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PubMed1982

Effect of acute zinc deprivation on plasma zinc and platelet aggregation in adult males.

In view of earlier results obtained with rodents, the present study was designed to investigate the effect of acute zinc deprivation in man on plasma zinc concentration and the response of platelets to aggregating agents. Three adult men consumed a formula diet based largely on soybean protein for 12 to 14 days. During the control period the diet was supplemented with 12 mg zinc per day. Without supplementation the diet supplied approximately 0.5 mg zinc per 3.0 Mcal; it contained 0.7 ppm zinc, and 0.2% phytate. After removal of the zinc supplement plasma zinc dropped rapidly and reached a minimum by the 5th day. There was a wide diurnal variation in plasma zinc concentration in one subject with the overnight fasting value being the highest and decreasing soon after the morning meal. Platelet aggregation in response to ADP and arachidonate was impaired when plasma zinc was 60 micrograms/dl or less and was restored to normal within 19 h of oral zinc supplementation. These results demonstrate that plasma zinc can be rapidly decreased by dietary zinc deprivation and that extracellular zinc plays an important role in platelet aggregation.

Adenosine Diphosphate↗

PubMed1993

Effects of dietary zinc restriction on postprandial changes in plasma zinc.

The principal objective of this study was to determine the effect of a short period of severe dietary zinc restriction on both prebreakfast and postbreakfast plasma zinc concentrations. After an overnight fast, plasma zinc was measured in five normal adults before and at 30-min intervals for 6 h after a standard zinc-free test meal. This test was performed after a week on a zinc-adequate diet and repeated after a week of severe dietary zinc restriction. Postabsorptive premeal plasma zinc did not change after a week of severe dietary zinc restriction but the posttest meal decline was significantly greater and the maximum decline less variable (15-23%). It is concluded that postprandial plasma zinc is more sensitive than prebreakfast plasma zinc to dietary zinc depletion. Recent zinc intake is one factor that determines the magnitude of the postprandial net efflux of zinc from the plasma compartment.

Adolescent↗

PubMed1994

Chronological loss of bone zinc during dietary zinc deprivation in neonatal pigs.

This research was conducted to measure the chronological changes in zinc concentrations of biopsied bone, hair, and plasma samples collected weekly during dietary zinc deprivation. Pigs 1-2 wk of age were fed a basal diet (< 1 microgram Zn/g) during a 1-wk depletion period and then assigned to one of three dietary regimens for 4 wk: a low-zinc diet (4 micrograms Zn/g) fed ad libitum, an adequate-zinc diet (100 micrograms/g) fed ad libitum, and an adequate-zinc diet restricted in intake to allow eight gain comparable with that of the low-zinc group. Bone zinc remained at approximately 120 micrograms/g dry wt for the control groups fed adequate zinc but steadily declined in pigs fed the low-zinc diet, leveling off at approximately 25% of the control values. Plasma and hair zinc concentrations also decreased but at a more rapid rate. Bone zinc is mobilizable in neonatal pigs, and biopsied bone zinc concentration is a reliable index of zinc status.

Aging↗

PubMed1995

Zinc supplementation during lactation: effects on maternal status and milk zinc concentrations.

The effects of a zinc supplement on maternal zinc status and milk zinc concentrations through > or = 7 mo of lactation were examined. Seventy-one lactating women received either a daily 15-mg zinc supplement (ZS, n = 40) or placebo (NZS, n = 31) started by 2 wk postpartum in a double-blind, randomized design. Overall mean zinc intakes were 13.0 +/- 3.4 mg/d for the NZS group and 25.7 +/- 3.9 mg/d (including supplement) for the ZS group. Plasma zinc concentrations of the ZS group were significantly higher than those of the NZS group (P = 0.05). Milk zinc concentrations declined significantly over the course of the study for all subjects but were not affected by zinc supplementation. The mean dietary zinc intake observed in the nonsupplemented group was adequate to maintain normal maternal zinc status and milk zinc concentrations through > or = 7 mo lactation. Similar controlled intervention trials in less well-nourished populations will be required to assess the impact of lower zinc intakes on milk zinc concentrations.

Adult↗

PubMed1998

Suboptimal zinc status in pregnant Malawian women: its association with low intakes of poorly available zinc, frequent reproductive cycling, and malaria.

A study of 152 rural Malawian women aged 23.2+/-5.5 y (x+/-SD) at 24 wk gestation included measurements of biochemical indexes of zinc (plasma and hair), protein (serum albumin), and infection (serum C-reactive protein, white blood cell count, and malaria), and dietary intakes (via three interactive 24-h dietary recalls). Data on health, demographic and socioeconomic status, family characteristics, reproductive history, and anthropometry were also collected. The study revealed a high prevalence of suboptimal zinc status: 36% of the women had low plasma and 46% had low hair zinc values. Median daily intake of zinc (9.0 mg) was low and poorly available: 61% was provided by cereals and 20% by flesh foods. Median intake of animal protein was only 5.6 g/d, and phytate intakes were high (1.4 g/d). Women consuming diets with phytate-zinc ratios > 17 (the median) had lower hair zinc concentrations (1.6 compared with 1.8 micromol/g, P < 0.03), were older (24 compared with 20 y, P < 0.02), and had a higher number of pregnancies (3 compared with 2, P < 0.02) than those consuming diets with a phytate-zinc ratio < 17. Frequent reproductive cycling was related to zinc status; hair zinc was higher for a prima- than for a multigravida (2.0 compared with 1.6 micromol/g, P < 0.01). Malaria prevalence was also associated with hair zinc (P < 0.05) but not with plasma zinc, after the number of pregnancies was controlled for. We conclude that low intakes of poorly available dietary zinc, frequent reproductive cycling, and malaria prevalence are three major factors in the etiology of suboptimal zinc status in these rural, pregnant Malawian women.

Adolescent↗

PubMed1998

Evaluation of zinc metabolism with use of stable-isotope techniques: implications for the assessment of zinc status.

Zinc stable isotopes can be applied to the identification of populations at risk for zinc deficiency and to monitoring the effects of zinc intervention studies designed to improve zinc nutriture. Techniques using these isotopes can provide information on how effectively the intestine is absorbing exogenous dietary zinc and conserving endogenous zinc. They can also yield estimates of the quantity of readily exchangeable zinc in the body. Data derived from stable-isotope studies can provide extensive information on zinc status and the bioavailability of dietary zinc, allowing researchers to relate zinc intake to physiologic and pathologic conditions. Application of these techniques in longitudinal studies can provide quantitative data on the effectiveness of prevention programs such as simple community measures aimed at reducing dietary phytate and zinc fortification and supplementation programs. Further, judicious application of zinc stable-isotope techniques could make an important contribution to progress toward the eradication of zinc deficiency in infants and young children in the developing world.

Animals↗

PubMed1979

Effect of glucocorticoids and zinc deficiency on femur and liver zinc in rats.

Male weanling rats were fed diets containing less than 1, 3, 6 oor 13 ppm zinc or stock rat diet for 3 weeks. Each dietary group was subdivided into a control group and a prednisolone-treated group (5 mg pred/kg body weight). Femur and liver zinc contents were determined by flame atomic absorption spectrophotometry. Prednisolone caused growth retardation at all levels of dietary zinc. A marked increase was seen in femur zinc content of prednisolone-treated rats fed zinc-deficient diets. No such increase was seen in rats fed diets adequate in zinc. No significant change was seen in liver zinc content of zinc-deficient rats due to prednisolone. By comparing femur zinc in rats fed zinc-deficient diets with femur zinc in weanling rats, it appears that prednisolone causes an increase in femur zinc in rats fed deficient diets by (a) preventing bone resorption, and (b) increasing femur uptake of dietary zinc. Because the effects of glucocorticoids in rats appear to differ from effects in man, similar studies in other species are recommended.

Animals↗

PubMed1982

Zinc utilization in pregnant and nonpregnant women fed controlled diets providing the zinc RDA.

Eight pregnant (P) women in their third trimester and 10 nonpregnant (NP) women participated in a 21-day confined metabolic study. The participants were fed semipurified liquid diets providing 20 mg zinc/day. Apparent zinc balance was calculated and parameters of zinc status assessed. Even though an adequate amount of a readily available form of zinc was fed, the P women consistently maintained lower mean serum zinc concentrations than the NP controls (69 micrograms/dl vs. 97 micrograms/dl). Although the dietary zinc intake was constant throughout the study, most subjects' salivary zinc levels varied greatly. In this study, salivary zinc concentrations was not a sensitive indicator of zinc intake. There were no differences in the concentrations of zinc in hair between the P and NP groups; mean values ranged from 180--220 ppm. In both groups, approximately 95% of the measured zinc output was lost in the feces and only 5% excreted in the urine. The P women tended to excrete more zinc in their urine than the NP women (900 micrograms/day vs. 650 micrograms/day), but they excreted less zinc in their feces. The P women demonstrated a greater apparent zinc retention than the NP women (1.9 +/- 0.6 vs. 0.9 +/- 0.5 mg/day). This difference, however, was not statistically significant (P greater than 0.05).

Absorption↗

PubMed1983

Severe zinc deficiency: effects on the distribution of nine elements (potassium, phosphorus, sodium, magnesium, calcium, iron, zinc, copper and manganese) in regions of the rat brain.

The effect of severe zinc deficiency on the distribution of nine elements (potassium, phosphorus, sodium, magnesium, calcium, iron, zinc, copper and manganese) in brain regions (olfactory lobes, right and left hippocampi, cerebellum and the rest of the brain) has been studied. After male rats (30 days old) were fed a zinc-deficient diet for 28 days, the zinc concentration of most brain parts was similar to zinc-adequate control values. Olfactory lobe zinc, on the other hand, was slightly depressed. However, the levels of other metals were dependent on zinc nutriture. Zinc deficiency caused an elevation in copper concentrations in most brain parts. Restriction of food intake caused a similar increase in brain copper but generally the effect was less than with zinc deficiency. Levels of calcium, manganese, sodium and potassium, in certain brain regions, also appeared to be altered by the zinc status of an animal. Of the minerals examined, only zinc and copper displayed asymmetrical distribution between the right and left hippocampus, and severe zinc deficiency did not affect lateral distribution of these trace metals in the hippocampus. The data suggest the hypothesis that changes in brain metal content, associated with zinc deficiency, contribute to the behavioral abnormalities that occur.

Animals↗

PubMed1984

Absorption, distribution and endogenous excretion of zinc by rats fed various dietary levels of inorganic tin and zinc.

Three studies were designed to determine the effects of various levels of tin (less than 1, approximately 100, approximately 200, approximately 500 and approximately 2000 micrograms tin/g diet) and zinc (approximately 15, approximately 30, approximately 52 micrograms zinc/g diet) on the metabolism of zinc by growing rats. Retention of zinc in tibia, kidney, liver and plasma was decreased significantly when rats consumed greater than or equal to 500 micrograms tin/g diet. Tibia zinc levels were also sensitive to lower levels of dietary tin, i.e., even 100 micrograms tin/g diet when rats were fed 51.8 micrograms zinc/g diet. Apparent absorption of zinc was significantly less when rats were fed approximately 200 or approximately 500 micrograms tin/g diet rather than a control diet containing 15.8 micrograms zinc/g diet and significantly less when rats were fed approximately 500 micrograms tin/g diet rather than approximately 200 micrograms tin/g diet with 29.7 micrograms zinc/g diet. The effect of dietary tin on fecal excretion of endogenous zinc and true absorption of zinc seemed to be dependent on the dose. Rats fed approximately 2000 micrograms tin/g diet lost significantly more zinc of endogenous origin in the feces than control animals. A significant decrease in true absorption of zinc was observed among those rats fed approximately 500 micrograms tin/g diet with 29.7 micrograms zinc/g diet. Increased consumption of zinc resulted in decreased apparent absorption of zinc, increased losses of endogenous zinc in the feces, and decreased true absorption of zinc.

Animals↗

PubMed1986

Zinc-vitamin A interaction in pregnant and fetal rats: supplemental vitamin A does not prevent zinc-deficiency-induced teratogenesis.

The influence of a higher-than-normal intake of vitamin A on the detrimental effects of zinc deficiency on vitamin A metabolism was investigated in pregnant Sprague-Dawley rats. At mating, rats were fed diets containing 100 (control), 4.5, or 0.5 micrograms/g zinc combined with 4 (control) or 8 micrograms retinyl acetate/g. Low intake of zinc, but not of vitamin A, caused food intake, total body weight change, fetal weight and placental weight to be low. Incidence of teratogenic effects was more pronounced in low zinc groups than in controls. Concentrations of vitamin A in maternal plasma and liver were affected by the amount of zinc in the diet. Dietary vitamin A, however, did not affect either of these parameters. Maternal plasma zinc concentration was affected only by low dietary zinc, whereas plasma copper and iron were unaffected by the dietary treatments. Maternal liver iron was higher in zinc-deficient rats than in controls; however, maternal liver zinc and copper concentrations were not altered by dietary treatments. No significant differences in vitamin A concentration of fetal liver, fetal plasma, or placenta were seen among the groups. Fetuses from zinc-deficient dams had significantly lower levels of liver vitamin A and liver zinc than did controls. Fetal liver iron was higher in zinc-deficient fetuses than in controls, whereas fetal liver copper was not affected by dietary treatment. These data suggest that supplemental dietary vitamin A does not ameliorate the effect of zinc deficiency on vitamin A metabolism during pregnancy.

Animals↗

PubMed1987

The effect of varying dietary zinc levels on the concentration and localization of zinc in rat bile-pancreatic fluid.

To determine if zinc homeostasis occurs by zinc output from bile-pancreatic secretions, the bile-pancreatic duct and intestine of rats were surgically cannulated, and bile-pancreatic fluid was collected 2 h/d from the day of surgery to 8 d after surgery. The rats were fed diets containing 10, 100 or 1000 micrograms Zn/g diet before and after surgery. The effect of surgery itself was significant; food intake was initially lower than presurgery levels, but returned to presurgery levels by d 5. Protein and zinc concentrations, and carboxypeptidase A (CpA) and carboxypeptidase B (CpB) activities in bile-pancreatic fluid increased after surgery and leveled off at approximately d 6. Among the dietary zinc groups, the concentration of zinc in bile-pancreatic fluid varied significantly, whereas concentrations of calcium and copper did not. Zinc concentration in bile-pancreatic fluid for d 1-8 postsurgery averaged 1.8, 3.2 and 4.4 micrograms Zn/g, in the groups fed 10, 100 and 1000 micrograms Zn/g diet, respectively. Because the percent of zinc ingested that was secreted in bile-pancreatic fluid, estimated to be 57, 9.5 and 1.2% for the groups consuming the diets containing 10, 100 and 1000 micrograms Zn/g diet respectively, was not similar in the three groups, the quantity of zinc in bile-pancreatic fluid is not proportionally related to the amount of zinc ingested. Our results therefore suggest that zinc secretion in bile-pancreatic fluid does not play a major role in zinc homeostasis. Molecular localization of zinc in bile-pancreatic fluid and measurement of activity of CpA and CpB indicated that zinc in bile-pancreatic fluid is associated primarily with these digestive enzymes.

Animals↗

PubMed1989

Effect of zinc deficiency and food restriction in rats on erythrocyte membrane zinc, phospholipid and protein content.

Zinc deficiency in rats increases the osmotic fragility of erythrocytes, suggesting a structural defect in the plasma membrane. The purpose of this study was to determine the effect of zinc deficiency on membrane components that might be responsible for the increased fragility. Immature male rats were fed for 3 wk a zinc-deficient (0.5 mg Zn/kg) or a control (100 mg Zn/kg) diet either ad libitum or pair-fed. Red blood cell membranes were analyzed for zinc after wet ashing in nitric-perchloric acid. The fatty acid composition of membrane phosphatidylcholine and phosphatidylethanolamine was determined by gas-liquid chromatography, and the protein composition was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The membrane zinc concentration was decreased by zinc deficiency, but returned to control levels upon repletion with a zinc-adequate diet for 3 d. The increased osmotic fragility was also restored to the control level during the same repletion period, suggesting that zinc is an important determinant of membrane stability. The phospholipid fatty acid composition was altered by zinc deficiency, but these changes were not rapidly reversed by repletion. The membrane cholesterol:phospholipid ratio was also increased by zinc deficiency. Zinc status had no influence on the membrane protein profiles of the components visualized by staining. Only the concentration of membrane zinc correlated with osmotic fragility during zinc depletion and repletion.

Analysis of Variance↗

PubMed1992

Nuclear zinc uptake and interactions and metallothionein gene expression are influenced by dietary zinc in rats.

Regulation of metallothionein gene expression by dietary zinc and the relationship of dietary zinc to nuclear zinc uptake was examined in growing rats. Zinc was fed at 5, 30 or 180 mg/kg, either in pelleted form for a 2-wk period (ad libitum) or for 2 h as a liquefied preparation (1 g in 4 mL). Two hours after the oral dose, the intestine and liver took up more zinc than other tissues. Nuclei purified from liver, kidney and spleen accumulated substantial amounts of zinc and directly reflected the dietary zinc level within the 2-h feeding period. Nuclei from kidney accumulated the largest amount of dietary zinc within 2 h, accounting for up to 6.2% of the total nuclear zinc concentration. Northern analysis demonstrated that metallothionein expression was proportional to dietary zinc intake in some tissues. It was greatest in kidney, followed in descending order by liver, intestine, spleen and heart. Thymus and lung metallothionein mRNA levels were not changed appreciably by dietary zinc intake. Chromatography of extracts from liver nuclei shows that 65Zn introduced into the portal supply is bound to discrete fractions of nuclear proteins. One of these fractions binds both 65Zn and a 32P-labeled oligonucleotide corresponding to the metal regulatory element of the metallothionein promoter. These results demonstrate that significant amounts of zinc from the diet are rapidly taken up by cell nuclei. Furthermore, they suggest that transcriptional regulation of the metallothionein gene and other genes with metal regulatory elements involves a direct interaction between the dietary supply and intranuclear factors that bind zinc.

Animals↗

PubMed2001

Differential regulation of zinc transporter 1, 2, and 4 mRNA expression by dietary zinc in rats.

Zinc metabolism is well regulated over a wide range of dietary intakes to help maintain cellular zinc-dependent functions. Expression of transporter molecules, which influence zinc influx and efflux across the plasma and intracellular membranes, contributes to this regulation. We have examined in rats the comparative response of zinc transporters 1, 2, and 4 (ZnT-1, ZnT-2 and ZnT-4) to dietary zinc. ZnT-1 and ZnT-4 are expressed ubiquitously, whereas ZnT-2 is limited to small intestine, kidney, placenta and, in some cases, the liver. When zinc intake was low (<1 mg Zn/kg), ZnT-2 mRNA was extremely low in small intestine and kidney compared with an adequate intake (30 mg Zn/kg). ZnT-1 and ZnT-2 mRNAs were markedly greater in both tissues when a supplemental zinc intake (180 mg Zn/kg) was provided. ZnT-4 was refractory to changes in zinc intake. When zinc was provided as a single oral dose (70 mg/kg body), ZnT-1 and ZnT-2 mRNA levels were increased many fold in small intestine, liver and kidney, whereas ZnT-4 gene expression was not changed. The expression of ZnT-1 and ZnT-2 is comparable to zinc-induced changes in metallothionein mRNA levels, suggesting a similar mode of regulation for these genes. The relative differential in regulation by zinc is ZnT-2 > ZnT-1 > ZnT-4. These data provide evidence that, in an animal model, zinc transporter expression is responsive to zinc under physiologically relevant conditions.

Administration, Oral↗

PubMed2003

Pancreatic metallothionein-I may play a role in zinc homeostasis during maternal dietary zinc deficiency in mice.

Herein, the function of pancreatic metallothionein (MT)-I during zinc deficiency in pregnancy was examined using transgenic mice, which constitutively express the mouse MT-I gene driven by the rat elastase I promoter. Pancreatic MT protein levels and zinc levels were elevated significantly in the transgenic mice compared with those in control mice. Pregnant transgenic and control mice were fed zinc-deficient (1 micro g/g beginning at d 8) or zinc-adequate (50 micro g/g) diets during pregnancy, and the effects on the morphology of embryos were determined at d 14 of pregnancy (d 1 = vaginal plug). As other indicators of zinc deficiency, maternal pancreatic MT levels, as well as the expression of zinc-regulated genes in the embryonic visceral yolk sac were examined. Under these experimental conditions of moderate dietary zinc deficiency, 21.3% of the embryos in control mice exhibited morphological defects, whereas only 5.8% of the embryos in the elastase-MT-I transgenic females had developed abnormally by d 14. Surprisingly, dietary zinc deficiency caused a >95% decrease in pancreatic MT protein concentration in these transgenic mice. This suggests the post-transcriptional control of MT protein levels during zinc deficiency because the rat elastase I promoter is not metal-regulated. The decrease in pancreatic MT protein levels was paralleled by a dramatic decrease in the relative abundance of MT-I mRNA and a dramatic increase in the relative abundance of the zinc/iron regulated transporter-related zinc transporter-4 (ZIP4) mRNA in the embryonic visceral yolk sac. Thus, the constitutive overexpression of pancreatic MT-I in these mice attenuated, but did not prevent the effects of maternal or embryonic zinc deficiency under these conditions. Overall, these findings are consistent with the hypothesis that mouse pancreatic MT-I may participate in providing a labile pool of maternal zinc for the developing embryo during periods of zinc deficiency.

Animals↗

PubMed1980

Hyperaccumulation of zinc by zinc-depleted Candida utilis grown in chemostat culture.

The steady-state levels of zinc in Candida utilis yeast grown in continuous culture under conditions of zinc limitations are <1nmol Zn2+/mg dry weight of cells. Unlike carbon-limited cells, zinc-depleted cells from a zinc-limited chemostat possess the capacity to accumulate and store zinc at levels far in excess of the steady-state level of 4 nmol/mg dry biomass observed in carbon-limited chemostat cultures. Zinc uptake is energy-dependent and apparently undirectional since accumulated 65Zn neither exists from preloaded cells nor exchanges with cold Zn2+. The transport system exhibits a high affinity for Zn2+ (Km =.36micrM) with a Vmaxof 2.2 nmol per minute per milligram dry weight of cells. Growth during the period of the uptake assay is responsible for the apparent plateau level of 35 nmol Zn2+/mg dry weight of cells achieved after 20-30 min in the presence of 65Zn at pH 4.5 and 30 degrees C. Inhibition of growth during the uptake assay by cycloheximide results in a biphasic linear pattern of zinc accumulation where the cellular zinc is about 60 nmol/mg dry weight after 1 h. The enhanced level of accumulated zinc is not inhibtory to growth. Zinc-depleted C. utilis contains elevated amounts of polyphosphate and this anionic evidence does not allow discrimination between possible regulation of zinc homestasis either by inhibitions of zinc efflux through control of the membrane carrier or by control of the synthesis of a cytoplasmic zinc-sequestering macromolecule.

Biological Transport, Active↗

PubMed1978

Urinary zinc excretion following infusions of zinc sulfate, cysteine, histidine, or glycine.

Zinc sulfate (40 mg elemental zinc) or one of three amino acids (5 or 10 g cysteine, 10 g histidine, or 10 g glycine) was infused into anesthetized dogs over a 60-min period. Plasma concentrations and urine excretions of zinc and five other cations, and glomerular filtration rates were determined before, during, and after these infusions. Infusions of zinc sufficient to produce a 20-fold increase in total plasma zinc concentrations had little effect on urinary zinc excretions (threefold increase) or plasma ultrafilterable zinc concentrations. Ten grams of cysteine urinary zinc excretions more than 100-fold, 5 g of cysteine increased zinc excretions more than 30-fold, 10 g of histidine increased zinc excretions sixfold, and 10 g of glycine had no effect. Cysteine infusions appeared to produce a net tubular secretion of zinc. Only histidine appeared to increase serum ultrafilterable zinc concentrations significantly. It would appear that plasma and urine concentrations of certain amino acids, specifically cysteine and histidine, along with polypeptides and other metabolites containing these amino acids, may be major determinants of urinary zinc excretion.

Animals↗