Body Zinc Research Articles

Serum zinc levels and zinc binding capacity in thalassemia

Recently, it has been reported that serum zinc binding capacity (ZnBC) is a very important criterion to evaluate body zinc (Zn) status. It has been shown that chronic Zn deficiency occur in the patients with thalassemia major (TM). Zn deficiency in TM may cause hyperzincuria, high ferritin levels, hepatic iron load, hepatic dysfunction. This study was undertaken to determine serum Zn levels and ZnBC in different thalassemia forms and sickle cell disease (SCD). The study has been carried out on 30 Thalassemia Major (TM), 34 Thalassemia Intermedia (TI), 31 Thalassemia Trait (TT) and 10 SCD. As control group, 13 healthy children and 20 adults were included. Serum Zn and ZnBC were determined by atomic absorption, then saturation index (SI%: serum Zn/ZnBC × 100) was calculated. Serum Zn levels in all patients were lower than control (p < 0.01). Serum ZnBC was at a normal level in patients with TT and TI but it was found to be lower in TM and SCD than control (p < 0.01). While serum Zn levels decrease and ZnBC increase in nutritional Zn deficiency, serum Zn levels decrease but ZnBC doesn't increase in patients with thalassemia.

Isolation and characterization of mammary cDNA differentially expressed in lethal milk mutation mice

AbstractLethal milk (lm) mutation in C57BL/6J inbred mice results in the reduction of zinc content in the milk and causes fatal neonatal zinc deficiency. Zinc injection to lm pups after birth helps them to overcome severe neonatal zinc deficiency and to maintain the normal body growth of lm pups. Thus, lm mutation displays a specific effect on the zinc content of the milk during lactation. The decrease in zinc content of the milk is not due to the low body zinc status in lactating lm dams. Also, oral zinc supplementation in lactating lm dams does not correct the low concentration of zinc in the milk. These findings suggest that lm mutation results in the defective cellular transport of zinc. The defective zinc transport might alter the expression of mammary genes because cellular zinc plays a critical role in diverse cellular functions. To investigate the effect of lm mutation on the expression of mammary genes, the differentially expressed cDNAs in lm mammary gland (MG) were explored using the mRNA differential display (DD) gel. One of the isolated cDNAs (M3) was expressed in the lm MG two times greater than that in the normal MG. The cloned partial M3 cDNA was shown to have the similarities to the unknown functional cDNAs in the yeast and human tissues. The M3 cDNA might have a common function in both lower and higher eukaryotes. The M3 mRNA is rich in the brain and the MG, but not in the liver and kidney. Hence, the M3 cDNA may have a certain function associated with the brain and the MG. More information regarding the cloned M3 cDNA might be provided by screening of the full length of M3 cDNA from cDNA library. J. Trace Elem. Exp. Med. 14:371–382, 2001. © 2001 Wiley‐Liss, Inc.

Body Weight-Specific Zinc Compartmental Masses in Girls Significantly Exceed Those Reported in Adults: A Stable Isotope Study Using a Kinetic Model

Maintaining optimal zinc status is important for normal growth and development in children, but minimal data are available regarding zinc metabolism in this age group. Our objectives were to utilize stable isotope-based compartmental modeling techniques to investigate zinc metabolism in healthy children; to expand a current stable isotope-based model to include red blood cell data; and to compare kinetic parameters in children with those previously reported in adults. Seven healthy girls, age 9.94 +/- 0.79 y, received 1.1 mg of a (67)zinc-enriched tracer orally and 0.5 mg of a (70)zinc-enriched tracer intravenously. Blood, urine and fecal samples were collected for 6 d. Stable isotope enrichments were measured by thermal ionization magnetic sector mass spectrometry. A six-compartment model based on a model previously reported in adults was used; the model excluded red blood cell data. Body weight-corrected masses of the body zinc compartments derived using this model were significantly greater in children than those reported in adults. Modification of the model to include a red blood cell compartment increased the total identifiable zinc mass of the nongastrointestinal compartments by approximately 2.5%. We conclude that compartmental modeling can be used to describe zinc kinetics in children, and that the body weight-corrected zinc pool masses are significantly greater in children than in adults.

Assessment of Marginal Zinc Status in Humans

The assessment of marginal zinc status is problematic. Currently, there is no universally accepted single measure to assess zinc status in humans. The development of a reliable measure of marginal or moderate zinc status would be useful for a variety of purposes. For example, a simple, yet sensitive and accurate measure of zinc nutritional status is critically needed to further our limited understanding of the possible associations between zinc status and the risk of developing various chronic diseases and in predicting favorable health outcomes in patient populations. A convenient and reliable zinc assessment tool is needed to identify subpopulations who are at a risk of zinc deficiency and as an objective guidepost to determine the need for initiation of zinc supplementation or zinc fortification of the food supply, as well in the refinement of recommendations of dietary zinc allowances. In frank zinc deficiency, clinical signs and static measures of zinc concentrations in a variety of readily available tissues, such as plasma, various blood cell types and hair, may uniformly confirm the presence of depleted body zinc stores. However, in general, the relative insensitivity or imprecision of these measurements has resulted in general disappointment in their use to assess marginal zinc status. Therefore, the search continues to find a useful and reliable marker of marginal zinc deficiency. In an attempt to speculate on possible future developments in the zinc status assessment field, a number of new and potentially promising approaches to this problem are highlighted.

A two-compartment Model for Zinc in Humans

The oral absorption of zinc, from a test meal of minced beef, mashed potatoes and peas, have been measured in 19 healthy adults using the radiotracer 65Zn. The oral absorption, expressed as a percentage of the administered dose, was 20 +/- 5% (mean +/- 1 SD) in good agreement with previous results. In a subset of 9 subjects, tracer retention in whole body and whole blood was followed out to one year. The data were fitted to a simple two compartment model yielding total body zinc (TBZn), the zinc content in each of the 2 compartments and zinc turnover. The TBZn values ranged from 15.5 to 35.9 mmol while zinc turnover ranged from 0.043 to 0.073 mmol/d in keeping with results reported for significantly more complicated compartmental models applied to more comprehensive 65Zn tracer data sets. Additionally, TBZn correlated well with total body potassium, a measure of lean body mass, measured by whole body counting of the naturally-occurring potassium radioisotope, 40K. The zinc content of the more rapidly turning over compartment ranged from 3.2 to 5.6 mmol in reasonable agreement with exchangeable zinc pool estimations reported for short term studies using stable zinc isotopes. Therefore, the simple dataset and model employed in the present study yielded information on the short- and long-term behaviour of zinc compatible with both more complex radiotracer studies and analytically more demanding stable isotope studies.

Costs of chronic waterborne zinc exposure and the consequences of zinc acclimation on the gill/zinc interactions of rainbow trout in hard and soft water

AbstractJuvenile rainbow trout were exposed to zinc in both moderately hard water (hardness = 120 mg CaCO3/L, pH = 8.0, Zn = 150 μg/L or 450 μg/L) and soft water (hardness = 20 mg CaCO3/L, pH = 7.2, Zn = 50 μg/L or 120 μg/L) for 30 d. Only the 450 μg/L zinc—exposed fish experienced significant mortality (24% in the first 2 d). Zinc exposure caused no effect on growth rate, but growth affected tissue zinc levels. Whole body zinc levels were elevated, but gills and liver showed no consistent increases relative to controls over the 30 d. Therefore, tissue zinc residues were not a good indicator of chronic zinc exposure. After the 30‐d exposure, physiological function tests were performed. Zinc was 5.4 times more toxic in soft water (control 96 h LC50s in hard and soft water were 869 μg/L and 162 μg/L, respectively). All zinc‐exposed trout had acclimated to the metal, as seen by an increase in the LC50 of 2.2 to 3.9 times over that seen in control fish. Physiological costs related to acclimation appeared to be few. Zinc exposure had no effect on whole body Ca2+ or Na+ levels, on resting or routine metabolic rates, or on fixed velocity sprint performance. However, critical swimming speed (UCrit) was significantly reduced in zinc‐exposed fish, an effect that persisted in zinc‐free water. Using radioisotopic techniques to distinguish new zinc incorporation, the gills were found to possess two zinc pools: a fast turnover pool (T1/2 = 3–4 h) and a slow turnover pool (T1/2 = days to months). The fast pool was much larger in soft water than in hard water, but at most it accounted for &lt;3.5% of the zinc content of the gills. The size of the slow pool was unknown, but its loading rate was faster in soft water. Chronic zinc exposure was found to increase the size of the fast pool and to increase the loading rate of the slow pool.

Effect of dietary zinc content and sources on the growth, body zinc deposition and retention, zinc excretion and immune response in chickens

1. In areas of intensive animal production heavy metals such as zinc (Zn), which is present at high concentrations in poultry excreta in relation to plant requirements, may be at the origin of soil phytotoxicity. This study was conducted in order to determine the effect of decreasing dietary Zn content on growth, plasma, tibia and whole body Zn concentrations, immune function, enzyme activity, Zn body retention and Zn concentration in excreta in broilers. 2. Two experiments were carried out using 160 and 80 1-day-old chicks. Broilers received diets with increased Zn contents of 20 to 190 mg/kg. In experiment 1, two sources of zinc methionine were compared to zinc sulphate. 3. A dietary Zn concentration of 45 mg/kg was sufficient to obtain normal broiler performance at 21 d of age. 4. Tibia and plasma Zn concentrations increased linearly with Zn dietary content and reached a plateau at 75 mg/kg, whereas the whole body Zn was saturated when the dietary Zn content was 90 mg/kg. 5. Antibody titres in response to SRBC injection and plasma alkaline phosphatase activity were not affected by dietary zinc concentration. 6. When the dietary Zn content was decreased from 190 to 65 mg/kg, body Zn retention was increased from 8% to 20% and Zn concentration in broiler manure was reduced by 75%. 7. Zn sources had no effect on the parameters measured in this study. 8. A nutritional approach, that is by lowering dietary Zn supplementation may reduce the risks of phytotoxicity in the soil resulting from excessive Zn concentration in manure.

Mobilization of lead by calcium versenate and dimercaptosuccinate in the rat.

1. Calcium disodium ethylenediaminetetraacetate (CaNa2 EDTA) and meso-2,3-dimercaptosuccinic acid (DMSA) individually and in permutation-combination in various doses (0.1, 0.2 and 0.4 mmol/kg bodyweight) were investigated for their efficacy to mobilize lead from vital tissues into urine and faeces and to restore the lead-sensitive biochemical parameters in lead pre-exposed rats with a view to develop the most acceptable treatment regimen for lead poisoning with a minimal loss of endogenous essential elements. 2. The combined therapy was more effective than a single chelator treatment. 3. The combination of 0.2 mmol/kg CaNa2EDTA + 0.4 mmol/kg DMSA caused a lower depletion of zinc, calcium and iron but possessed almost equal capability to that of 0.4 mmol/kg CaNa2EDTA + 0.4 mmol/kg DMSA to produce urinary as well as faecal excretion of lead, to reduce the tissue burden of lead, including that of the brain, and to reverse lead-induced biochemical alterations. 4. The combination of 0.2 mmol/kg CaNa2EDTA + 0.4 mmol/kg DMSA has shown a definite improvement over previously reported combinations in terms of removal of lead from tissues, particularly the brain, restoration of urinary delta-aminolevulinic acid levels and a decrease in the loss of body zinc and is, therefore, recommended for the treatment of lead intoxication.

Measurement of zinc in clinical samples.

and serum specimens and either may be analysed. Thus, most investigations of zinc-associated clinical problems require analysis of specimens of plasma or serum. In certain situations it is appropriate to determine urinary excretion while whole blood, erythrocyte, leucocyte or hair concentrations are relevant to some studies.i-' Typical concentrations of zinc in these specimens are shown in Table 2. A few workers have monitored the zinc concentrations of plasma fractions (e.g. zinc bound to albumin, transferrin, and amino acids), in attempts to develop more sensitive parameters of zinc status than the total serum zinc concentration.' 7 However, this line of investigation has not proven helpful. Methods for plasma fractionation of zinc are complex, involving techniques such as electrophoresis and ultrafiltration, which require large volumes of sample and risk contamination errors. Results can be of academic interest but clinically useful markers of zinc status have not been identified. Analyses of tissues, foodstuffs Zinc is an essential trace element for animals and man.' It is a cofactor for a large number of enzymes in virtually all metabolic pathways, is a component of transcription activation factorsthe zinc fingers, is involved in neurotransmitter function, immune activity and the action of hormones such as insulin. Thus, zinc is of major importance in physiology and biochemistry and, by implication, to the health of the individual. Deficiency of zinc is manifest by a variety of symptoms (Table 1) and though uncommon, excessive exposure will also cause morbidity.? No more than 1% of the total body zinc is present in the circulation with around four-fifths of this fraction contained in the red cells. Plasma, therefore, contains about 0·2% of the total body load of zinc most of which is bound to albumin with the remainder found in 1)(-2 macroglobulin and amino acid complexes. High concentrations of zinc are found in tissues where cell turnover is rapid, such as the liver, testes and intestinal mucosa. The major zinc reservoirs include muscle, bone, skin and hair, but zinc is not readily mobilized from these sites in times of deficiency. Zinc deficiency will develop if there is inadequate dietary intake or absorption, excessive loss or failure to meet an increased demand. Investigation of zinc nutritional status is appropriate when there are symptoms suggestive of perturbation of zinc metabolism (Table 1), in patients receiving total parenteral nutrition, artificial diets or other nutritional setbacks, and where there is occupational exposure.? Despite the very low proportion of total body zinc in the plasma and the influence of the acute phase response, total plasma zinc concentration is the most useful indicator of deficiency.I: Concentrations of zinc are similar in plasma

Zinc kinetics in preterm infants: a compartmental model based on stable isotope data.

Zinc is an essential nutrient for growth; however, little is known about zinc kinetics (absorption, distribution, and excretion) in preterm infants (< 38-wk gestation). Zinc kinetics were studied in two preterm infants (gestational ages, 32 and 33 wk) following oral or intravenous administration of a stable isotope (70Zn). Plasma, red blood cells (RBC), urine, and feces were sampled for up to 30 days. Isotope enrichment was measured in tissues by inductively coupled plasma (ICP)-mass spectrometry, and zinc was determined by ICP-atomic emission spectrometry. Data were analyzed by compartmental analysis using SAAM31. Zinc intake increased during the studies, and, because body zinc was not in steady state, both tracer (70Zn) and tracee (Zn) data were fitted using analogous models. A model for adults [M. E. Wastney, R. L. Aamodt, W. F. Rumble, and R. I. Henkin. Am. J. Physiol. 251 (Regulatory Integrative Comp. Physiol. 20): R398-R408, 1986] was modified to fit data from the preterm infants. RBC data were fitted using one compartment (vs. 2 in adults), and an adult RBC subsystem was included in the model to account for zinc introduced during blood transfusions. Exchange of zinc between compartments that were not sampled was based on zinc distribution in neonates. Absorption was 42 and 34%, and endogenous fecal excretion, based on intravenous data, was 15 micrograms.kg-1.day-1. The model can be used to quantify changes in zinc kinetics of preterm infants with age, weight, and zinc intake for evaluating nutritional requirements with growth.

Lead exposure and conventional and ambulatory blood pressure: a prospective population study. PheeCad Investigators

- To evaluate in a prospective fashion the association between low-level lead exposure and blood pressure. - Prospective cohort study. - General population. - A random population sample (N=728; 49% men; age range, 20-82 years) was studied in Belgium for 1985 through 1989 and reexamined for 1991 through 1995. - At baseline and follow-up, blood pressure was measured by conventional sphygmomanometry (15 total readings) and at follow-up also by 24-hour ambulatory monitoring. Lead exposure was estimated from blood lead and zinc protoporphyrin concentrations. Multivariate analyses controlled for sex, age, body mass index, smoking and drinking habits, physical activity, exposure at work, social class, menopausal status, use of medications (antihypertensive medication, oral contraceptives, hormonal replacement therapy), hematocrit or hemoglobin, serum total calcium concentration, 24-hour urinary sodium and potassium excretion, and gamma-glutamyltransferase activity. - At baseline, mean (SD) systolic/diastolic conventional blood pressure was 130 (17)/77 (9) mm Hg. The mean blood lead concentration was 0.42 micromol/L (8.7 microgram/dL), and the mean zinc protoporphyrin concentration was 1.0 microgram per gram of hemoglobin. Over the 5.2-year median follow-up, the mean blood lead concentration dropped by 32% (0.14 micromol/L [2.9 microgram/dL]) (P<.001). Small but significant (P<.01) changes occurred in systolic (-1.5 mm Hg) and diastolic (+1.7 mm Hg) conventional blood pressure and in zinc protoporphyrin concentration (+0.5 microgram per gram of hemoglobin). Over the follow-up period, no consistent associations emerged between the changes in conventional blood pressure and in blood lead or zinc protoporphyrin concentrations. In addition, after adjustment for sex, age, and body mass index, blood lead and zinc protoporphyrin concentrations at baseline did not predict the development of hypertension in 47 patients (risk ratio for doubling of the initial lead concentration, 1.2; 95% confidence interval, 0.7-2.0). In a time-integrated analysis in which each person was characterized by all available measurements, conventional blood pressure did not correlate with blood lead or zinc protoporphyrin concentrations in a consistent manner. Similarly, the mean (SD) 24-hour blood pressure at follow-up (119 [11]/71 [8] mm Hg; N=684) did not show a consistent relationship with blood lead or zinc protoporphyrin concentrations at baseline or at follow-up. - Lead exposure at the intensity studied (<l.45 micromol/L [<30 microgram/dL]) was not consistently associated with increased conventional or 24-hour blood pressure in the general population or with increased risk of hypertension. These findings argue against the hypothesis that current lead exposure levels are associated with excess cardiovascular morbidity and mortality caused by hypertension.

Zinc needs and homeostasis during lactation.

During lactation there is an increased maternal loss of essential trace element zinc that is secreted into milk. During the first six months of lactation a mean of approximately 1.1 mg d-1 of zinc is secreted into human milk, which decreases to 0.6 mg d-1 during the next six months of lactation. The increased maternal need for zinc must be met through an increased dietary intake or homeostatic mechanisms which could compensate for the secretion of zinc into milk. These homeostatic mechanisms may include an increase in absorption, reduced excretion (urine and faecal endogenous losses) and the use of maternal pools of zinc, such as bone. Enhanced zinc absorption during lactation has been reported for lactating women whose intake of zinc is less than half of the current recommendation. Urinary zinc excretion by lactating women has also been observed to be significantly decreased up to 6 months postpartum compared to women who have never been pregnant. Approximately 30% of total body zinc is associated with bone. During lactation maternal bone resorption and reduction in one mineral content has been observed. Since urinary zinc excretion is reduced during lactation, this bone resorption could supply a portion of the zinc that is incorporated into milk. Thus, during lactation, homeostatic mechanisms which include an enhanced zinc absorption, reduced urinary zinc excretion and zinc from bone resorption could partially compensate for the secretion of zinc into human milk. These homeostatic mechanisms need to be considered when dietary recommendations for zinc intake are made for lactating women.

A compartmental model of zinc metabolism in adult men used to study effects of three levels of dietary copper

The effect of dietary copper level on zinc metabolism in five healthy adult men was studied using compartmental modeling. The subjects were fed one level of dietary zinc (11.2 +/- 1.6 mg/day) and three levels of dietary copper (1.68, 0.785, and 7.52 mg/day). The stable isotope tracers 70Zn and 67Zn were administered intravenously (3 times) and orally (4 times), respectively. Plasma, urinary, and fecal 67Zn and 70Zn levels were measured. An existing model of zinc metabolism was used as a basis for our model. Model rate constants were modified to simulate multiple oral and intravenous doses of stable isotope tracers given during the 90-day study. Most rate constant changes occurred in the absorption and excretion pathways. The model predicted that movement of zinc through the gastrointestinal tract increased when the highest level of copper was fed and the urinary zinc excretion rate tended to increase. The fractional rate constant representing absorption of zinc decreased slightly when the highest level of copper was fed. Total body zinc was predicted to be approximately 2,000 mg, with 95% in tissues other than the liver, red blood cells, or plasma and approximately 2.25% in the blood (with 95% of that in the red blood cells), which follows expected zinc masses within the body and those predicted by previous models.

The importance of food and water as sources of zinc during exposure of Gammarus pulex (Amphipoda)

The bioaccumulation of zinc by the freshwater shrimp Gammarus pulex (L.) and adsorption by its food, conditioned horsechestnut leaves (Aesculus hippocastanum L.), in two zinc exposure concentrations were studied in the laboratory. The bioconcentration factors (BCF), uptake and elimination rate constants, and assimilation rate from food were calculated for one exposure concentration using a two-trophic-level model of a food chain. The BCF of the conditioned horse chestnut leaves was more than five times higher than that of G. pulex, and the assimilation rate of zinc from food by Gammarus was only 1.4%. As with many other animals, G. pulex was able to regulate its total body zinc level, and to accumulate most of the metal from water rather than from its food.

Zinc and copper balances in healthy adult males during and after 17 wk of bed rest

The effects of long-term bed rest on zinc and copper balances were measured in seven healthy men. Volunteers aged 22-54 y (mean +/- SD, 34 +/- 12 y), 168-185 cm in height (173 +/- 5 cm), and 64-86 kg in weight (74 +/- 9 kg) remained on a metabolic ward for 29 wk. Subjects were ambulatory during weeks 1-5, remained in continuous bed rest for weeks 6-22, and were reambulated during weeks 23-29. Copper and zinc were measured in weekly urine and fecal composites. Dietary intakes provided (mean +/- SD) 19.2 +/- 1.2 mumol Cu (1.22 +/- 0.08 mg), 211 +/- 11 mumol Zn (13.81 +/- 0.72 mg), 25.2 +/- 1.2 mmol Ca (1011 +/- 46 mg), 1086 +/- 46 mmol N (15.21 +/- 0.65 g), and 48.1 +/- 1.4 mmol K (1489 +/- 44 mg)/d. Bed rest increased fecal zinc excretion and decreased zinc balance, whereas copper balance was unchanged. Reambulation decreased fecal zinc excretion and increased both zinc and copper balances. These results suggest that during long-term bed rest or space flight, individuals will lose total body zinc and will retain more zinc and copper when they reambulate.

Assessment of zinc status in juvenile Atlantic salmon ( Salmo salar) by measurement of whole body and tissue levels of zinc

Duplicate groups of 40 g Atlantic salmon were fed dry pelleted diets based on cod muscle meal as a protein source for 8 weeks. The basal diet contained 17 mg Zn/kg to which 0, 10, 20, 40 or 80 mg Zn/kg diet, respectively, were added as ZnSO 4·7H 2O. After 8 weeks, 15 fish from each dietary treatment were marked and then they were fed the basal diet for another 4 weeks. Fish were sampled after 2, 4, 8 and 12 weeks. Blood samples were withdrawn and serum was analyzed for zinc concentration and alkaline phosphatase (AP) activity. Liver, kidney, vertebrae and intestine were removed from ten fish in each dietary treatment. A further ten fish were used for whole body mineral analyses. There were no significant differences in growth due to different dietary zinc concentrations and this, together with data on alkaline phosphatase and iron levels, showed that the basal diets contained sufficient zinc to prevent overt zinc deficiency symptoms. Zinc concentrations in the whole body and tissues, however, were significantly influenced by dietary zinc level. On the basis of the dietary zinc concentration required to maintain whole body zinc and serum zinc concentrations within the normal range, it was concluded that the dietary zinc requirement of juvenile Atlantic salmon is between 37 and 67 mg Zn/kg dry diet under our test conditions. Hence, until more data are available, juvenile Atlantic salmon diets based almost entirely on marine fish protein should contain > 67 mg Zn/kg dry diet.

The changes of metabolism balance of zinc and copper in gastric juice with widely varying dietary zinc intake.

The concentrations of zinc and copper in gastric juice of humans who had widely varying dietary zinc intake were evaluated. In order to compare this with zinc and copper levels of normal dietary individuals, we also determined the zinc and copper levels in healthy individuals' plasma and in cancer patient's natural tissue, all of whom had normal diets. The correlation coefficients between zinc and copper were 0.71, 0.45, and 0.55, respectively, in gastric juice, plasma, and tissue of normal dietary subjects. Such correlation changed and was destroyed when there was a high zinc level in gastric juice. When gastric juice zinc level changed from mean value 16.8 mumol/L to 262.5 mumol/L, the correlation coefficient varied from 0.71 to -0.04, and the copper level also varied from mean value 8.96 mumol/L to 4.89 mumol/L. These findings probably give the evidence to suggest that a high zinc level will restrain the copper level and break the balance of the human body's zinc and copper metabolism.

On the excretion of zinc by the shore crabCarcinus maenas(L.)

Abstract The shore crab Carcinus maenas (L.) does not excrete zinc taken up and accumulated when exposed to 100 µg Zn l−1, but does excrete a proportion (c. 70%) of the zinc taken up from 3162 µg Zn l−1 over 21 days. Ofthe zinc excreted at this exposure, only 4% is excreted in the urine. There was a linear relationship between zinc concentrations in urine and blood. Food was found to be an important Zn source to the crab, and excretion ofZn accumulated from food again depended on dose. None of a c. 25 µg Zn dose in food was excreted in 12 days; of 210 µg absorbed from a 250 µg Zn dose in a meal 46% was retained after 12 days, and 113 µg was excreted (22% in the faeces, 1% in the urine and 77% probably via the gills). C. maenas lost c. 20% of the body zinc content with the moult, even after withdrawal into the soft tissues of some of the zinc there accumulated (both from food and water).

Mild to moderate zinc deficiency in short children: Effect of zinc supplementation on linear growth velocity

Twenty-one prepubertal, short Japanese children (11 boys) without endocrine abnormalities were identified as having mild-to-moderate zinc deficiency by zinc kinetics studies (zinc body clearance > or = 20 ml/kg per hour). Only one child had a serum zinc level < 65 micrograms/dl (cutoff level). A total of 10 children (5 boys) received 5 mg/kg per day of zinc sulfate for 6 months; 11 untreated children (6 boys) served as control subjects. During treatment, calorie intake (p < 0.01), growth velocity (p < 0.01), serum zinc, calcium, and phosphorus concentrations, alkaline phosphatase activity (p < 0.001), percentage of tubular reabsorption of phosphorus (p < 0.05), ratio of maximal tubular reabsorption rate for phosphorus to the glomerular filtration rate (p < 0.05), serum osteocalcin level (p < 0.01), and plasma insulin-like growth factor 1 (p < 0.05) were significantly increased, but urinary excretion of growth hormone was unchanged in the zinc-supplemented group. All these values were unchanged in the untreated children. We conclude that zinc supplementation is effective for inducing growth in short children with zinc deficiency, and that body zinc clearance tests facilitate detection of marginal zinc deficiency.

Zinc metabolism and metallothionein expression in bone marrow during erythropoiesis

Zinc metabolism and metallothionein induction in rat bone marrow were investigated during induced erythropoiesis. Redistribution of body zinc was measured with 65Zn after acute blood loss in rats fed zinc-restricted or zinc-adequate diets. Uptake of 65Zn by bone marrow was related to time after blood loss, metallothionein induction, and dietary zinc status. Increased 65Zn uptake by marrow of zinc-restricted rats suggests a minimal amount of zinc is necessary to support expansion of the erythrocytic compartment. Zinc induction of marrow metallothionein also occurred in rats in which anemia was produced using phenylhydrazine. Anemic rats which were administered zinc had higher concentrations of marrow metallothionein compared with control rats. Induction of marrow metallothionein by zinc in nonanemic rats required prior treatment with erythropoietin. Percoll fractionation showed marrow metallothionein was most abundant in erythroblasts. These experiments suggest metallothionein synthesis occurs in erythropoietin-sensitive precursor cells in the marrow in response to increased zinc accessibility.