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PubMed1992

Smoking alters the relationship between maternal zinc intake and biochemical indices of fetal zinc status.

Maternal smoking impairs fetal zinc status. This study was designed to clarify the effect of smoking on the relationship between maternal zinc intake and zinc status in mother and fetus. Zinc was measured with atomic-absorption spectroscopy. Statistical analyses consisted of descriptive statistics, simple correlations, and stepwise multiple regression. The results suggest that maternal plasma zinc, red blood cell zinc, and alkaline phosphatase at term are not related to maternal zinc intake. In the nonsmoking parturient both cord-vein plasma zinc and cord-vein alkaline phosphatase activity are positively related to maternal zinc intake. In the smoking parturient there is no relationship between maternal zinc intake and fetal zinc status except for a negative relation with cord-vein plasma zinc. Relations between maternal zinc intake and placental zinc can be shown with stepwise-multiple-regression techniques. The data suggests that maternal zinc intake is related not to maternal zinc status but to fetal zinc status in a normal pregnancy. The relation is altered in the pregnancy complicated by smoking.

Alkaline Phosphatase↗

PubMed2002

Zinc homeostasis during lactation in a population with a low zinc intake.

BACKGROUND: There is a major increase in endogenous zinc excretion, specifically via the mammary gland, in early human lactation. Whereas fractional absorption of dietary zinc has been reported to increase in early human lactation, it is not known to what extent adaptive mechanisms may maintain zinc homeostasis, especially when dietary zinc intake is relatively low. OBJECTIVE: The objective of this study was to quantitate major variables of zinc homeostasis during early lactation in subjects from a population whose habitual dietary zinc intake is low. DESIGN: We studied 18 free-living lactating women from a rural community of northeast China whose infants were exclusively breast-fed. The subjects were studied at approximately 2 mo of lactation with use of stable isotopes of zinc and metabolic collection techniques. Milk volume was measured with use of a deuterium enrichment method. RESULTS: The mean (+/-SD) secretion of zinc in milk was 2.01 +/- 0.97 mg/d, the intake of zinc was 7.64 +/- 1.61 mg/d, and the fractional absorption of zinc was 0.53 +/- 0.09, for a total daily zinc absorption of 4.00 +/- 0.71 mg/d. Endogenous zinc excretion in urine and feces was 0.30 +/- 0.10 and 1.66 +/- 0.97 mg/d, respectively. CONCLUSIONS: Zinc balance, including zinc secreted in breast milk, was maintained at approximately 2 mo of lactation in women whose habitual diet was low in zinc. Homeostasis was achieved by high fractional absorption of zinc and intestinal conservation of endogenous fecal zinc.

Adult↗

PubMed1991

Maintenance of zinc-dependent hepatic functions in rat hepatocytes cultured in medium without added zinc.

Hepatocytes were cultured with Waymouth's media containing zinc at concentrations of 1 (the endogenous zinc concentration of basal medium), 16 and 48 mumols Zn/L to examine the effects of extracellular zinc on a variety of zinc-related functions. The zinc concentrations were chosen with the intention of simulating zinc-deficient, adequate and excess extracellular conditions. Basal medium had no effect on cell zinc, metallothionein (MT) or MTmRNA for up to 48 h but reduced delta-aminolevulinic acid dehydratase (delta-ALA-D) activity to 75% of the initial level by 3 h. The addition of zinc at 16 or 48 mumols Zn/L during the initial 3 h of culture did not prevent the decrease in delta-ALA-D activity. Reintroducing zinc at concentrations of 16 or 48 mumols Zn/L to hepatocytes after the initial 3 h of culture in basal medium significantly increased cell zinc, MT and MTmRNA levels and fully restored delta-ALA-D activity by 24 h. Medium zinc had no apparent effect on membrane integrity assessed as leakage of lactate dehydrogenase activity into culture media or de novo protein synthesis as examined by two-dimensional gel electrophoresis of 35S-labeled proteins. Hepatocytes cultured in basal medium resisted losses in cell zinc concentration even when EDTA and bovine serum albumin were present in culture medium. Kinetic experiments using 65Zn suggest hepatocytes maintain zinc concentrations by reducing zinc efflux. The ability of hepatocytes cultured in basal (1 mumol Zn/L) medium to maintain cell zinc content and some zinc-dependent functions underscores the difficulty of producing zinc deficiency in primary hepatocyte culture.

Actins↗

PubMed2004

The release of zinc ions from and cytocompatibility of two zinc oxide dressings.

OBJECTIVE: These in vitro studies examined the release of zinc ions from and the response of human dermal fibroblasts to two zinc oxide-medicated dressings: one with zinc oxide in an ointment base and one using polyvinylpyrrolidone (PVP), a hydrophilic polymer for the binding of zinc oxide particles. METHOD: Zinc release from the dressings in buffered-saline (pH 7.4) was studied through a high-pore-density membrane (pore size, 0.40 microm) in a two-compartment model at 37 degrees C for three hours. Cytocompatibility of the dressings and 500 micromol/l of zinc ions was assessed using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay after exposure to monolayers of confluent normal human dermal fibroblasts to the dressing extracts for four hours. RESULTS: The zinc release rate from PVP-bound zinc oxide was more than two-fold higher than from zinc oxide in the ointment. Extract of the zinc oxide ointment, containing 150 micromol/l solubilised zinc, elicited a cytotoxic reaction, while the zinc oxide-PVP extract, containing 410 micromol/l solubilised zinc, and 500 micromol/l zinc chloride were non-cytotoxic to the fibroblasts. CONCLUSION: Zinc release in a simulated wound milieu appears to be inhibited when zinc oxide is incorporated in a lipophilic vehicle. It is hypothesised that the ointment vehicle induced cytotoxicity rather then the solubilised zinc oxide. DECLARATION OF INTEREST: None.

Administration, Cutaneous↗

PubMed1976

Zinc metabolism and homeostasis in rats fed a wide range of high dietary zinc levels.

Zinc metabolism and homeostasis were studied in young growing rats fed a 38 ppm zinc diet with added zinc levels ranging from 0 to 8400 ppm for 21 days. High dietary zinc did not cause toxicity symptoms. Stable zinc in feces increased linearly with dietary zinc intake but fecal 65Zn, from a single oral dose, did not increase above the 1200 ppm dietary level. Stable zinc in liver, kidney, and tibia increased two to three times with 2400 ppm added zinc, but was not further elevated until 8400 ppm was fed. Stable zinc in muscle and heart was not affected appreciably by dietary zinc level. In all tissues, 65Zn retention was drastically reduced with 1200 ppm added dietary zinc. Additional dietary zinc reduced 65Zn in muscle and heart but had little effect on liver and kidney 65Zn. The data indicate that rats have fairly effective homeostatic control mechanisms for tissue zinc below about 7200 ppm dietary zinc. Whereas, with dietary zinc up to about 1200 ppm, decreasing absorption is the main route of homeostatic control, above this level, more rapid zinc turnover rates and increasing endogenous zinc excretion appear to have major importance.

Animals↗

PubMed1985

[Zinc concentrations and total amount of zinc in seminal plasma of infertile men with special reference to prostatic secretory function].

The exact relationship between seminal plasma zinc and fertility is not known. Zinc is secreted mainly by the prostate, and zinc concentration in seminal plasma is regarded as an excellent indicator of prostatic secretory function. However, low zinc concentration may result not only from poor secretory function of the prostate but also from dilution due to excessive secretion of seminal vesicular fluid. This assumption is supported by the present result that zinc concentration was inversely correlated with fructose concentration. Therefore zinc concentration is thought to reflect prostatic function in proportion to seminal vesicular function. Total amount of zinc in seminal plasma seems to be an appropriate indicator for prostatic secretory function. In the present study, concentrations and total amount of zinc were examined in seminal plasma of men with various fertility problems. There were no significant differences between men with normal spermodiagram and those with abnormal spermodiagram, seminal inflammation or varicocele in concentration or total amount of zinc. No changes were observed in any of them after various therapies including oral zinc sulfate. However, the percentage of men with normal spermodiagram was low in the group with extremely low or high zinc concentration and total sperm count tended to increase with increase in total amount of zinc. Furthermore, the spermatozoal motility was better in the prostatic fraction than in the vesicular fraction of split ejaculates, and the percentage of men with decreased motility and normal sperm concentration was significantly high in the group with lower zinc concentration or decreased total amount of zinc. These observations indicate that prostatic secretion has a stimulatory effect on spermatozoal motility. The secretory activities of the prostate and the seminal vesicle are generally known to be closely controlled by androgens, but our findings indicate that the secretory functions of these accessory organs are independent because there was no correlation between total amount of zinc and fructose. Analysis of the relative concentrations in prostatic secretion, split ejaculates, and seminal plasma confirmed an almost exclusively prostatic origin of zinc. As part of the routine andrologic examination, measurement of concentration and total amount of zinc in seminal plasma is useful for evaluating prostatic function, but measurement of acid phosphatase, magnesium, calcium or potassium will provide almost as much information, since they also seem to be secreted primarily by the prostate.

Adult↗

PubMedDate not supplied

Zinc metabolism and homeostasis: the application of tracer techniques to human zinc physiology.

Tracer kinetic techniques based on zinc stable isotopes have a vital role in advancing knowledge of human zinc physiology and homeostasis. These techniques have demonstrated the complexity of zinc metabolism, and have been critical to estimating the size and interrelationships of those pools of zinc that exchange rapidly with zinc in plasma and which are likely to be especially important for zinc dependent biology. This paper presents findings from recent research linking a steady state compartmental model with non-steady state post-prandial sampling from the intestine, utilizing a combination of intestinal intubation/perfusion and stable isotope tracer kinetic techniques. The gastrointestinal tract has a central role in maintaining whole body zinc homeostasis. While the fractional absorption of zinc from a meal depends on the quantity of exogenous zinc and on such dietary factors as phytic acid, the fractional absorption does not appear to be dependent on the size of the rapidly exchanging pool of the host. In contrast, the quantity of endogenous zinc excreted via the intestine is positively correlated with both the amount of absorbed zinc and the zinc 'status' of the host, and thus this process has an equally critical role in maintaining zinc homeostasis. The observed alterations in zinc metabolism in some disease states can be understood in the context of known homeostatic processes. In other conditions, however, such alterations as inflammation-associated hyperzincuria and zinc redistribution, the links between homeostatic perturbation and cellular biology are yet to be explained. Thus the challenge remains for research at the whole body level to carefully characterize zinc distribution and exchange under diverse circumstances, while research at the cellular level must elucidate the regulatory processes and the factors to which they respond.

Digestive System↗

PubMed1981

Studies on the bioavailability of zinc in humans: effects of heme and nonheme iron on the absorption of zinc.

The change in the concentration of plasma zinc after oral administration of zinc was used as the index of zinc absorption in the study of the interaction of zinc and iron in the human intestine. With zinc sulfate as the source of inorganic zinc, and ferrous sulfate as the source of nonheme iron, a ratio of Fe/Zn of 1:1 slightly inhibited zinc absorption while Fe/Zn ratio of 2:1 and 3:1 substantially inhibited zinc uptake. No effect on zinc absorption was observed, however, when heme iron, as heme chloride, was ingested in a 3:1 Fe/Zn ratio with inorganic zinc. Atlantic oysters providing about 54 mg of zinc were consumed with or without 100 mg of ferrous iron; Fe/Zn ratio was 2:1. With this "organic" form of zinc, iron did not significantly affect zinc absorption. The evidence for competitive interaction of zinc and iron was strongest with nonheme iron and inorganic zinc. Thus, the possibility that intrinsic iron in formulas for feeding infants and in vitamin-mineral supplement might inhibit the absorption of zinc justifies concern about the Fe/Zn ratio in the formulation of these products.

Adult↗

PubMed1981

Effect of phytate:zinc molar ratio and isolated soybean protein on zinc bioavailability.

The effect of phytate to zinc (Zn) molar ratio on zinc bioavailability was evaluated in rats. The bioavailability was determined by giving an oral dose of 65Zn and measuring the liver uptake and disappearance from the gastrointestinal tract after 4 hours and fecal and urinary 65Zn excretion from 24 to 168 hours. Rats were fed a diet containing 12 ppm zinc from zinc sulfate with and without phytic acid from sodium phytate for 14 days. At the end of 14 days feeding, the rats were intubated with a homogenized diet containing 12 ppm zinc, one microCi 65Zn and graded levels of phytic acid so that the phytate:Zn molar ratio varied from 0 to 100. Zinc bioavailability was significantly reduced only in the rats fed diets containing phytate and intubated diet containing phytate:zinc molar ratio of 12.5 and above. The results from this study also indicated that measuring 65Zn disappearance and uptake was a valid bioassay for determining zinc bioavailability. The effect of isolated soybean protein on extrinsic zinc bioavailability was also evaluated in rats fed zinc adequate and zinc deficient diets. The results showed that zinc bioavailability was significantly reduced by replacing egg white protein with isolated soybean protein only when the rats were fed zinc deficient diet prior to single oral dose of 65Zn mixed with test proteins. The effect of isolated soybean protein on intrinsic zinc bioavailability for the growing rats was also evaluated. The results demonstrated that the zinc bioavailability in isolated soybean protein can be improved by fortifying with zinc so that the phytate:Zn molar ratio is less than 10.

Animals↗

PubMed2005

Determination of relative bioavailability of zinc in a petit suisse cheese using weight gain and bone zinc content in rats as markers.

The aim of the study was to determine the relative bioavailability of zinc gluconate stabilized with glycine in a Petit Suisse cheese from an infant dessert. Weight gain and bone zinc content were the nutritional responses evaluated for the diets of different zinc content: 2 ppm (basal) and 5, 10, and 30 ppm from zinc gluconate stabilized with glycine and zinc sulfate. Nonlinear regression analysis of the fitted curves for weight gain determined a relative zinc bioavailability of 100% for the Y max ratio and 96% for Ymax/t1/2 ratio for zinc gluconate stabilized with glycine (R2=0.7996 for zinc sulfate and 0.8665 for zinc gluconate stabilized with glycine). The slope ratio analysis from linear regression of femur zinc determined a relative zinc bioavailability of 93% for zinc gluconate stabilized with glycine (R 2=0.8693 for zinc sulfate and 0.8307 for zinc gluconate stabilized with glycine). Zinc gluconate stabilized with glycine has similar bioavailability as zinc sulfate in a Petit Suisse cheese nutritional matrix, with the advantage that the stabilized compound does not modify the sensorial characteristics of the fortified cheese.

Animals↗

PubMedDate not supplied

Zinc homeostasis and functions of zinc in the brain.

The brain barrier system, i.e., the blood-brain and blood-cerebrospinal fluid barriers, is important for zinc homeostasis in the brain. Zinc is supplied to the brain via both barriers. A large portion of zinc serves as zinc metalloproteins in neurons and glial cells. Approximately 10% of the total zinc in the brain, probably ionic zinc, exists in the synaptic vesicles, and may serve as an endogenous neuromodulator in synaptic neurotransmission. The turnover of zinc in the brain is much slower than in peripheral tissues such as the liver. However, dietary zinc deprivation affects zinc homeostasis in the brain. Vesicular zinc-enriched regions, e.g., the hippocampus, are responsive to dietary zinc deprivation, which causes brain dysfunctions such as learning impairment and olfactory dysfunction. Olfactory recognition is reversibly disturbed by the chelation of zinc released from amygdalar neuron terminals. On the other hand, the susceptibility to epileptic seizures, which may decrease vesicular zinc, is also enhanced by zinc deficiency. Therefore, zinc homeostasis in the brain is closely related to neuronal activity. Even in adult animals and probably adult humans, adequate zinc supply is important for brain functions and prevention of neurological diseases.

Amygdala↗

PubMed1998

The glutathione redox couple modulates zinc transfer from metallothionein to zinc-depleted sorbitol dehydrogenase.

The release and transfer of zinc from metallothionein (MT) to zinc-depleted sorbitol dehydrogenase (EC 1.1.1.14) in vitro has been used to explore the role of MT in cellular zinc distribution. A 1:1 molar ratio of MT to sorbitol dehydrogenase is required for full reactivation, indicating that only one of the seven zinc atoms of MT is transferred in this process. Reduced glutathione (GSH) and glutathione disulfide (GSSG) are critical modulators of both the rate of zinc transfer and the ultimate number of zinc atoms transferred. GSSG increases the rate of zinc transfer 3-fold, and its concentration is the major determinant for efficient zinc transfer. GSH has a dual function. In the absence of GSSG, it inhibits zinc transfer from MT, indicating that MT is in a latent state under the relatively high cellular concentrations of GSH. In addition, it primes MT for the reaction with GSSG by enhancing the rate of zinc transfer 10-fold and by increasing the number of zinc atoms transferred to four. 65Zn-labeling experiments confirm the release of one zinc from MT in the absence of glutathione and the more effective release of zinc in the presence of GSH and GSSG. In vivo, MT may keep the cellular concentrations of free zinc very low and, acting as a temporary cellular reservoir, release zinc in a process that is dynamically controlled by its interactions with both GSH and GSSG. These results suggest that a change of the redox state of the cell could serve as a driving force and signal for zinc distribution from MT.

Animals↗

PubMed1998

Zinc-induced inactivation of the yeast ZRT1 zinc transporter occurs through endocytosis and vacuolar degradation.

The ZRT1 gene encodes the transporter responsible for high affinity zinc uptake in yeast. ZRT1 is transcribed in zinc-limited cells and its transcription is repressed in zinc-replete cells. In this report, we describe a second, post-translational mechanism that regulates ZRT1 activity. In zinc-limited cells, ZRT1 is a stable, N-glycosylated plasma membrane protein. Exposure to high levels of extracellular zinc triggers a rapid loss of ZRT1 uptake activity. Our results demonstrate that this inactivation occurs through zinc-induced endocytosis of the protein and its subsequent degradation in the vacuole. Mutations that inhibit the internalization step of endocytosis also inhibited zinc-induced ZRT1 inactivation and the major vacuolar proteases were required to degrade ZRT1 in response to zinc. Furthermore, immunofluorescence microscopy showed that ZRT1 is localized to the plasma membrane in zinc-limited cells and that the protein is transferred to the vacuole via an endosome-like compartment upon exposure to zinc. ZRT1 inactivation is a relatively specific response to zinc; cadmium and cobalt ions trigger the response but less effectively than zinc. Moreover, zinc does not alter the stability of several other plasma membrane proteins. Therefore, zinc-induced ZRT1 inactivation is a specific regulatory system to shut off zinc uptake activity in cells exposed to high extracellular zinc levels thereby preventing overaccumulation of this potentially toxic metal.

Carrier Proteins↗

PubMed2000

Zinc transporters that regulate vacuolar zinc storage in Saccharomyces cerevisiae.

All cells regulate their intracellular zinc levels. In yeast, zinc uptake is mediated by Zrt1p and Zrt2p, which belong to the ZIP family of metal transporters. Under zinc limitation, ZRT1 and ZRT2 transcription is induced by the Zap1p transcriptional activator. We describe here a new component of zinc homeostasis, vacuolar zinc storage, that is also regulated by Zap1p. Zinc-replete cells accumulate zinc in the vacuole via the Zrc1p and Cot1p transporters. Our results indicate that another zinc transporter, Zrt3p, mobilizes this stored zinc in zinc-limited cells. ZRT3 is a Zap1p-regulated gene whose transcription increases in low zinc. Zrt3p is also a member of the ZIP family and it localizes to the vacuolar membrane. The effects of ZRT3 mutation and overexpression on cell growth, cellular zinc accumulation and intracellular labile zinc pools are all consistent with its proposed role. Furthermore, we demonstrate that zrt3 mutants inefficiently mobilize stored zinc to offset deficiency. Thus, our studies define a system of zinc influx and efflux transporters in the vacuole that play important roles in zinc homeostasis.

Amino Acid Sequence↗

PubMed1977

Zinc excretion in young women on low zinc intakes and oral contraceptive agents.

Zinc excretion under conditions of negligible zinc intake (0.17 mg/day) was measured in women taking a combination oral contraceptive agent (+OCA) and in women with normal menstrual cycles (-OCA). A semipurified, constant formula diet, providing negligible amounts of zinc, copper and iron, but adequate levels of other essential nutrients, was fed. During the 35--day study, serum and urinary zinc declined more markedly in the +OCA than -OCA groups. Serum zinc dropped 47% in the +OCA and 21% in the -OCA; urinary zinc declined 83% and 62% in the two groups. After pre-study, zinc was cleared from the gut, fecal zinc decreased about 40% in both groups. Whole body integumental zinc losses were similar for both groups, about 0.7 mg/day. For -OCA, zinc losses via this route were higher during the luteal phase than during menstruation. Menstrual fluid zinc contents were negligible and similar for both groups, about 5 microgram/day. The data suggest that accessible zinc stores are not extensive and that depletion of these stores, as a result of the low-zinc diet, caused the fall in serum zinc. The use of OCA influenced the response to the low-zinc diet, but endogenous zinc losses calculated for day 1 were nearly the same for both groups, about 1.6 mg/day.

Adolescent↗

PubMed1978

Plasma whole blood and urine zinc in the assessment of zinc deficiency in the rat.

Serial measurements of plasma, whole blood, and urine zinc have been made in young adult rats fed zinc deficient and zinc supplemented diets for a total period of 65 days. After commencing a zinc deficient diet plasma zinc fell within 48 hours to 25% of control values and remained at this level throughout the period of study. A substantial diurnal variation was observed in plasma zinc, and the level was significantly lower in the fasting state. Whole blood zinc was unaffected by fasting, showed no diurnal variation, and remained at control values even after 65 days of zinc deficient diet. Urine zinc fell to very low values, 10 days after commencing a zinc deficient diet, but after 30 days rose to control values. Under controlled conditions plasma zinc can be used as an indication of zinc deficiency. Whole blood zinc is of no value in the detection of zinc deficiency. Urine zinc concentration varies with time following a zinc deficient diet.

Animals↗

PubMed1981

Effects of dietary zinc levels on zinc concentrations in tissues of common carp.

Common carp always has higher zinc concentration in viscera than other carps. To determine the relationship between the dietary zinc level and zinc concentration in common carp, the fish were fed diets containing 17, 294, 1,007 and 1,974 ppm zinc for 8 weeks, and the zinc concentration in each tissue was measured. It was found that the group of fish fed 17 ppm zinc had the highest growth rate. When the dietary concentration of zinc was lower than 294 ppm, the zinc concentrations in the tissues were similar during the 8 weeks of experiment. The zinc accumulated in the fish when the dietary zinc concentration was higher than 1,007 ppm. Zinc accumulated first in the digestive tract, then in the skeletal tissues and then in skin and muscle. Common carp and silver carp were fed the same diet from hatchling till adult. The results indicated that no matter whether the feed was natural food or artificial feed containing 300 ppm of zinc or artificial feed containing 25 ppm of zinc, the zinc concentrations in common carp were several times higher than silver carp. We concluded that the fact that common carp had higher zinc concentrations than other carps was not caused by the diet, but might arise from the fact that the absorption rate of zinc was higher.

Animals↗

PubMed1985

Zinc utilization in young men fed adequate and low zinc intakes.

Zinc absorption and balances were measured in six young men who were confined while participating in a 75-d metabolic study. A diet of conventional food providing either 16.5 or 5.5 mg Zn/d was fed. Apparent absorption of zinc was calculated from the zinc balance data and from the absorption of a zinc stable isotope added to the diet. The apparent zinc absorption calculated from the isotope data was about 25% when 16.5 mg zinc was fed; it increased to about 53 and 49% after 13 and 42 d, respectively, when 5.5 mg zinc was fed. Total zinc absorption fell from 4.1 mg/d to 2.7-2.9 mg/d during the low zinc period, however. This zinc absorption was sufficient to maintain crude zinc balances in five of the six subjects. Neither serum nor urinary zinc levels changed significantly during the period of feeding low levels of zinc. It appears that zinc absorption readily responds to changes in dietary zinc and that an intake of 5.5 mg Zn/d for about 8 wk does not cause serum or urinary zinc level to fall.

Absorption↗