True absorption and endogenous fecal excretion of manganese in relation to its dietary supply in growing rats

A conventional balance study with 48 male weanling rats was conducted to determine true absorption and endogenous fecal excretion of manganese (Mn) in relation to dietary Mn supply, following the procedures of a previously adapted isotope dilution technique. After 10 d on a diet with 1.5 ppm Mn, eight animals each were assigned to diets containing 1.5, 4.5, 11.2, 35, 65, or 100 ppm Mn on a dry-matter basis. Three days later, each rat was given an intramuscular⁵⁴Mn injection and kept on treatment for a balance period of 16 d. Apparent Mn absorption assessed for the final 8 d, averaged 8.6 μg/d without significant treatment effects, although Mn intake ranged from 18.6 to 1200 μg/d, in direct relation to dietary Mn concentrations. Mean fecal excretion of endogenous Mn for the six treatments was 0.9, 2.7, 7.4, 11.0, 16.3, and 17.7 μg/d, respectively. These values delineate the rates to which true absorption exceeded apparent rates. True absorption, as percent of Mn intake, averaged 28.7, 15.9, 11.7, 6.1, 3.4, and 2.0, respectively, as compared with mean values of 23.9, 10.9, 6.2, 3.4, 1.2, and 0.5 for percent apparent absorption. It was concluded that both true absorption and endogenous fecal excretion markedly responded to Mn nutrition and that the reduction in the efficiency of true absorption was quantitatively the most significant homeostatic response for maintaining stable Mn concentrations in body tissues.     

Radioisotope-dilution technique for determining endogenous manganese in feces of the growing rat

A conventional balance study with growing rats was conducted to evaluate experimental conditions for determining endogenous fecal manganese (Mn) excretion and, hence, true Mn absorption by the isotope-dilution technique. Thirty-four rats, with a mean initial live weight of 60 g, allotted to three groups of 8 animals and one group of 10 animals, were injected intramuscularly with a⁵⁴Mn tracer dose and sacrificed after 4, 8, 12, and 16 d, respectively. In liver and serum, the specific radioactivity of Mn was the lowest among the tissues analyzed and its exponential rate of decrease over the period of d 4–16 was the highest. During the 8-d period, from d 9–16, apparent Mn absorption averaged 14.1% of intake (128.5 μg Mn/d). Assuming that the specific activity of Mn in liver of d 11 or, alternatively, in serum of d 16, was on the average representative of that of endogenous Mn in feces of d 9–16, it was computed that Mn of endogenous origin accounted for 9.0 and 9.3% of the total fecal excretion of the metal, and that true absorption amounted to 21.9 and 22.1% of Mn intake, respectively.     

Copper absorption in young men fed adequate and low zinc diets

Copper absorption was measured at two levels of dietary zinc in six healthy young men who were confined to a metabolic unit for a 75 d study of zinc utilization. A diet of conventional foods was fed, providing either 16.5 or 5.5 mg zinc and 1.3 mg copper daily. Copper absorption was determined by feeding⁶⁵Cu, a stable isotope of copper, once during the 16.5 mg Zn diet and near the beginning and end of the 5.5 mg Zn diet. Apparent copper absorption averaged 48.1% when the 16.5 mg Zn diet was fed. This was significantly higher than the averages of 37.2 and 38.5% when the 5.5 mg Zn diet was fed. Absorption also differed significantly among subjects. Fecal copper did not differ between diets or among subjects. All subjects were in positive copper balance at both levels of dietary zinc. These results suggest that a dietary zinc intake slightly above the Recommended Dietary Allowance of 15 mg/d does not increase fecal copper loss and does not interfere with copper absorption.     

Zinc and copper in human cerebrospinal fluid

Zinc and copper have been estimated in CSF of 14 normal volunteers, nine men and five women. Zinc was analyzed by limited-aspiration flame atomic absorption spectrophotometry using a deuterium continuum light source. Copper was analyzed in 0.1% HNO₃ by flameless atomic absorption spectrophotometry with a graphite cuvette on a flameless atomizer. Recovery of added zinc varied less than 5% and that of the added copper varied less than 8%. CSF zinc was 31.5±19.8 μg/L (mean ± 1 SD); CSF copper, 7.5±3.1 μ/L. Values obtained for CSF zinc are about 1/2 those we and others obtained previously, the decrease related almost exclusively to removal of interference by the CSF matrix, which produced spuriously elevated values without use of the deuterium light source. Values obtained for CSF copper were approximately one-tenth those we and others had obtained previously. The decrease related, in part, to the removal of matrix effects, but also to improvement of the signal-to-noise ratio present in other techniques.     

Urinary Excretion of Zinc and Metabolic Control of Patients with Diabetes Type 2

The objective of this study was to assess urinary excretion of zinc and evaluation parameters of metabolic control in type 2 diabetic patients. Thirty-one type 2 diabetic patients, of both genders, with 5.8 ± 5.6 years average time of the disease, age range 20–60 years, were selected. Evaluation of the nutritional status was performed using anthropometric measurements. To evaluate food consumption, the 3-day alimentary log method was used, and its analysis was performed using a software. Determination of urinary zinc was by atomic absorption spectrophotometry. From the obtained results, it was concluded that 51.6% of the patients were overweight. The mean of found waist circumference was 100.4 and 92.2 cm for men and women, respectively. Blood glucose and glycated hemoglobin values were higher than reference values, and plasma albumin concentration was adequate. The median of found urinary zinc excretion was 474.9 μg/24 h, within normal standards (300–600 μg/day). Regarding diet composition, calorie and protein concentration were above recommendation, while mean zinc concentration was adequate. This data allow the conclusion that the evaluated patients presented adequate urinary zinc excretion in comparison with reference values.     

Absorption,endogenous excretion,and balance of zinc in growing rats on diets with various sugars replacing starch

The effect of partially replacing starch for various sugars on the apparent and true absorption, endogenous excretion, and balance of zinc was investigated in a study with growing rats. Six groups of five or six animals with an initial live weight of 39.4 +/- 2.7 g were fed diets that had the same Zn content (22 mg/kg), but differed in the sugar content: 1. Starch only (56%); 2. Glucose (15%); 3. Fructose (15%); 4. Sucrose (30%); 5. Galactose (15%); and 6. Lactose (30%). At the start of a 15-d fecal and urinary collection period, each animal was given an intramuscular injection of 380 kBq 65Zn for estimating endogenous Zn excretion by isotope dilution. The ratio of the specific activity of fecal Zn (after 12 d) to that of urinary Zn (after 9 d) was applied to reflect the ratio of endogenous to total fecal Zn collected from day 10 to 15. This ratio averaged 0.59, without significant differences among treatments. For this period, apparent and true absorption averaged 87.1 and 94.7% of Zn intake, respectively, and did not significantly differ among diets. Urinary excretion of 65Zn and of stable zinc by the galactose-fed rats was markedly higher than that by the other animals. Their Zn balance was, per unit weight gain, comparable with that of the other groups (30.7 vs 28.2 to 30.2 micrograms/g).     

Zinc Nutritional Status in Adolescents with Down Syndrome

Studies have evidenced that zinc metabolism is altered in presence of Down syndrome, and zinc seems to have a relationship with the metabolic alterations usually present in this syndrome. In this work, the Zn-related nutritional status of adolescents with Down syndrome was evaluated by means of biochemical parameters and diet. A case–control study was performed in a group of adolescents with Down syndrome (n = 30) and a control group (n = 32), of both sexes, aged 10 to 19 years. Diet evaluation was accomplished by using a 3-day dietary record, and the analysis was performed by the NutWin program, version 1.5. Antropometric measurements were performed for evaluation of body composition. The Zn-related nutritional status of the groups was evaluated by means of zinc concentration determinations in plasma and erythrocytes, and 24-h urinary zinc excretion, by using the method of atomic absorption spectroscopy. The diet of both groups presented adequate concentrations of lipids, proteins, carbohydrates, and zinc. The mean values found for zinc concentration in erythrocytes were 49.2 ± 8.5 μg Zn/g Hb for the Down syndrome group and 35.9 ± 6.1 μg Zn/g Hb for the control group (p = 0.001). The average values found for zinc concentration in plasma were 67.6 ± 25.6 μg/dL for the Down syndrome group and 68.9 ± 22.3 μg/dL for the control group. The mean values found for zinc concentration in urine were 244.3 ± 194.9 μg Zn/24 h for the Down syndrome group and 200.3 ± 236.4 μg Zn/24 h for the control group. Assessment of body composition revealed overweight (26.7%) and obesity (6.6%) in the Down syndrome group. In this study, patients with Down syndrome presented altered zinc levels for some cellular compartments, and the average zinc concentrations were low in plasma and urine and elevated in erythrocytes.     

Copper absorption,endogenous excretion,and distribution in Sprague-Dawley and lean (Fa/Fa) Zucker rats

We previously observed a rapid reduction in plasma ceruloplasmin activity in lean Zucker (Fa/Fa) rats fed a marginal copper (Cu)-deficient diet compared to similarly fed obese Zucker (fa/fa) and lean Sprague-Dawley rats. In an effort to understand the mechanisms underlying this response, we utilized the isotope dilution method to investigate the absorption and excretion of Cu in lean Zucker rats fed control and marginal Cu diets. Sprague-Dawley (SD) and homozygous lean Zucker rats were fed either a Cu-adequate (Cont; 7.5 μg Cu/g diet) or a low Cu (Low; 1.1 μg Cu/g diet) casein-based diet for 23 d. Two weeks following initiation of the dietary treatment, each rat was injected intramuscularly (im) with 11.2 μCi of⁶⁷Cu. Urine and feces were collected daily. On the 9th d following isotope injection, rats were killed and tissues collected. Significant dietary effects were observed in the relative absorption and endogenous fecal excretion of⁶⁷Cu. The tissue distributions of nonisotopic Cu and⁶⁷Cu activity were also different between dietary treatments. Tissues from rats fed the low-Cu diet typically had high concentrations of⁶⁷Cu and low concentrations of nonisotopic Cu compared to controls. An increase in relative⁶⁷Cu absorption was evident for rats fed the low-Cu diet (57.2 and 39.3%, for SD Low, Zucker Low, respectively, and 17.9, and 28.5% SD Cont and Zucker Cont, respectively). Rats fed the low-Cu diet also had reductions in endogenous fecal excretion of⁶⁷Cu compared to their respective controls. Although strain effects were not evident for either percent Cu absorption or endogenous fecal Cu excretion, the relative adaptive changes appeared more marked for the Sprague-Dawley rats compared to the lean Zucker rats.     

Type II diabetes mellitus,congestive heart failure,and zinc metabolism

Zinc status was assessed in patients with type II diabetes mellitus and congestive heart failure (CHF). Three groups of patients were enrolled into the study: Group 1: 15 patients with type II diabetes mellitus and CHF; Group 2: 20 patients with isolated type II diabetes mellitus; and Group 3: nine patients with isolated CHF. Twenty-four-hour urine was measured for creatinine, protein, and zinc, and blood was drawn for creatinine, proteins, liver enzymes, hemoglobin A₁c, and zinc. Insulin treatment and hemoglobin A₁c were comparable in the diabetic patients of groups 1 and 2, but group 1 was also treated with captopril and diuretics like the CHF patients of group 3. Plasma zinc levels were statistically similar in all three groups, but urinary zinc excretion (μmol/24 h) and urinary zinc: creatinine (μmol/mmol) ratio were significantly higher in the type II diabetics and CHF group (27.2±1.5; 1.69±0.6, respectively) compared to the diabetic patients alone (19.4±0.76; 0.97±0.3, respectively) and the CHF patients (9.7±0.3; 0.62±0.3, respectively). Patients with type II diabetes mellitus and CHF were treated with higher doses of captopril than the CHF patients (56.25±24 mg vs 18.8±11 mgP<0.05). Thus, patients with type II diabetes mellitus and CHF excrete larger amounts of zinc, which may eventually lead to zinc deficiency.     

Intestinal iron absorption in chickens

Intestinal iron absorption in chickens was studied in vivo, using an intestinal perfusion technique in closed circuit. The results obtained show that iron absorption, at 30 min intervals, is a linear function of test solution iron concentrations of up to 776 μg Fe/20 mL. At higher concentrations, iron saturation occurs. The mucosal epithelial cells seem to be less a limiting factor than in rats. However, in chickens, the binding capacity of plasma might play an important role in the regulation of iron absorption. Iron absorption versus time was analyzed in 15, 30, 60, and 120 min periods for the iron concentration of 14 μg Fe/20 mL. Intestinal iron absorption showed a linear relationship between these two parameters. A period of perfusion of either 30 or 60 min by a solution of 14 μg Fe/20 mL appears suitable since no interference by a saturation process can then occur.     

Lead increases urinary zinc excretion in rats

The major purpose of this study was to determine whether acute or chronic Pb exposure would increase urinary excretion of zinc in the rat. Four groups of unanesthetized rats were given 0, 0.03, 0.3, or 3 mg Pb (as acetate) kg intravenously, and urinary excretion of zinc, sodium, and potassium was monitored for 6 h. Only at the highest dose was urinary Zn excretion significantly elevated; there were no significant changes in sodium and potassium excretion at any dose. Two other groups of rats were studied for 9 weeks in metabolism cages before and during administration of either 500 ppm Pb (as acetate) or equimolar Na acetate in the drinking water. Two days after Pb treatment and continuing through day 35, Zn excretion was elevated in the Pb-exposed animals; beyond this day, zinc excretion became similar in the two groups. The difference in Zn excretion was not the result of lower water intake by the Pb-treated animals. At sacrifice (70 days after starting Pb exposure), Pb-exposed animals had lower Zn content of the plasma and testis, but there was no difference in kidney Zn. Plasma renin activity was significantly higher in Pb-exposed animals. We conclude that chronic Pb exposure in rats can result in some degree of decreased tissue zinc, which is, at least in part, secondary to increased urinary losses of zinc.     

Induction of metallothionein in rat tissues following subchronic exposure to mercury shown by radioimmunoassay

Although the analysis of metallothionein (MT) by radioimmunoassay (RIA) is not a common technique, its use is preferred over other methods since it offers the advantages of sensitivity and specificity. In this paper we present data on the basal levels of MT in rat tissues and physiological fluids of female Sprague-Dawley rats. The mean basal MT concentrations of the following organs and fluids were determined by RIA to be: liver (9.8 μg/g), kidney (68 μ/g), brain (0.8 μg/g), spleen (1.0 μg/g), heart (5.4 μg/g), plasma (11 ng/ml), and urine (200–300 μg/g creatinine). Following subcutaneous exposure to inorganic mercury (0.2 μmol/kg/d, 5 d a week for up to 4 wk), the metal accumulated primarily in the kidney. There was also a simultaneous accumulation of zinc in the liver and of zinc and copper in the kidney. Induction of MT did take place in liver, kidney, brain, and spleen. No increases in the MT contents of blood and urine were noted. The excess zinc and copper in the kidney of exposed animals were found to be associated predominantly with MT. No overt signs of mercury toxicity were noted in these animals and the incidence of proteinurea was nil. The data are discussed with reference to methods of MT determination in animal tissues and in relation to mercury metabolism and toxicity.     

Response of Selenium Status Indicators to Supplementation of Healthy North American Men with High-Selenium Yeast

The essential nutrient selenium is required in microgram amounts [recommended dietary allowance (RDA) = 55 μg/day, 699 nmol/day] and has a narrow margin of safety (upper tolerable intake limit = 400 μg/day, 5 μmol/day). We conducted a randomized placebo-controlled study of high-selenium yeast, the form used in most supplements (300 μg/day, 3.8 μmol/day), administered to 42 free-living healthy men for 48 weeks. Dietary intakes of selenium, macronutrients, and micronutrients were not different between groups and did not change during the study. Supplementation more than doubled urinary selenium excretion from 69 to 160 μg/day (876 to 2,032 nmol/day). Urinary excretion was correlated with recent selenium intake estimated from 3-day diet records: urinary selenium excretion = 42 μg/day (533 nmol/day) + 0.132 × dietary selenium intake, p < 0.001. Dietary selenium intake was not significantly correlated with the other indicators of selenium status, presumably because urinary selenium excretion reflected recent intake, and tissue selenium was homeostatically controlled. After 48 weeks of supplementation, plasma selenium was increased 60% from 142 to 228 μg/l (1.8 to 2.9 μmol/l), and erythrocyte selenium was approximately doubled from 261 to 524 μg/l (3.3 to 6.6 μmol/l). Selenium concentrations increased more modestly in hair (56%) and platelets (42%). Platelets were the only blood component in which glutathione peroxidase activity was significantly related to selenium content. Selenium levels decreased rapidly after the end of supplementation, and there were no significant differences in selenium status indicators between groups by week 96. The absorption, distribution, and excretion of selenium from high-Se yeast were similar to selenium in foods.     

Zinc bone loss in chronic renal failure and chronic metabolic acidosis

The effects of chronic metabolic acidosis (CMA) on zinc (Zn) bone content and urinary excretion were examined in the presence of normal or reduced renal function together with some aspects of calcium (Ca) metabolism. Four groups of rats were compared. All were fed a 30% protein and 9 mg Zn/100 g diet. Two were uremic (U): The first developed acidosis (UA), which was suppressed in the other (UNA) by NaHCO₃ supplement. Two other groups had normal renal function: One was normal (CNA), and the other had NH₄Cl in the drinking water and acidosis (CA). Femur total Zn and Ca content was markedly reduced by CMA and was not affected by uremia. Zn urinary excretion was increased by CMA and unaltered by uremia. Ca urinary excretion was markedly reduced in uremic rats, but was enhanced in both acidotic conditions. Urinary Ca and Zn showed a strong correlation in uremic and in control rats. Plasma parathormone and 1,25(OH)₂D₃ were unchanged by CMA. These data are in agreement with a direct primary effect of CMA on bone in releasing buffers. CMA induces bone resorption and a parallel decrease of mineral bone components, such as Ca and Zn, with little or no role of PTH, 1,25(OH)₂D₃ and of uremia itself.     

Urinary levels of metallothioneins and metals in subjects from a semiindustrialized area in Tarragona Province of Spain

The monitoring of heavy metals is important if adverse effects on health are to be avoided. In humans, metallothionein (MT) has been used as a biomonitor for the assessment of cadmium (Cd). In the present study, subjects drawn from the population of Tarragona Province (NE Spain) were investigated. Urinary MT, zinc (Zn), and copper (Cu) concentrations, corrected for creatine concentrations, were determined in 625 samples from healthy subjects aged between 10 and 65 yr. Mean values of MT and Cu in females were higher than those in males, with levels of 29.5 (23.8) vs. 22.7 (24.9) μg MT/creatinine (p<0.001) and 4.8 (6.1) vs 3.4 (4.9) μg Cu/g creatinine (p<0.001). No differences between males and females were observed with respect to urinary Zn: 78.0 (66.4) vs 73.0 (85.5) μg/g creatinine, respectively (p=0.332). Significantly higher MT, Zn, and Cu values were observed in the females aged 15–19 yr and, in the age group of 50–54 yr, only in the Zn and Cu values, when compared with those in males. Significant positive correlations of MT vs Zn and Cu as well as correlations of Zn vs Cu levels were observed in both genders. The present findings confirm the proposed role of MT as a biomonitor of mineral status.     

Zinc deficiency decreases plasma erythropoietin concentration in rats

In 1985, Paterson and Bettger found hypoplastic hematopoiesis in severely zinc-deficient rats. Therefore, we investigated plasma erythropoietin concentration in zinc-deficient rats. Forty 4-wk-old male Sprague-Dawley rats were assigned into 4 dietary treatment groups of 10 for the 4-wk study: zinc-deficient group (4.5 mg zinc and 35 mg iron/kg; −Zn), iron-deficient group (30 mg zinc/kg, no supplemental iron; −Fe), zinc/iron-deficient group (4.5 mg zinc/kg, no supplemental iron; −Zn−Fe), and control group (AIN-93G; Cont). Water intake determined at d 19 was similar among all treatment groups. At d 27–28, bioimpedance was measured. The intracellular water/extracellular water ratio was significantly increased in the −Zn group (p<0.05). Compared to the Cont, group, the plasma erythropoietin concentration was increased by iron deficiency and decreased by zinc deficiency (p<0.01). Hematocrit was significantly decreased in both the −Fe and −Zn−Fe groups and was significantly increased in the −Zn group (p<0.01). Transferrin saturation in the −Fe and −Zn−Fe groups was significantly lower than the Cont group (p<0.01), and that of the −Zn group was highest among all groups. The low plasma erythropoietin concentration might account for depressed hematopoiesis associated with zinc deficiency.     

Serum and liver zinc,copper, and iron in chicks infected withEimeria acervulina orEimeria tenella

Two-wk-old broiler chicks were inoculated via crop intubation withEimeria acervulina at two doses: 10⁵ or 10⁶ sporulated oocysts/bird or withEimeria tenella at a dose of 10⁵ sporulated oocysts/bird. Serum and liver samples were collected on days 3 and 6 post-inoculation (PI). There were no significant changes in serum or liver zinc, copper, and iron concentrations in any of the infected groups by 3 d PI. However, on d 6, PI serum protein was significantly reduced in all of the infected groups compared to their pair-fed controls. The chicks infected withE. tennella had significantly reduced serum zinc (1.20 vs 1.77 μg/mL) and iron (0.44 vs 1.28 μg/mL) concentrations and significantly elevated serum copper (0.28 vs 0.17 μg/mL) and ceruloplasmin levels (20.33 vs 11.11 μg/mL) compared to their pair-fed counterparts. Those chicks infected withE. acervulina (10⁶ oocysts/bird) exhibited significantly reduced serum iron concentration by 6 days PI (0.90 vs 1.14 μg/mL). Liver zinc was significantly increased in the chicks infected withE. tenella (349 vs 113 μg/g dry liver wt), as was copper (24 vs 19 μg/g), whereas liver iron concentration was significantly reduced (172 vs 243 μg/g) compared to pair-fed controls. At both dose levels, the chicks infected withE. acervulina exhibited a significant reduction in liver iron by 6 d PI. Hepatic cytosol metals generally reflected whole tissue levels. Metallothionein (MT)-bound zinc was significantly elevated in the chicks infected withE. tenella. Iron bound to a high molecular weight, heat-stable protein fraction (presumably cytoplasmic ferritin) was significantly reduced in chicks infected withE. acervulina, as well as those infected withE. tenella. Collectively, the changes in serum zinc, copper, and iron concentrations, as well as the changes in hepatic zinc and MT-zinc concentrations in the chicks infected withE. tenella were similar to changes evoked during an acute phase response to infection. It is possible that a secondary bacterial infection or inflammation stemming from erosion of the lining of the cecum may play a role in the response of trace element metabolism to theE. tenella infection. Mentions of a trademarkr, proprietary product or specific equipment does not consitute a guarantee or warranty by the US Department of Agriculture and does not imply its approval to the exclusion of other products.     

Effects of maternal marginal zinc deficiency on myelin protein profiles in the suckling rat and infant rhesus monkey

In the current study, the effects of marginal Zn deficiency on myelin protein profiles in neonatal rats and rhesus monkeys were investigated. Following mating, rats were fed a Zn-adequate diet,ad libitum (50 μg Zn/g; 50 Zn AL), or a marginal Zn diet (10 μg Zn/g) from day 0 (10 Zn d0) or day 14 (10 Zn d14) of gestation to day 20 postnatal. An additional group of dams was restricted-fed the control diet to the food intake of the 10 Zn d0 group (50 Zn RF). Day 20 pup plasma and liver Zn concentrations in the 10 Zn groups were lower than in the 50 Zn groups. In a parallel experiment, rhesus monkeys were fed a Zn-adequatead libitum diet (100 μg Zn/g) or a marginal Zn diet (4 μg Zn/g diet; MZD) throughout gestation and lactation. Day 30 monkey infant plasma and liver Zn levels were similar in the MZD and control groups. Rat brain and monkey brain cortex weights were similar among the dietary groups. The amount of myelin recovered (mg protein/g brain) from day 20 rat pups from the 10 Zn groups was lower than that recovered from the 50 Zn rat pups. Myelin recovery from the MZD and control monkey infants was similar. When myelin protein profiles were characterized, it was found that the percentages of high-molecular-weight (HMW) proteins and Wolfgram protein were higher, whereas the percentages of small and large basic proteins were lower in myelin from the 10 Zn d0 and 50 Zn RF pups compared to the distribution in the 50 Zn AL rat pups. Results for the 10 Zn d0 and 10 Zn d14 pups were similar for all of the parameters studied. The percentage of HMW proteins was higher and that of basic protein lower in myelin from MZD monkey infants compared to the percentage of these proteins in myelin from controls. Although the interpretation of the rat data is complicated because of the anorexia associated with the Zn deficiency, the observed changes in monkey myelin protein profiles provide strong evidence that maternal Zn deficiency affects myelination in the offspring.     

Development of zinc deficiency in Zn labeled, fully grown rats as a model for adult individuals

The development of zinc deficiency in adults was studied in a metabolism experiment involving 31 adult, female rats labeled homogenously with 65Zn. The animals were fed restricted amounts (8 g/day) of a semisynthetic diet containing either 58 microgram Zn/g (control, n = 7) or 2 microgram Zn/g (Zn deficiency, n = 24). Control animals were sacrificed at day 0 (n = 3) and day 29 (n = 4). Zinc deficient animals were sacrificed at day 1, 2, 4, 7, 11, 16, 22, and 29 (3 animals per group). The development of zinc deficiency comprised 4 phases: (I) Fecal Zn excretion needed several days to adjust to the low level of Zn intake. The high initial Zn loss via feces was counterbalanced mainly by Zn mobilization from the skeleton. (II) During the 2nd week of deficiency Zn mobilization from tissue storage changed transiently to soft tissues (mainly muscle and fat tissue). (III) After the 2nd week the skeleton resumed to mobilize Zn. (IV) At the end of the study the skeleton Zn storage was exhausted and alkaline phosphatase activity indicated severe Zn deficiency. Urinary Zn excretion was too small to contribute quantitatively to changes in Zn metabolism during any phase of Zn deficiency. In conclusion, adults may compensate a deficient Zn supply by mobilizing tissue Zn for several weeks: The skeleton revealed to be the major short-term as well as long-term source of whole body tissue Zn that can be mobilized.     

Effects of interaction between65Zn,cadmium, and copper in rats

Distribution and retention of zinc in the presence of cadmium and copper was studied in rats exposed repeatedly to these metals. The experiment was performed on white rats of the Wistar strain. The animals were divided into four groups/five rats each: 1)⁶⁵ZnCl₂; 2)⁶⁵ZnCl₂+CdCl₂; 3)⁶⁵ZnCl₂+CuCl₂; and 4) control group. Rats were administered sc every other day for two weeks:⁶⁵ZnCl₂−5 mg Zn/kg; CdCl₂−0,3 Cd/kg; and CuCl₂−2 mg Cu/kg. The zinc content was measured in rat tissues by γ-counting. Effect of Cd and Cu on subcellular distribution of zinc in the kidney and liver and on the level of metallothionein were also examined. Whole body retention of zinc under the influence of cadmium was lower than that observed in animals treated with zinc alone. However, copper increased twofold the whole body retention of zinc. Cadmium elevated the accumulation of zinc only in the kidneys nuclear fraction and liver soluble fraction. In the kidneys and liver, copper elevated the accumulation of zinc, in the nuclear, mitochondrial, and soluble fractions. The level of metallothionein-like proteins (MT) in the kidneys after a combined supply of zinc and copper was significantly increased with respect to the group of animals treated with zinc alone. These results indicated complex interactions between cadmium, copper, and zinc that can affect the metabolism of each of the metals.