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PubMed1989

Clinical zinc deficiency during zinc-supplemented formula.

A 2 1/2-month old preterm infant had failure to gain weight with high caloric intake, and had generalized persistent dermatitis and mild diarrhea. The patient was being fed zinc-supplemented cow's-milk-based formula (Osterfeed). High caloric intake of 8 weeks' and topical treatment of 11 weeks' duration were futile. A thorough investigation revealed low serum zinc concentration. Administration of zinc sulfate 150 mg/day resulted in brisk weight gain and complete clearing of skin lesions. The infant maintained normal levels of zinc 4 months after zinc therapy was discontinued, while being fed unmodified cow's milk and a diet of corn flour. The probability that zinc-supplemented formulas do not meet the high zinc requirements of premature infants is raised. The importance of plasma or serum zinc examination in preterm infants with slow growth velocity or failure to gain weight despite adequate caloric intake, with or without skin lesions and diarrhea, is emphasized.

Body Weight↗

PubMed1990

The effect of zinc levels in fetal circulation on zinc clearance across the in situ perfused guinea pig placenta.

Although zinc is essential for normal fetal growth and development, little is known about factors that influence its transfer across the placenta. The in situ perfused guinea pig placenta model was used to study the influence of the zinc concentration of fetal circulation on maternofetal placental zinc transfer. A placenta of the anaesthetized sow was perfused (on the fetal side) with a physiological perfusate via the umbilical vessels, with the fetus excluded. The sow was infused intravenously with 65zinc as a tracer of placental Zn clearance, and with antipyrine as an indirect indicator of maternal placental blood flow. Maternal plasma and placental effluent samples collected at intervals were counted for 65zinc by gamma counter, and the absorbance of nitrosated antipyrine was measured at 350 nm. Varying the mean zinc concentration in the perfusate from 0.176 to 1.87 mg/L had no effect on relative zinc clearance calculated as zinc clearance/antipyrine clearance (mean +/- SEM; 0.085 +/- 0.010 vs. 0.114 +/- 0.018; n = 6; p greater than 0.05). The results suggest that short-term changes in fetal zinc status do not influence placental zinc transfer.

Animals↗

PubMed1992

The effect of zinc chloride dentifrices on plaque growth and oral zinc levels.

The antiplaque potential of zinc salts has been previously demonstrated. The purpose of the present investigation was to establish the effect of zinc chloride dentifrices on plaque growth and on the concentration of zinc in saliva and plaque. Zinc levels in saliva and plaque were measured by atomic absorption spectrophotometry. Elevated zinc levels were observed in saliva and in plaque for 1 hour after contact with a zinc chloride dentifrice. Increased concentrations of zinc were also observed in plaque residue. Further analysis of data showed that subjects with high rates of plaque growth benefited more from the zinc dentifrices than did those with low rates of plaque growth.

Adult↗

PubMed2005

The European Union risk assessment on zinc and zinc compounds: the process and the facts.

A risk assessment on zinc and zinc compouns was carried out withn the framework of Council Regulation 793/93/EEC on Existing Chemicals. This risk assessment basically followed the European Union (EU) technical guidance documents (TGDs). These TGDs are built on the current knowledge on quantitative risk assessments, mainly for organic chemicals. This article describes the tailor-made approach for the zinc risk assessment. This work lasted almost a decade and involved the contributions of all EU member states and industry, who discussed the risk assessment during technical meetings. The risk assessment is initially based on scientific findings but is interrelated with pragmatic considerations. It follows a comprehensive approach, covering both environmental and human health. In the environmental part, new methodologies were developed to deal with the natural background of zinc, essentiality, speciation, and the use of species sensitivity distributions. The major results and the process of drawing conclusions of the risk assessment are outlined: potential environmental risks of zinc and zinc compounds may occur at local and regional scales in surfacewater, sediment, and soil. No potential health risks were identified for consumers and man indirectly exposed via the environment. For workers, potential health risks were identified only for zinc oxide and zinc chloride.

Animals↗

PubMed1991

Effects of zinc methionine and zinc oxide on performance, blood characteristics, and antibody titer response to viral vaccination in stressed feeder calves.

Ninety steers with an average weight of 214 kg were purchased at 2 feeder calf sales and transported 70 to 100 km. On arrival at the feedlot, steers were weighed and identified, blood was withdrawn, and the steers were vaccinated against bovine herpesvirus-1 (BHV-1) and parainfluenza3 (PI3), using a modified live vaccine, and randomly assigned to treatment groups. Treatments were: control (no supplemental zinc; zinc methionine; and zinc oxide. The control diet contained 26 mg of zinc/kg diet, and zinc was added in treatments 2 and 3 to provide 25 mg of supplemental zinc/kg diet. Neutralizing antibody titers were determined on serum samples taken on days 0 and 14 as a measure of the immune response to BHV-1 and PI3 vaccination. Weight gains for the 28-day study were similar across treatments. Dry matter intake tended to be higher in steers fed supplemental zinc from either source, because steers fed zinc methionine and zinc oxide consumed 5.2 and 4.4% more feed, respectively, than controls. Antibody titers against BHV-1 tended to be higher in steers supplemented with zinc methionine on day 14. Differences between treatments were not found for PI3 titers. Mortalities did not occur and morbidity rate was low.

Animals↗

PubMed1987

[Interaction between copper and zinc in sheep parenterally treated with zinc oxide].

Changes in copper and zinc concentrations in the blood serum of sheep were studied in clinical conditions for sixty days in relation to the intramuscular application of zinc oxide at a dose of 10 mg Zn per kg liveweight; zinc oxide was administered in a developmental preparation. Serum concentrations of zinc started increasing significantly the eighth day after administration (p less than 0.01), the maximum values were found out on the twelfth day (21.19 +/- 3.89 mumol X l-1). Significantly higher concentrations of zinc in the blood serum of test sheep were observed as soon as on the eighth day (p less than 0.01), in comparison with the untreated group, and they persisted till the end of investigation (p less than 0.01). Simultaneously with the changes in serum zinc concentrations, copper metabolism was influenced when the statistically higher values of copper concentrations in the blood serum of the test group were recorded the eighth and twelfth days (p less than 0.01), in comparison with the control animals. In the remaining period, serum copper concentrations did not show any mathematical dependence and the equalization to the original values in the treated group occurred at the end of the experiment. The above-mentioned results from the sheep treated with zinc oxide refer to a possibility of influencing mutually the copper and zinc metabolism also parenterally; this could be utilized during the treatment of secondary deficiencies, or toxicosis.

Animals↗

PubMed1987

An epidemiologic study of mortality in veal calves subsequent to an episode of zinc toxicosis on a California veal calf operation using zinc sulfate-supplemented milk replacer.

Ninety-five 3- to 6-month old male Holstein veal calves were evaluated after an episode of zinc toxicosis, to describe clinical signs and to identify management and/or host-related factors that may have contributed to death. Clinical signs appeared 23 days after feeding of milk replacer commenced. Of 85 calves examined, 64 had pneumonia (75.5%), 62 had ocular signs (72.9%), 46 had diarrhea (54.1%), 34 were anorectic (40.0%), 15 were bloated (17.6%), 8 had cardiac arrhythmias (9.4%), 3 had convulsions (3.5%), and 3 were polydipsic/polyphagic (3.5%). Clinical signs began to appear when calves each were being fed approximately 1.5 to 2.0 g of zinc/day and exposed to a cumulative zinc intake of 42 to 70 g, from a milk replacer containing 706 micrograms of elemental zinc/g of milk replacer. Of 95 calves studied, 1 died before zinc was supplemented, 16 died during the episode, 12 were euthanatized, 1 was lost to follow-up evaluation, 1 was culled, and 64 were slaughtered. Deaths attributable to zinc toxicosis were observed between 25 and 53 days after the milk replacer was supplemented with zinc. Calves died while being exposed cumulatively to 30 to 66 g of zinc. The factors of previous pneumonia severity, age, cumulative daily exposure to zinc, and calf location within a bay were examined for possible associations with mortality, using stepwise logistic regression. Though younger calves tended to have a higher mortality than older calves, neither age category nor severity of pneumonia, before zinc supplementation, accounted for a significant mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗

PubMed1980

Comparison of the efficiency of zinc injected as metal or oxide for zinc deficiency treatment in sheep.

Efficiency of zinc injection as metal or oxide suspended in purified oil has been compared with control in three groups of seven ewes (39 kg). The zinc injected as oxide is liberated more rapidly from the injection site and the plasma zinc reachs a higher level than with zinc metal. However the effect of zinc metal injection lasts longer. Plasma copper behaves as an inflammation index. It rises more with zinc oxide injection. Both forms, metal or oxide are well tolerated by sheep without any side effect. Zinc oxide may be injected for more intensive but shorter treatment when zinc metal offers the best delayed effect.

Animals↗

PubMed1989

Role of zinc in regulating the testicular function. Part 1. Effect of dietary zinc deficiency on serum levels of gonadotropins, prolactin and testosterone in male albino rats.

Hypogonadism is a major manifestation of zinc deficiency in both humans and animals. In this study, we try to elucidate the main role of zinc in regulating the testicular function. Ninety male weanling albino rats were divided into three groups: control, zinc-deficient (ZD), and zinc-supplemented (ZS) groups. Six rats from each group were sacrificed every two weeks over a total period of ten weeks. Serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL) and testosterone (T) were estimated by radioimmunoassay technique. Serum zinc concentrations were also determined. Data revealed that serum zinc concentrations were significantly low in ZD group compared to both control and ZS groups. Normal FSH and LH but low PRL and T levels were demonstrated in sera of ZD group compared to both control and ZS groups. We came to the following conclusions: zinc deficiency has no effect on the pituitary gonadotropin output. Zinc deficiency affects the testicular function either directly through its effect on the testicular steroidogenesis and/or indirectly through its effect on the pituitary synthesis and/or secretion of PRL.

Animals↗

PubMedDate not supplied

Treatment of Wilson's disease with zinc. I. Oral zinc therapy regimens.

The standard therapy for preventing copper accumulation in Wilson's disease, D-penicillamine, has been a life-saving drug, but it has many side effects and some patients are completely intolerant. We have been using oral zinc as another approach to the therapy for Wilson's disease, with copper balance studies as the key initial assessment of the adequacy of a given dose or regimen of zinc therapy. We earlier reported that an intensive regimen of zinc (zinc taken every 4 hr) was effective in controlling copper balance. We have now shown with balance studies that a simplified zinc therapy regimen of 50 mg zinc taken 3 times per day is effective in controlling copper balance. Preliminary work presented here with other simplified regimens also indicate their effectiveness. These studies increase the data base, in terms of copper balance, for zinc therapy of Wilson's disease, and expand the dose range and regimens of zinc which have been shown to control copper balance.

Adult↗

PubMed1995

Cloning and functional characterization of a mammalian zinc transporter that confers resistance to zinc.

A cDNA encoding a zinc transporter (ZnT-1) was isolated from a rat kidney cDNA expression library by complementation of a mutated, zinc-sensitive BHK cell line. This cDNA was used to isolate the homologous mouse ZnT-1 gene. The proteins predicted for these transporters contain six membrane-spanning domains, a large intracellular loop and a C-terminal tail. ZnT-1 is homologous to zinc and cobalt resistance genes of yeast. Immunocytochemistry with an antibody to a myc epitope added to the C-terminus of ZnT-1 revealed localization to the plasma membrane. Transformation of normal cells with a mutant ZnT-1 lacking the first membrane-spanning domain conferred zinc sensitivity on wild-type cells, suggesting that ZnT-1 functions as a multimer. Deletion of the first two membrane-spanning domains resulted in a non-functional molecule, whereas deletion of the C-terminal tail produced a toxic phenotype. Mutant cells have a slightly higher steady-state level of intracellular zinc and high basal expression of a zinc-dependent reporter gene compared with normal cells. Mutant cells have a lower turnover of 65Zn compared with normal cells or mutant cells transformed with ZnT-1. We propose that ZnT-1 transports zinc out of cells and that its absence accounts for the increased sensitivity of mutant cells to zinc toxicity.

Amino Acid Sequence↗

PubMedDate not supplied

Zinc and metallothionein levels and expression of zinc transporters in androgen-independent subline of LNCaP cells.

Zinc levels in the prostate have been reported to be associated with the development and progression of malignant prostate cells. To investigate the reason why the zinc content decreases during the progression of prostate cancer to an androgen-independent state, we compared the expression levels of metallothionein and zinc transporters between androgen-responsive LNCaP cells and its androgen-independent subline, AIDL cells. AIDL cells showed lower zinc levels than LNCaP cells and comparable levels of androgen receptor expression to LNCaP cells, consistent with some clinical aspects of androgen-independent prostatic cancer. AIDL cells exhibited a lower expression of zinc transporter 1 (ZnT1) and higher expression of ZnT3 than LNCaP cells. The content of metallothionein, which is a major zinc-binding protein, was significantly lower in AIDL cells than in LNCaP cells. Furthermore, the expression of ZnT3 mRNA was decreased by incubating LNCaP cells in medium containing hormone-stripped fetal calf serum and increased by addition of synthetic androgen R1881 to the medium, whereas the intracellular zinc levels were not affected under these conditions. These findings suggest that factors such as ZnT1 and metallothioneins other than ZnT3 are associated with the low intracellular zinc content in AIDL cells.

Androgens↗

PubMed1985

Metallothionein content and zinc status in various tissues of rats treated with iodoacetic acid and zinc.

Metallothionein (MT) content was determined in 11 tissues of saline-treated rats, and 18 h after single IP injections of iodoacetic acid (IA, 15 and 30 mg/kg) or zinc sulfate (20 mg zinc/kg). Zinc increased MT content in eight tissues, being most effective in pancreas, liver, and small intestine. After IA, MT increased in liver, muscle, pancreas, and thymus, the highest amount being in liver. Increased levels of total tissue zinc were observed in those tissues which clearly responded to the treatments with elevated MT levels, such as liver, kidney, small intestine, and pancreas. MT induction by zinc in these tissues was associated with an accumulation of zinc not bound to MT. In the IA-treated rats non-MT zinc accumulated in liver and pancreas. It is concluded that induction of MT by zinc and in particular by organic chemicals such as IA without exogenously supplied metals interferes with zinc homeostasis and the physiological role of MT in liver and extrahepatic tissues of the rat.

Animals↗

PubMed1988

Zinc plasma levels after oral zinc tolerance test in nonalcoholic cirrhosis.

Zinc absorption was examined in 25 nonalcoholic cirrhotic patients using the oral zinc tolerance test and comparing results to a healthy control group. With 22.5 mg elementary zinc, the increase in plasma zinc was significantly lower in the cirrhotic patients than in the control group with P less than 0.01 in the first and second hours and P less than 0.05 in the fourth hour. The zinc malabsorption may result from an abnormal small intestinal mucosa. Indeed small intestinal biopsies in all patients showed partial shortening and prominent distension of villi and intense stromal edema with inflammatory cell infiltration of the lamina propria. However, it is not clear whether these intestinal changes are due to zinc deficiency or to portal hypertension. Thus zinc malabsorption appears to contribute to zinc deficiency in nonalcoholic cirrhotics and seems to result, in part, from pathological changes in the mucosa.

Adult↗

PubMed1983

Zinc effects on glutathione metabolism relationship to zinc-induced protection from alkylating agents.

Several aspects of the effects of zinc on the metabolism of glutathione were examined in the Chinese hamster cell (line CHO) and in three derived sublines which differ in their resistance to the thiol reactive heavy metal cadmium. In the parental CHO cell, which does not induce the synthesis of metallothionein in response to zinc, glutathione levels remained approximately constant during the first 6 hr of zinc exposure. In the resistant cell lines, which induce the synthesis of metallothionein in response to zinc, the glutathione levels dropped transiently during zinc exposure. In all cell lines except the most cadmium resistant line, the glutathione levels after 12 hr were increased up to 3-fold relative to pretreatment levels. Similarly, the glutathione S-transferase activity measured by the conjugation of 1-chloro-2,4-dinitrobenzene to glutathione was increased after 9-12 hr of zinc treatment in all except the most highly cadmium resistant cell line. Glutathione reductase was not affected consistently by zinc treatment; however, the level of activity of this enzyme in the most highly cadmium resistant line was two to three times greater than that observed in the other cell lines. These effects are considered in relation to the zinc-induced protection of these cells from the toxic effect of the alkylating agent melphalan.

Animals↗

PubMed1983

Metabolism of zinc and copper in the neonate: zinc thionein in developing rat brain, heart, lung, spleen, and thymus.

In a continuing study of the importance of metallothionein (MT) in the growth and development of neonates, zinc and copper metabolism in rat brain, heart, lung, spleen, and thymus has been analyzed in 5, 10, 15, 20, and 25 day old rats. Total, cytosol, and MT zinc and copper concentrations and organ contents were determined. Zinc, but very little, if any copper was associated with MT in these organs. Concentrations ranged from 0.03 to 3.3 micrograms Zn in MT/g; organ contents ranged from 0.003 to 2.2 micrograms Zn in MT/organ. Brain exhibited the highest concentrations and contents of zinc in MT, approaching the levels found in kidneys. Rank order of organ contents of zinc in MT was brain greater than lung greater than heart, spleen, thymus, during this neonatal growth period. When organ growth was rapid, a large percentage (20-95%) of the cytosolic zinc present in these organs was associated with MT, as has been previously observed with liver, kidneys, and testes. None of these organs undergoes the dramatic changes in zinc and copper metabolism previously observed in neonatal rat liver and gastrointestinal tract, and in maturing testes. They are more comparable to kidneys in their concentrations of zinc in MT. Like testes, little copper is found in these organs.

Animals↗

PubMed1989

T-lymphocyte dysfunction in the elderly associated with zinc deficiency and subnormal nucleoside phosphorylase activity: effect of zinc supplementation.

The present study was conducted in an attempt to explore a possible mechanism for zinc-deficiency-induced T-lymphocyte dysfunction in the elderly. Eight elderly subjects aged 65-78 years served in this study. All subjects were anergic, zinc-deficient and had low activity of erythrocyte nucleoside phosphorylase. Baseline values for zinc status and immunological indices were established after which subject were treated with zinc acetate (60 mg elemental zinc per day given orally) for a period of 4 1/2 months. Zinc supplementation resulted in a significant increase in the concentrations of zinc in plasma (P less than 0.001), erythrocytes (P less than 0.05), lymphocytes (P less than 0.001) and neutrophils (P less than 0.005). The activity of nucleoside phosphorylase in erythrocytes increased significantly (P less than 0.001) as a result of zinc treatment. This was associated with significant improvement in the delayed cutaneous hypersensitivity reactions.

Acetates↗

PubMed2005

Role of zinc and zinc transporters in the molecular pathogenesis of diabetes mellitus.

Diabetes is one of the most common chronic diseases in the United States. An estimated 18.2 million people in the US (6.3%) have diabetes; among them 2.8 million are African Americans (AAs). On average, AAs are twice as likely to have diabetes as European Americans (EAs) of similar age. AAs disproportionately suffer from various diseases in the US. Many of these diseases include hypertension, cardiovascular disease (CVD), diabetes mellitus (DM-beta predominantly Type II), and cancers of the prostate and pancreas. A number of risk factors such as smoking, a high fat diet, little physical activity, stress, and meager access to health care have been the subject of numerous investigations. However, the factor of the interaction between genetics and the environment has received very little attention in the scientific community. Of note, the content of zinc in pancreatic beta gells is among the highest in the body; however, very little is known about the uptake and storage of zinc inside these cells. We hypothesize that one of the major reason AAs disproportionally suffer from DM (as well as some other illnesses like prostate cancer, CVD and hypertension) is due to their inherent inability to transport appropriate amount of zinc in the crucial cell types that require relatively higher amount of zinc than the other cell types. In this article, we will explore in detail the possible genetic and environmental link between human zinc transporters (hZIPs) and their differential expressions in the islet beta cells from AAs as compared to other racial groups, particularly EAs, in both normal healthy individuals and diabetic patients. We hypothesize that the hZIPs play an important role in the development of diabetes, and the main reason AAs disproportionately suffer from DM (as well as other illnesses like prostate and pancreatic cancers, hypertension, and CVD) as compared to EAs may be due the low degree of expressions of the critical zinc transporters in the beta cells. Understanding the molecular events in the pathogenesis of DM with regards to regulation of zinc uptake would be critical to the evaluation of the natural history of diabetes in humans and especially in various racial groups. If a direct link between zinc transport and diabetes can be established, then a special nutritional formula, medication or other intervention might be especially designed to test the ability to decrease the incidence of this disease in DM susceptible groups, particularly in AAs.

Carrier Proteins↗