleotidase, were unchanged during the study. There were no significant changes in EZP masses or kinetic parameters. A three-compartment model indicated that the masses of plasma zinc and total EZP averaged 3.25 +/- 0.58 and 147.8 +/- 33.2 mg, respectively, at the four time points studied. Plasma zinc mass turned over at an average of 5.3 times per hour. There was an 11% reduction (P = 0.06) in plasma zinc flux 3 wk after the start of the low zinc diet period, but it returned to baseline values after 10 wk of zinc restriction. The results suggest that total EZP mass is maintained when dietary zinc is reduced to 4.6 mg/d over a 10-wk period.

Adult↗

PubMed1984

Changes in plasma zinc content after exercise in men fed a low-zinc diet.

For 30 days five healthy men aged 23-57 yr consumed a diet adequate in zinc (8.6 mg/day); they ate a low-zinc diet (3.6 mg/day) for the next 120 days and then received a zinc-supplemented (33.6 mg/day) diet for 30 days. Copper intake was constant at 1.8 mg/day. Aerobic capacity was determined periodically during each diet period. Relative zinc balance (% of control) declined during depletion (r = -0.28, P less than 0.009). Pre- and postexercise zinc concentrations decreased when dietary zinc was restricted (r = -0.61, P less than 0.0001 and r = -0.78, P less than 0.0001) and increased with supplementation (r = 0.61, P less than 0.008 and r = 0.76, P less than 0.0003, respectively). Both plasma zinc and hematocrit increased (P less than 0.01) after maximal exercise. To minimize the effect of hemoconcentration during exercise, the van Beaumont quotient (J. Appl. Physiol. 34: 102-106, 1973) was calculated using pre- and postexercise hematocrit and plasma zinc. The initial quotient of 1.8 +/- 1.8% (mean +/- SE) declined (P less than 0.05) to -7.4 +/- 2.3% during depletion. With zinc repletion, the quotient increased to 6.9 +/- 3.6%, which was greater (P less than 0.05) than the quotient in depletion but similar to the initial quotient. The quotient was a strong predictor (r = 0.71, P less than 0.0005) of the change in relative zinc balance during zinc depletion. In contrast, no changes were found in plasma copper content. These data suggest that zinc mobilization from tissues is impaired during zinc depletion, and they validate the use of the van Beaumont quotient as an index of change in body zinc stores.

Adult↗

PubMed1993

Alterations in intestinal uptake and compartmentalization of zinc in response to short-term dexamethasone therapy or excess dietary zinc in piglets.

Premature infants receive high dietary zinc and often glucocorticoids as a treatment for chronic lung disease. A piglet model was developed to investigate intestinal zinc transport and distribution of tissue zinc in response to treatment with short-term (5 d) glucocorticoid therapy or a high zinc diet. Piglets (13-15 d old; n = 21) were randomly allocated to: 1) dexamethasone (DEX) therapy (1.5 mg/kg intramuscularly twice a day), 2) high zinc diet (15.3 mmol/kg), or 3) control group (0.3 mmol dietary zinc/kg and saline intramuscularly twice a day). Pig weight, formula intake, urine volume, and blood glucose were monitored. At necropsy, tissue samples were obtained to measure zinc in plasma and zinc and metallothionein in liver and small intestinal mucosa. Velocity of zinc uptake by intestinal brush border membrane vesicles was measured using 65Zn tracer. Maximum uptake rate and Km for zinc uptake by brush border membrane vesicles were significantly greater (p < 0.05) in DEX compared with control and high zinc groups. DEX-treated piglets had a significantly lower (p < 0.05) zinc efflux rate across brush border membrane vesicles compared with that of the control. The high zinc group had a higher liver (p < 0.05) and mucosal (p < 0.05) zinc content and higher liver metallothionein concentration (p < 0.001) compared with the control and DEX groups. Weight gain over 5 d was not different among groups. Daily blood glucose was higher (p < 0.05) in DEX versus control and high zinc groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1998

[Relationship between body surface zinc loss and dietary zinc intake in children].

OBJECTIVE: To study the effects of body surface loss of zinc on the determination of dietary supply of zinc. METHODS: Body surface loss of zinc was determined in 24 preschool children with normal zinc nutrition (Group A) and zinc malnutrition (Group B). RESULTS: Body surface loss of zinc was 0.25 and 0.23 mg daily in Groups A and B with dietary zinc intake of 5.45 and 5.03 mg, respectively, and 0.29 and 0.25 mg daily with dietary zinc intake of 7.20 and 6.73 mg, respectively. The body surface loss of zinc accounted for five percent of the total. CONCLUSION: Considering the loss of zinc from body surface, it is suggested that dietary zinc supply be increased by 21 percent. When children is in good status of zinc nutrition, body surface loss of zinc correlates proportionally with their dietary zinc intake.

Child↗

PubMed1992

Effect of replacement of "zinc finger" zinc on estrogen receptor DNA interactions.

Exposure of bovine estrogen receptor to the metal chelators EDTA and 1,10-phenanthroline results in a loss of nonspecific DNA binding, presumably because of the removal of "zinc finger" zinc. Nonspecific DNA binding, as measured by a DNA-cellulose binding assay, can be restored by dialysis of the aporeceptor against buffer containing zinc, cadmium, and cobalt but not with buffer containing copper or nickel. More detailed studies were carried out using a bacterially expressed polypeptide encompassing the DNA binding domain of the human estrogen receptor. Apopolypeptide fails to bind DNA specifically, as measured by mobility shift assay using a consensus estrogen response element hexamer containing oligonucleotide, but DNA binding was restored by dialysis of the apopolypeptide against buffer containing zinc, cadmium, and cobalt but not with buffer containing copper or nickel. Dissociation constants of zinc- and cadmium-reconstituted polypeptide for the estrogen response element hexamer (66 and 48 nM, respectively) are virtually indistinguishable from native polypeptide (Kd = 48 nM) whereas cobalt-reconstituted polypeptide has a lower affinity (Kd = 720 nM). However, native, zinc-, cadmium-, and cobalt-reconstituted polypeptides gave identical results in a methylation interference assay. Competition experiments with zinc and copper or nickel suggest that copper and nickel are able to bind to zinc finger residues but do so nonproductively. The relative affinities copper greater than cadmium greater than zinc greater than cobalt greater than nickel for the polypeptide were determined by a zinc blot competition assay. The ability of cadmium and cobalt to substitute for zinc in the zinc fingers demonstrates a structural "flexibility" in the DNA binding domain as each of these metals has slightly different ionic radii. On the other hand, subtle differences in DNA binding affinity and/or specificity could exist, which may not be detectable here. Also, the ability of metals to substitute for zinc in the DNA binding domain suggests that metal substitution in these zinc fingers in vivo may be of relevance to the toxicity and/or carcinogenicity of some of these metals.

Animals↗

PubMed1991

Effects of zinc supplementation on zinc status and immunity in haemodialysis patients.

The depression of immunity to various antigens in chronic uremia is a frequently encountered phenomenon. Zinc deficiency might well be an important factor in its genesis. The aim of this study was to investigate the role of zinc deficiency in this reduced immune response. Two groups of 7 patients on haemodialysis who had failed to respond with seroconversion to an earlier vaccination against hepatitis B were revaccinated. One group received zinc by the addition of zinc chloride to the dialysate. Before initiation of the study zinc in plasma and leucocytes was measured. No difference in plasma and leucocyte zinc was observed between the two groups. Zinc in leucocytes was lower in patients than in a group of healthy volunteers (61.5 pmol/10E6 cells +/- 4.6 versus 73.8 +/- 5.6, p less than 0.005). Plasma zinc showed no difference between patients and healthy volunteers. During zinc supplementation zinc in plasma rose in the patient group receiving zinc (10.4 mmol/L +/- 1.5 to 14.2 +/- 1.9, p less than 0.005). However, no rise in leucocyte zinc was seen. At the end of the trial seroconversion had occurred in 2 patients in each group. It is concluded that zinc supplementation in haemodialysis patients does not lead to the restoration of leucocyte zinc to normal levels. Neither did it lead to an enhanced antibody response in our population after revaccination of haemodialysis patients against hepatitis B.

Adult↗

PubMed1988

Calmodulin, zinc and calcium concentration in tissues of zinc- and calcium-deficient rats.

To demonstrate the effect of zinc and/or calcium deficiency on calmodulin concentration and also the antagonistic behavior of zinc and calcium in metabolism, four groups of eight rats each were provided the following diets in equal amounts: group I, the basic diet with 63 ppm zinc and 0.88% calcium; group II, the calcium-deficient diet (0.0043% calcium); group III, the zinc-deficient diet (1.1 ppm zinc); and group IV, the combined zinc/calcium-deficient diet. The zinc-deficient diet significantly reduced the zinc concentration in serum (72%), femur (65%), pancrease (34%), muscle (23%), testis (11%) and brain (7%), and elevated the calcium concentration in testis (19%) and brain (24%), but did not affect calcium concentration in serum, pancreas and muscle. Likewise, calcium deficiency reduced the calcium concentration in serum (56%), femur (40%), pancreas (16%), muscle (43%), testis (19%) and brain (24%), and elevated the zinc concentration in femur (22%), although the zinc concentration in serum, pancreas, muscle and testis remained unaffected. Combined zinc and calcium deficiency elevated both the zinc as well as the calcium concentration in serum, femur and muscle, as compared to zinc or calcium deficiency alone. The alkaline phosphatase activity was reduced by 52% during zinc deficiency and was elevated by a factor of 2.5 during calcium deficiency. The calmodulin concentrations in muscle, testis and brain, as determined by radioimmunoassay, were elevated during both zinc as well as calcium deficiency, although this elevation could not be confirmed in every case.

Animals↗