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The pharmacokinetics of zinc from zinc gluconate: a comparison with zinc oxide in healthy men.

OBJECTIVE: Zinc supplementation is beneficial in some clinical conditions such as age-related macula degeneration (AMD). It has been suggested that zinc absorption is influenced by the form in which zinc is ingested. Therefore, the pharmacokinetics of zinc gluconate (organic) were compared with those of zinc oxide (inorganic). METHODS: 12 healthy male subjects aged between 21 and 31 years (24 years median) orally received daily doses of 20 mg metal zinc as zinc gluconate and 17.4 mg metal zinc as zinc oxide under randomized crossover conditions for 14 days each with at least 14 days as a washout. Zinc plasma concentrations were measured by means of inductively coupled plasma-atomic emission spectroscopy. RESULTS: C(max) was found 18.3% (10.3 - 26.3%) higher following multiple-dose administration of zinc gluconate as compared to zinc oxide (mean; 0.95% confidence interval of the relative differences between both treatment conditions; p < 0.05). AUC(0-24h) was noted 8.1% (1.9 - 14.3%) higher after zinc was given as zinc gluconate when compared to zinc oxide (p < 0.05) whereas t(max) did not differ between both treatment conditions. CONCLUSIONS: Zinc absorption in humans could be improved by zinc complexation with gluconate.

Adult↗

The adaptive response to dietary zinc in mice involves the differential cellular localization and zinc regulation of the zinc transporters ZIP4 and ZIP5.

The ZIP5 gene encodes a protein closely related to ZIP4, a zinc transporter mutated in the human genetic disorder acrodermatitis enteropathica. Herein, we demonstrate that mouse ZIP5 and ZIP4 genes are co-expressed in several tissues involved in zinc homeostasis (intestine, pancreas, embryonic yolk sac). However, unlike expression of the ZIP4 gene, which is induced during periods of zinc deficiency, ZIP5 gene expression is unaltered by dietary zinc. Immunohistochemistry localizes ZIP5 to the basolateral surfaces of enterocytes, acinar cells, and visceral endoderm cells in mice fed a zinc-adequate diet. However, this protein is removed from these cell surfaces and internalized during dietary zinc deficiency. In contrast, ZIP4 is induced and recruited to the apical surface of enterocytes and endoderm cells during zinc deficiency. In the pancreas, ZIP4 is expressed in beta-cells, whereas ZIP5 is expressed in acinar cells. These results suggest that the function of ZIP5 is antagonistic to that of ZIP4 in the control of zinc homeostasis; rather than functioning in the acquisition of dietary zinc, as does ZIP4, ZIP5 may function in the removal of zinc from the body. Thus, during periods when dietary zinc is replete, ZIP5 may function to remove zinc from the blood via the pancreas and intestine, the major sites of zinc excretion in mammals, whereas the acquisition of dietary zinc by intestinal ZIP4 would be minimal. In contrast, during periods of dietary zinc deficiency when secretion of zinc by the pancreas and intestine is minimized, ZIP5 is removed from the cell surface, and the intestinal uptake of zinc is augmented by induction of ZIP4.

Amino Acid Sequence↗

[Determination of metabolic availability of zinc and estimation of zinc requirements through changes in the activity of metallo-zinc enzymes].

Data on the zinc requirements of animals vary widely with the type of diet or kind of zinc compound considered, as they are dependent on the kind of definition and estimation of mineral requirements used which, in turn, are based on the analytical content of the mineral in the diet. Actually, requirements for a particular trace element are the same for any diet provided differences in the rate of absorption and metabolic availability of the element are taken into consideration. A suggestion is made in the present paper to utilize changes in the activity of different metallo-zinc enzymes as a method for determining the degree of metabolic availability of zinc. Within the framework of a repletion trial young male rats were fed a semisynthetic casein diet containing 1.2 ppm of zinc for a 14-day period of zinc depletion followed by a 15-day repletion period during which the rats received a diet containing 4.5 ppm or 12 ppm of zinc. In this trial the pattern of activity of the alkaline phosphatase in serum and in the femoral bones was studied and the level of pancreatic carboxypeptidase A and B was estimated. The data thus obtained were compared with those of pair-fed control animals and control animals fed a libitum. (96 ppm of dietary zinc). The results of the present trial show the metabolic availability of zinc can be determined by measuring the level of activity of these metallo-zinc enzymes. A suitable model was established. Moreover, attempts have been made to show in which way the zinc demands of growing, full-grown, pregnant and lactating animals may be estimated by measuring changes in the degree of activity of these metallo-zinc enzymes. A definition is, in this case, given by that amount of zinc which allows for an optimum activity of the different metallo-zinc enzymes. Such data are applicable only to a particular diet or are valid only for a particular zinc compound. Principally, it is much better to relate the Zn requirements of the animal to the level of absorbable and metabolically available zinc. The present model has been suggested to provide a possibility for measuring the metabolic availability of zinc in the body.

Alkaline Phosphatase↗

Metallothionein knockout and transgenic mice exhibit altered intestinal processing of zinc with uniform zinc-dependent zinc transporter-1 expression.

A role for metallothionein in intestinal zinc absorption has been the subject of considerable debate. If metallothionein affects zinc absorption, then those factors that induce metallothionein synthesis (e.g., heavy metals, hormones) should alter zinc absorption and homeostasis. The present studies used metallothionein transgenic mice (overexpressing) and metallothionein knockout mice (no expression of metallothionein-1 or metallothionein-2) to examine directly the effects of metallothionein on zinc absorption, independent of secondary effects that could be caused by metallothionein inducers. Zinc absorption was examined by administering a single oral zinc dose (0.5 mmol/kg) by feeding tube to metallothionein transgenic and metallothionein knockout mice and measuring the serum zinc concentration. Two hours after the dose, the serum zinc concentration was 2.3 times higher in metallothionein knockout mice than in their control strain. Conversely, the concentration was elevated only one third as much in the metallothionein transgenic mice as in their controls after the zinc dose. We found that the serum zinc concentration was inversely related to the level of metallothionein protein. The intestinal zinc content was higher in the metallothionein knockout mice, however, suggesting that metallothionein did not reduce zinc absorption by simply sequestering zinc in the mucosa. The expression of the zinc transporter ZnT-1 was directly related to the serum zinc level and was independent of the level of metallothionein. These results further support metallothionein as an important component for reducing the efficiency of zinc absorption at elevated zinc intakes.

Animals↗

Use of zinc tolerance test and 24-hour urinary zinc content to assess oral zinc absorption.

OBJECTIVES: The sensitivity of one plasma and two urinary methods to assess zinc absorption after oral dosing were compared over the dose range of 10 to 100 mg. METHODS: Eleven healthy subjects participated in this four-way crossover design study. After an overnight fast, the subjects received a single oral dose of zinc acetate corresponding to 10, 25, 50, or 100 mg of elemental zinc. Plasma zinc concentrations were measured at baseline (pre-zinc administration) and hourly intervals post-zinc administration for 9 hours. Urine was collected for 24 hours prior to and for 24 hours after zinc administration. During this 48-hour period, subjects consumed an isocaloric, caffeine-free diet containing 18 mg of elemental zinc per day. RESULTS: The area under the plasma zinc concentration versus time curve (PZAUC) increased linearly with doses between 10 and 50 mg, then flattened out. By contrast, urinary zinc excretion was approximately linear with doses in the 25 to 100 mg range, but no differences were observed in urinary zinc excretion after doses of 10 and 25 mg. CONCLUSIONS: Plasma zinc concentration is a useful method of evaluating oral zinc absorption from doses of 10 to 50 mg. Urinary zinc excretion is an alternative method of assessing zinc absorption, particularly when doses of 50 to 100 mg of elemental zinc are administered.

Administration, Oral↗

Zinc absorption and intestinal losses of endogenous zinc in young Chinese women with marginal zinc intakes.

The objective of this study was to determine fractional absorption of exogenous zinc and intestinal excretion of endogenous zinc in women of childbearing age whose habitual dietary zinc intake was marginal. The target population (L group) comprised residents of a remote farming village in northeast China and the control subjects (M group) were residents of Beijing. Mean (+/-SE) calculated dietary zinc intakes were 5.2 +/- 0.2 and 8.1 +/- 0.2 mg/d, respectively. The phytate-zinc molar ratio in the diet of both groups was approximately 10:1. 70Zn was administered intravenously before breakfast and 67Zn orally with three main meals in 1 d. Subsequently, all feces were collected quantitatively until the second visible marker had been excreted and 12-h urine samples were collected on days 3-9. Fractional absorption was determined by measuring cumulative fecal excretion of nonabsorbed 67Zn and endogenous fecal zinc by isotope-dilution technique (70Zn). Fractional absorption values for L and M groups, respectively, were 0.31 +/- 0.03 and 0.34 +/- 0.03 (P=0.45). Corresponding figures for endogenous fecal zinc were 1.30 +/- 0.07 and 2.34 +/- 0.20 mg Zn/d (P<0.001). Both the estimated total size of the pools of zinc that exchange with zinc in plasma within 2 d (r=0.762, P<0.001) and the excretion of endogenous zinc in the feces (r=0.706, P<0.0001) were positively correlated with calculated total daily zinc absorption. We conclude that fractional absorption of zinc does not differ between women consuming marginal and adequate quantities of zinc in their diets, but endogenous zinc is conserved effectively by the intestine in women whose habitual dietary zinc is marginal.

Absorption↗

Comparative absorption of zinc picolinate, zinc citrate and zinc gluconate in humans.

The comparative absorption of zinc after oral administration of three different complexed forms was studied in 15 healthy human volunteers in a double-blind four-period crossover trial. The individuals were randomly divided into four groups. Each group rotated for four week periods through a random sequence of oral supplementation including: zinc picolinate, zinc citrate, and zinc gluconate (equivalent to 50 mg elemental zinc per day) and placebo. Zinc was measured in hair, urine, erythrocyte and serum before and after each period. At the end of four weeks hair, urine and erythrocyte zinc levels rose significantly (p less than 0.005, p less than 0.001, and p less than 0.001) during zinc picolinate administration. There was no significant change in any of these parameters from zinc gluconate, zinc citrate or placebo administration. There was a small, insignificant rise in serum zinc during zinc picolinate, zinc citrate and placebo supplementation. The results of this study suggest that zinc absorption in humans can be improved by complexing zinc with picolinic acid.

Administration, Oral↗

Zinc nutrition in healthy subjects and patients with taste impairment from the view point of zinc ingestion, serum zinc concentration and angiotensin converting enzyme activity.

OBJECTIVE: To estimate the zinc nutrition in healthy subjects and patients with taste impairment. Dietary zinc intake, zinc concentration in the serum and the ratio of apo/holo-activities of angiotensin converting enzyme (ACE), a zinc dependent enzyme in the serum (ACE ratio) were used as indices. SUBJECTS: Healthy paramedical volunteers from a local hospital and patients with taste impairment seen in the Department of Otolaryngology, Tokushima University Hospital. MEASUREMENTS: Dietary zinc intake was estimated with the food frequency questionnaire (FFQ). Zinc concentration in the serum was measured by means of atomic absorption spectrometry. The ACE activity in the serum was measured spectrophotometrically as the activity of holo-ACE, which contains zinc and shows full ACE activity. The activity of apo-ACE, which dose not contain zinc, was determined as the increase of its activity over that of the initial holo-ACE activity after the addition of zinc to the serum in vitro. ACE ratio was used as a more sensitive indicator of zinc nutrition than measuring zinc concentration in the serum. RESULTS: There were no differences in dietary intake of zinc after adjusting for energy and zinc concentration in the serum between patients and age-adjusted healthy subjects. The ACE ratio in patients with taste impairment was significantly higher than that in age-adjusted healthy subjects (P<0.05). CONCLUSION: Our date demonstrate that zinc deficiency is a predominant factor underlying taste impairment and we hypothesize that patients with taste impairment may have malabsorption of dietary zinc.

Adult↗

Correction of interleukin-2 gene expression by in vitro zinc addition to mononuclear cells from zinc-deficient human subjects: a specific test for zinc deficiency in humans.

A nutritional deficiency of zinc in humans is widespread in the developing world, and a conditioned zinc deficiency is observed in many diseased states, the elderly population, and pregnant women of both developed and developing nations. It was recently reported that zinc is required for Nuclear Factor-kappaB (NF-kappaB) activation and gene expressions of both interleukin-2 (IL-2) and interleukin-2 receptor alpha (IL-2Ralpha) and beta in HUT-78, a Th0 human malignant lymphoblastoid cell line. In this study, it has been reported for the first time that zinc is also required for gene expression of IL-2 and IL-2Ralpha in primary cells. Isolated peripheral blood mononuclear cells (MNCs) from zinc-deficient elderly subjects was used for this study. NF-kappaB activation was shown to have decreased in the MNCs from zinc-deficient subjects, which was corrected by in vivo zinc supplementation. It was further shown that either in vivo zinc supplementation or the addition of zinc in vitro to MNCs from zinc-deficient subjects results in correction of the gene expression of IL-2 and IL-2Ralpha. Therefore, it was proposed that in vitro addition of zinc to MNCs for correction of gene expression of IL-2 in humans may be used as a specific test for zinc deficiency. Although currently no known specific laboratory test exists for the diagnosis of zinc deficiency in humans, the use of correction of IL-2 messenger RNA (mRNA) with in vitro zinc addition to MNCs from zinc-deficient subjects may be very useful.

Aged↗

Zinc tolerance tests in zinc deficient and zinc supplemented diets.

Seven men consumed a low-zinc (3.3 mg/day) diet for 8 wk, followed by zinc-repletion (+15 mg/day) for 12 days. Zinc tolerance tests (50 mg) were administered initially and following depletion and repletion periods. Plasma zinc after 2 h in the zinc tolerance test was marginally higher after both the depletion (p less than 0.06) and repletion (p less than 0.001) periods as compared to the initial test. No changes were seen in parotid zinc tolerance tests or fasting levels of zinc in plasma or parotid saliva. In a subsequent study, zinc tolerance tests were given to normal subjects before and after 12 days of zinc supplementation (15 mg/day). Again, zinc levels in plasma were increased following zinc supplementation at the 2nd h post-zinc dose, but levels in saliva did not change. The elevation of plasma zinc curves with both zinc deficiency and supplementation suggests that this test is not a reliable indicator of zinc status.

Adult↗

Effects of dietary zinc upon tissue zinc and percent unsaturated plasma-zinc binding capacity.

Calves were fed 520 ppm zinc for 21 days, then placed on a low zinc diet (20 ppm zinc) for 35 days to determine the biological availability of zinc reserves of tissue. Concentrations of zinc in liver and kidney were elevated greatly by feeding high dietary zinc for 21 days and continued to increase with time. On the low zinc diet, the tissue burden of zinc decreased within 35 days to those comparable to calves initially fed low zinc. Likewise, both zinc in plasma and percent capacity of unsaturated plasma for binding zinc were near negative controls 21 days after removal of calves from high zinc diets. Tissue stores of zinc will not maintain adequate zinc in blood for extended periods, and hence, they probably will not sustain optimal feed intakes and growth rates of calves on low-intakes of zinc.

Animals↗

Absorption of zinc from wheat products fortified with iron and either zinc sulfate or zinc oxide.

BACKGROUND: Several chemical forms of zinc have been proposed for food fortification, but information is needed on their absorption from common cereals having varied phytate content. OBJECTIVE: The goal was to measure zinc absorption from wheat products fortified with iron sulfate and either zinc sulfate or zinc oxide. DESIGN: Adult volunteers received either low-phytate bread (n = 11) or higher-phytate porridge (n = 11) once weekly on 2 or 3 occasions. The foods were fortified with 1 of the 2 zinc salts (60 mg elemental Zn/kg wheat flour) during week 1 and with the other during week 2, in random order. (65)Zn in the same chemical form as the fortificant was incorporated in each food to assess zinc absorption with the use of whole-body counting. The porridge group received an additional test meal fortified with zinc oxide during week 3, but the (65)Zn tracer was given as an oral solution of (65)ZnCl(2). RESULTS: Zinc absorption from bread (13.8%; 95% CI: 11.8%, 16.2%) was significantly (P < 0.001) greater than from porridge (6.4%; 5.5%, 7.6%), presumably because of the greater phytate content of the porridge. With control for food type, there were no significant differences in zinc absorption from meals fortified with zinc sulfate or zinc oxide (P = 0.24). When the porridge was fortified with zinc oxide and labeled with (65)ZnCl(2), absorption of the tracer (8.9%; 7.1%, 11.0%) was significantly (P = 0.007) greater than when (65)ZnO was incorporated in the porridge (5.6%; 4.5%, 6.9%). CONCLUSIONS: Either zinc oxide or zinc sulfate can be used to fortify wheat products consumed by presumably healthy persons. Isotopic tracers used to assess the absorption of mineral fortificants should have the same chemical form as the fortificant.

Adult↗

Methodology for assessing zinc bioavailability: efficacy estimates for zinc-methionine, zinc sulfate, and zinc oxide.

The bioavailability of zinc-methionine (ZnMET) was compared to that of feed-grade ZnSO4.H2O using three different diets: purified (crystalline amino acid [AA]), semipurified (soy isolate), and complex (corn-soybean [C-SBM]) diet. With the Zn-deficient purified or semipurified diet, weight gain and tibia Zn responded linearly to both ZnSO4.H2O and ZnMET supplementation. Common-intercept, multiple linear regression indicated differences in Zn bioavailability between ZnMET and ZnSO4.H2O for both diets as indicated by bone Zn. With the ZnSO4.H2O standard set at 100%, bioavailability of Zn from ZnMET was 117% (P less than .05) in the AA diet and 177% (P less than .01) in the soy isolate diet. The ZnMET was also compared to ZnSO4.H2O in a C-SBM diet containing 117 mg of Zn/kg. When high levels of Zn were added to this diet (0, 250, 500, and 750 mg/kg of supplemental Zn), consistent tissue Zn responses did not occur beyond the first increment. Addition of lower levels of supplemental Zn (0, 5, 10, 20, 30, 40 and 50 mg/kg) to a Zn-unsupplemented C-SBM basal diet (45 mg/kg of Zn), however, resulted in a broken-line, two-slope response in tibia Zn for both ZnMET and ZnSO4.H2O. Inflection points occurred at 60 and 54 mg of Zn/kg of diet for ZnSO4.H2O and ZnMET, respectively. The ratio of slopes (ZnMET:ZnSO4.H2O) below the inflection points was 206% (P less than .01), indicating that Zn was considerably more bioavailable in ZnMET than in ZnSO4.H2O for chicks consuming C-SBM diets. When feed-grade ZnO was compared to feed-grade ZnSO4.H2O in chicks consuming C-SBM diets, bone Zn slopes below the respective inflection points indicated that Zn was 61% bioavailable in ZnO relative to ZnSO4.H2O.

Animal Feed↗

Bioavailability of zinc in several sources of zinc oxide, zinc sulfate, and zinc metal.

Three zinc depletion-repletion assays were carried out with chicks to determine Zn bioavailability in five sources of ZnO, three sources of ZnSO4.H2O, and two sources of Zn metal. A standard 23% CP corn-soybean meal diet was fed during the first 3 d posthatching, after which it was replaced with a Zn-deficient soy concentrate diet (13.5 mg Zn/kg) until d 7. On d 8 after an overnight period of feed withdrawal, chicks were fed for 12 d the Zn-deficient basal diet containing 0, 4.76, and 9.90 (Assay 1); 0, 5.06, or 10.12 (Assay 2); or 0, 4.73, or 9.13 (Assay 3) mg/kg supplemental Zn from analytical grade (AG) ZnSO4.7H2O (22.7% Zn) to generate a standard response curve. The AG and feed-grade (FG) Zn sources being evaluated were then provided at a level that would fall within the standard curve. Weight gain (Assays 1, 2, and 3) and total tibia Zn (Assay 1) responded linearly (P<.01) to Zn supplementation from ZnSO4.7H2O. Weight gain regressed on supplemental Zn intake gave standard-curve equations with fits (r2) ranging from .94 to .97. In Assay 1, regression of total tibia Zn (Y, in micrograms) on supplemental Zn intake (X, in milligrams/12 d) gave the equation Y = 13.2+6.74X (r2 = .90). Standard-curve methodology was used to estimate relative Zn bioavailability (RBV), with RBV of Zn in the ZnSO4.7H2O standard set at 100%. Four sources of FG ZnO were evaluated: Source 1 (78.1% Zn, hydrosulfide process, U.S.), Source 2 (74.1% Zn, Waelz process, Mexico), Source 3 (69.4% Zn, China), and Source 4 (78.0% Zn, French process, Mexico). Analytical-grade ZnO (80.3% Zn) was also evaluated. Feed-grade ZnO Sources 1 and 4 as well as AG ZnO produced average RBV values that were not different (P>.10) from the standard, but average RBV values for FG Source 2 and FG Source 3 were only 34 (P<.05) and 46% (P<.05), respectively. All sources of ZnSO4.H2O, which included two FG sources (source 1, 36.5% Zn; source 2, 35.3% Zn) and one food-grade source (36.5% Zn), were not different (P>.10) in RBV from the ZnSO4.7H2O standard. Two Zn metal products, Zn metal dust (100% Zn) and Zn metal fume (91.5% Zn), were also evaluated, and they were found to have Zn RBV values of 67 (P<.05) and 36% (P<.05), respectively. Feed-grade sources of ZnO vary widely in color, texture, Zn content, and Zn bioavailability.

Animal Feed↗

Zinc absorption estimated by fecal monitoring of zinc stable isotopes validated by comparison with whole-body retention of zinc radioisotopes in humans.

Knowledge about zinc availability from human diets is limited due to methodological difficulties. Recently developed stable isotope techniques for estimating dietary zinc absorption were compared with radioisotope techniques in five men and three women. Stable and radioactive zinc isotopes were simultaneously administered. Fecal excretion of the isotopes as well as whole-body retention of the radioactive zinc isotope was monitored. Concentration of stable zinc isotope label in fecal samples was determined by inductively coupled plasma mass spectrometry by fully quantitative measurements and from inductively coupled plasma mass spectrometry isotope ratios combined with analysis of total zinc content using atomic absorption spectrometry. Zinc absorption estimated from whole-body retention was 27 +/- 6% (mean +/- SD), estimated zinc absorption obtained by fecal monitoring of radioisotope was 26 +/- 9%, and the two stable zinc measurements resulted in values of 29 +/- 12 and 33 +/- 12%, respectively. There was no significant difference in zinc absorption estimated from whole-body retention and with the fecal monitoring methods. Recovered stable zinc isotope label was significantly lower than recovered radioisotope. For individual fecal samples, systematic differences of 16% and 12%, respectively (P < 0.05), between the radioisotope recovery and the recovery of stable isotopes with the two methods for measurement was observed. The stable zinc isotope technique for measurement of zinc absorption resulted in mean results similar to those of the radioisotope technique, but with a larger variation in the measurements.

Adult↗

Abundance of zinc ions in synaptic terminals of mocha mutant mice: zinc transporter 3 immunohistochemistry and zinc sulphide autometallography.

The mocha mouse is an autosomal recessive pigment mutant on mouse chromosome 10 caused by a deletion in the gene for the delta subunit of the adaptor-like complex AP-3. Based on zinc transporter 3 (ZnT3) immunohistochemistry, zinc TSQ fluorescence and a modified Timm method, previous studies found a lack of histochemically-detectable zinc and a substantial reduction in the ZnT3 immunoreactivity. It has, therefore, been suggested that the mocha mouse could serve as a model for studies of the significance of zinc ions in zinc-enriched (ZEN) neurons. We have chosen the mocha-zinc-model in a study of the significance of ZEN neurons in hypoxia-caused damage in mouse brain. In order to establish that the model was either void of zinc ions or had a significantly decreased level of zinc ions in their ZEN terminals, we repeated the studies that had lead to the above assumption, the only methodology difference being that we used the zinc specific Neo-Timm method instead of the Timm method applied in the original study. We found that, although the ZnS autometallography (AMG) technique revealed a reduction in staining intensity as compared to the littermate controls, there were still plenty of zinc ions in the ZEN terminals, in particular visible in telencephalic structures like neocortex and hippocampus. At ultrastructural levels the zinc ions were found in a pool of vesicles of the ZEN terminals as in the control animals, but additionally zinc ions could be traced in ZEN neuronal somata in the neocortex and hippocampus. The mossy fibres in the hippocampus of mocha mice also bind with TSQ, though less than in the controls. We found ZnS AMG grains in ZEN neuronal somata, which were also immunoreactive for ZnT3. Our study confirmed the decreased ZnT3 immunoreactivity in ZEN terminals of the mocha mouse found in the original study. Based on these findings, we suggest that the mocha mouse may not be an ideal model for studies of the histochemically-detectable zinc ion pool of the central nervous system.

Animals↗

Comparative toxicity of a zinc salt, zinc powder and zinc oxide to Eisenia fetida, Enchytraeus albidus and Folsomia candida.

The pore water zinc concentration and the calcium chloride extracted zinc fraction are higher in the soils spiked with a zinc salt (ZnCl2) compared to soils spiked with zinc oxide or zinc powder. Based on total zinc concentrations in the soil, the acute toxicity of zinc salt to the compost worm Eisenia fetida, the potworm Enchytraeus albidus and the springtail Folsomia candida was lower compared to zinc oxide and zinc powder. However, when expressed on the basis of pore water concentrations or calcium chloride extracted fractions, acute toxicity was higher for zinc salt, which indicated that dermal uptake via the pore water is not the only route of uptake. Chronic toxicity of zinc salt, zinc oxide and zinc powder was similar when based on total concentrations in the soil which again indicates that the pore water route of uptake is not the only route of exposure but that oral uptake is also important.

Animals↗

Salivary zinc as an index of zinc status in women fed a low-zinc diet.

The effect of a low-zinc diet on saliva and plasma levels was studied in 12 healthy young women. A diet low in zinc (3.2 mg/day) was fed to the subjects for 22 days. Subjects were determined to be in satisfactory zinc status via analysis of the zinc levels of their diet, hair, plasma, and saliva. During the low-zinc diet, concentrations of zinc in whole mixed saliva remained relatively stable for each individual and related significantly to the percentage sediment in the saliva. However, mixed saliva zinc did not respond to dietary depletion. Plasma zinc levels declined, but not significantly. Zinc levels of salivary sediment, which consisted primarily of epithelial cells, significantly (p less than 0.05) decreased from initial values of 126 +/- 28 microgram/g to final levels of 94 +/- 14 microgram/g after the low-zinc diet. These results suggest that mixed saliva zinc is not a useful index of zinc status; however, salivary sediment zinc may be a sensitive parameter if contamination can be avoided.

Adult↗