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PubMed2004

Effects of dietary zinc levels, phytic acid and resistant starch on zinc bioavailability in rats.

BACKGROUND: Owing to its fermentability, it has been advocated that resistant starch (RS) has a positive effect on the absorption of minerals by increasing their solubility in the hindgut. In marginally zinc-deficient rats, the enhancement of zinc bioavailability by RS occurs mostly when the diet contains phytic acid. AIM OF THE STUDY: This study aims to investigate the effect of dietary zinc level and phytic acid on the cecal zinc pools and zinc bioavailability of rats fed RS. METHODS: Wistar rats (male, 3wk old) were divided into eight groups (n = 6), and fed diets containing either 5% cellulose (control fiber: insoluble and low fermentable) or 20 % RS (test fiber: soluble and fermentable), with or without the addition of 1% sodium phytate, at the 10 and 30 mg/kg dietary zinc levels, for 21 days. RESULTS: At 10 mg Zn/kg, RS increased femur zinc concentration only in the group receiving the phytate-containing diet, while at 30 mg Zn/kg it increased femur zinc concentration in rats fed both phytate-free and phytate-containing diets. The total content of zinc in the cecum was increased by the higher dietary zinc level and tended to be increased by the addition of phytate, which is assumed to impair zinc absorption in the small intestine. Feeding RS lowered cecal pH values, which correlated with increasing values of zinc solubility (r = -0.3471; P < 0.05). The later was, in turn, directly associated with zinc apparent absorption (r = 0.3739; P < 0.05). CONCLUSIONS: The increase in zinc bioavailability by RS occurs when dietary zinc levels are adequate and/or zinc absorption is impaired in the small intestine, increasing the influx of unabsorbed zinc into the cecum and favoring the increase of zinc bioavailability when RS fermentation lowers the cecal pH.

Animals↗

PubMed1988

Relationship between plasma zinc, angiotensin-converting enzyme, alkaline phosphatase and onset of symptoms of zinc deficiency in the rat.

Recent evidence suggests that changes in plasma zinc concentration may play a central role in the development of early lesions of zinc deficiency. The aim of the following work was to better understand events occurring in plasma during the onset of zinc deficiency, and to investigate biochemical mechanisms by which plasma zinc may exert its effects. Fifty male weanling rats of 90 g weight were allocated to five treatment groups of ten rats each. Treatments were: 1, zinc deficient, mixed diet (1-2 mg Zn per kg): 2, zinc deficient, self-select diet; 3, zinc repleted; 4, control, pair fed; 5, control, ad libitum fed. With the exception of treatment 1, which consisted of a 25% casein diet, all rats were offered protein as a separate component of the diet. Control rats received zinc in the drinking water (100 mg l-1). The sequence of events following initiation of zinc deficiency were: reduced plasma zinc concentration (2 days), reduced plasma angiotensin-converting enzyme and alkaline phosphatase activities (3-4 days), reduced feed intake and growth (5-6 days) and reduced percentage protein intake (12 days). Plasma zinc concentration in the deficient rats was inversely correlated with the growth rate of the rat over the previous 24 h. Zinc repletion resulted in marked overshoot in plasma zinc concentration (300%) and converting-enzyme activity (150%) within 24 h, but a return to normal within 72 h. Alkaline phosphatase activity responded likewise, albeit more slowly. Protein self selection had no effect on the manifestations of zinc deficiency, although reduced protein intake was associated with lower plasma zinc concentration. The results provide evidence of a role for plasma zinc in the development of early clinical signs of zinc deficiency, possibly acting biochemically through reduced activity of zinc-dependent peptidases such as angiotensin-converting enzyme.

Alkaline Phosphatase↗

PubMed2005

Long-term moderate zinc supplementation increases exchangeable zinc pool masses in late-middle-aged men: the Zenith Study.

BACKGROUND: Zinc supplementation may be beneficial for health. Assessing exchangeable zinc pools may be a useful approach to evaluate zinc status. OBJECTIVE: We evaluated the effects of long-term supplementation with 2 moderate doses of zinc on the mass of exchangeable zinc pools. DESIGN: Three groups of healthy, late-middle-aged men (n = 16 per group) participated in a stable-isotope zinc kinetic study after 6 mo of daily supplementation with 0 (placebo), 15, or 30 mg Zn. At the end of the supplementation period, each subject received an intravenous injection of 0.89 mg (70)Zn, and the plasma zinc disappearance curve was monitored for the next 10 d. Two approaches were used to determine the characteristics of the exchangeable zinc pools: 1) formal 3-compartmental modeling and 2) a simplified determination of the total mass of the rapidly exchangeable zinc pool (EZP). RESULTS: In the placebo group, the exchangeable zinc pool masses for the 3 considered pools were as follows: 2.15, 12.7, and 100.5 mg Zn. The rapidly exchangeable zinc pool mass in the placebo group was 143 mg Zn. Zinc supplementation significantly increased the exchangeable zinc pool masses regardless of the approach used to determine these pools. In addition, these data confirm that exchangeable zinc pool masses correlate positively with total zinc intake and negatively with subject age and do not correlate with plasma zinc concentrations. CONCLUSION: Our data show that long-term supplementation with 2 moderate doses of zinc is an efficient way to increase exchangeable zinc pool masses in late-middle-aged men.

Aged↗

PubMed1983

Intestinal metallothionein: effect of parenteral and enteral zinc exposure on tissue levels of mice on controlled zinc diets.

An investigation of changes in duodenal metallothionein (MT) levels following zinc exposure was conducted. Mice fed zinc-deficient (less than 1 ppm zinc) or zinc-supplemented (50 ppm) diets showed no increase in duodenal MT levels 24 hours after exposure to 17 mumol/kg zinc by gastric intubation. However, both MT induction and zinc incorporation were measured in the liver indicating transport of zinc via the intestinal mucosa. Only a small increase in [35S]cystine was observed to be incorporated into the MT fractions of duodenal homogenate obtained from zinc-exposed mice. Thus no statistically significant increase in duodenal MT was detected on single oral exposure of mice to zinc sulfate. Repetitive parenteral or enteral doses of zinc sulfate spaced 12 hours apart resulted in significant increases in duodenal MT. However, increases in MT by dietary zinc were not found until a 300 ppm zinc diet was used. No difference could be detected in duodenal MT levels of pair-fed animals fed zinc-deficient or 50 ppm zinc diet for 14 days. Similarly, no statistically significant difference in 65Zn uptake by in situ perfused duodenal sections could be detected in mice maintained on zinc-deficient or 100 ppm zinc diet for 1 month. These findings suggest that intestinal MT functions as a rapidly turned over zinc storage protein rather than a zinc regulatory protein.

Animals↗

PubMed1992

Dietary protein, as egg albumen: effects on bone composition, zinc bioavailability and zinc requirements of rats, assessed by a modified broken-line model.

The effect of dietary protein concentration on zinc bioavailability, requirements and incorporation into bones was investigated in growing rats. Zinc requirements were determined by the broken-line method. Protein did not affect either absorption or biological half-life of 65Zn added to the diet. Zinc requirements based on weight gain or tibia zinc were generally greater when rats were fed 30% rather than 15% egg white. When fed 30% rather than 15% egg white, zinc-deficient rats gained less weight and tended to incorporate less zinc into bone, whereas zinc-adequate rats gained weight similarly and incorporated more zinc into bone. Dietary protein concentration apparently elevated the maximum amount of zinc incorporated into bones of rats fed adequate zinc. When dietary zinc was adequate (25 mg/kg diet), tibia zinc concentrations increased linearly with dietary concentrations of 15, 25, 35 and 45% egg white. When dietary zinc was adequate, higher protein diets resulted in lower tibia nitrogen, and higher tibia zinc, without substantial changes in tibia size or calcium concentration. These results indicate that high protein diets increase zinc requirements and bone zinc deposition, the latter being a consequence of altered bone zinc metabolism, rather than improved zinc bioavailability.

Administration, Oral↗

PubMed1996

Metallothionein I and II protect against zinc deficiency and zinc toxicity in mice.

Metallothionein (MT)-bound zinc accumulates when animals are exposed to excess zinc and is depleted under conditions of zinc deficiency, suggesting that MT serves as a means of sequestering excess zinc as well as a zinc reservoir that can be utilized when zinc is deficient. To examine the importance of MT for these processes, mice with null alleles of both MT I and MT II genes were created and the zinc concentration and histological appearance of multiple organs assessed. At birth, the hepatic zinc concentration of these MT-null mice was lower than that of wild-type controls (0.27 +/- 0.02 vs. 0.65 +/- 0.11 micromol zinc/g tissue, P < 0.05). During the next 3 wk of suckling zinc-replete (95 micrograms zinc/g diet) dams, the hepatic zinc concentration of controls fell to 0.42 +/- 0.04 micromol/g but was unchanged in the MT-null mice (0.28 +/- 0.04 micromol/g). The most prominent histological anomaly observed at 3 wk of age was the presence of swollen Bowman's capsules in the kidneys of MT-null mice. When nursing MT-null dams were fed a severely zinc-deficient (1.5 microg/g) diet, kidney development in the MT-null pups was retarded as indicated by the retention of the nephrogenic zone and incomplete tubule development. We suggest that the lack of a hepatic reservoir of zinc jeopardizes the developing kidney in the MT-null mice. In addition to being more sensitive to dietary zinc restriction, MT-null mice are more sensitive to zinc toxicity. When adult mice were challenged with a ramping dose of zinc up to a total of 3700 micromol zinc/kg body weight, MT-null mice had a greater incidence of pancreatic acinar cell degeneration compared with control mice despite accumulating less zinc (2.72 +/- 0.46 vs. 1.23 +/- 0.52 micromol zinc/g pancreas, control and MT-null, respectively, P < 0.05). The results of these experiments suggest that MT I and MT II can protect against both zinc deficiency and zinc toxicity.

Animals↗

PubMed2006

Iron and zinc supplementation improved iron and zinc status, but not physical growth, of apparently healthy, breast-fed infants in rural communities of northeast Thailand.

Iron deficiency is prevalent in children and infants worldwide. Zinc deficiency may be prevalent, but data are lacking. Both iron and zinc deficiency negatively affect growth and psychomotor development. Combined iron and zinc supplementation might be beneficial, but the potential interactions need to be verified. In a randomized, placebo-controlled trial using 2 x 2 factorial design, 609 Thai infants aged 4-6 mo were supplemented daily with 10 mg of iron and/or 10 mg of zinc for 6 mo to investigate effects and interactions on micronutrient status and growth. Iron supplementation alone increased hemoglobin and ferritin concentrations more than iron and zinc combined. Anemia prevalence was significantly lower in infants receiving only iron than in infants receiving iron and zinc combined. Baseline iron deficiency was very low, and iron deficiency anemia was almost nil. After supplementation, prevalence of iron deficiency and iron deficiency anemia were significantly higher in infants receiving placebo and zinc than in those receiving iron or iron and zinc. Serum zinc was higher in infants receiving zinc (16.7 +/- 5.2 micromol/L), iron and zinc (12.1 +/- 3.8 micromol/L) or iron alone (11.5 +/- 2.5 micromol/L) than in the placebo group (9.8 +/- 1.9 micromol/L). Iron and zinc interacted to affect iron and zinc status, but not hemoglobin. Iron supplementation had a small but significant effect on ponderal growth, whereas zinc supplementation did not. To conclude, in Thai infants, iron supplementation improved hemoglobin, iron status, and ponderal growth, whereas zinc supplementation improved zinc status. Overall, for infants, combined iron and zinc supplementation is preferable to iron or zinc supplementation alone.

Anemia, Iron-Deficiency↗

PubMedDate not supplied

Clinical studies on zinc metabolism during total parenteral nutrition as related to zinc deficiency.

In 99 adult patients receiving controlled total parenteral nutrition (TPN), a study was made on the time course of concentrations of zinc in plasma, erythrocyte and urine in relation to the development of zinc deficiency. Zinc deficiency developed in 11 cases receiving TPN solutions not containing zinc. The plasma zinc level was significantly lower at the time of onset of zinc deficiency than in normal subjects, before the procedure of TPN, or at the time of symptomatic relief achieved by administration of zinc. The erythrocyte zinc level was slightly but not significantly lower at time of onset of zinc deficiency than in normal subjects, before TPN or at time of symptomatic relief. The urinary zinc level at time of onset of zinc deficiency was significantly lower than that in normal subjects or at the time of symptomatic relief but not significantly lower than that before TPN. A comparison between patients developing and those not developing zinc deficiency within 4 wk of the outset of TPN showed that only the plasma zinc level was significantly lower in the former than the latter group. The urinary zinc level also tended to be lower, although not significantly, in the former than the latter group but varied widely. No difference was present between the groups as to the erythrocyte zinc level. Zinc deficiency developed in none of those patients who had a plasma zinc level of 50 micrograms/dl or more but in five of 10 (50%) patients with less than 50 micrograms/dl and in all three with less than 30 micrograms/dl of zinc in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2002

Body zinc distribution profile during N-methyl-N-nitrosourea-induced mammary tumorigenesis in rats at various levels of dietary zinc intake.

Zinc distribution is apparently altered in breast cancer patients. It is unclear if this apparent zinc redistribution is a consequence of altered zinc nutrition or tissue-specific response to breast cancer. Our objectives were to assess effects of N-methyl-N-nitrosourea-treatment and N-methyl-N-nitrosourea-induced mammary tumorigenesis on body zinc-distribution profile in rats and to assess effects of dietary zinc intake on the body zinc-distribution profile during N-methyl-N-nitrosourea treatment and N-methyl-N-nitrosourea-induced mammary tumorigenesis in rats. Female Sprague-Dawley rats were assigned to zinc-deficient (3 mg/kg diet) or zinc-adequate (31 mg/kg diet) ad libitum or pair-fed group. Rats were sham treated or N-methyl-N-nitrosourea treated (50 mg/kg body weight; Experiment 1 or 40 mg/kg body weight; Experiment 2) (n = 6). In both experiments, the zinc concentration was significantly higher (6-19 times) in mammary tumor than in mammary gland. Tissue zinc concentration was essentially unaffected by N-methyl-N-nitrosourea treatment and tumor bearing, but was reduced by zinc deficiency in the bone, kidney, and liver. Overall, higher mammary tumor zinc concentration and absence of zinc redistribution during N-methyl-N-nitrosourea treatment and N-methyl-N-nitrosourea-induced mammary tumorigenesis, regardless of zinc intakes, indicates zinc accumulation in mammary tumors. Because zinc is essential for growth and cancer is characterized by uncontrolled growth, this zinc accumulation suggests an involvement of zinc in N-methyl-N-nitrosourea-induced rat mammary tumorigenesis.

Animals↗

PubMed2004

Role of vitamin-zinc interactions on in vitro zinc uptake by human erythrocytes.

In vitro zinc uptake by human erythrocytes was studied under a range of zinc concentrations representing three different plasma zinc levels i.e., zinc deficient [0.35-0.61 ppm], zinc normal [0.74-1.59 ppm], and zinc excess [1.65-2.3 ppm]. Further, interactions of physiological levels of riboflavin, flavin adenine dinucleotide (FAD), nicotinic acid, nicotinamide adenine dinucleotide (NAD), thiamine, thiamine pyrophosphate (TPP), folic acid, and ascorbic acid with zinc uptakes were studied in independent experiments. In control experiments, as compared to the normal zinc state, the rate of change of zinc uptake over change in zinc levels was 1.6 times in the excess state and 0.12 times in the deficient state, indicating three distinct patterns. Under the zinc-deficient state, thiamine significantly enhanced the zinc uptakes (p< 0.05), whereas ascorbic acid and riboflavin inhibited zinc uptakes (p< 0.05). The percent hemolysis of the cells was also significantly lower in the presence of thiamine (p< 0.05). Under normal and excess zinc states, the vitamin-zinc interactions were not significant. The results suggest that with erythrocytes as the vehicles, thiamine might be playing an enhancer role in uptake of zinc, whereas the action of ascorbic acid might be inhibitory for zinc uptakes under deficient zinc states.

Dose-Response Relationship, Drug↗

PubMed1978

Effects of early wound healing and wound treatment with zinc tape on intestinal absorption and distribution of zinc in rats.

In rats operated with large excisional skin wounds which were not treated with zinc tape, the serum zinc concentration was decreased at every observation time during the first post-operative day and the absorption of zinc from the intestine was increased. Slight decreases in the zinc concentration were seen in some tissues while liver zinc was very high. In rats with wounds treated with zinc tape, serum zinc was markedly increased at 6 hours, lower but above control levels at 7 and 12 hours and markedly increased again at 24 hours. The absorption of zinc from the intestine was low. Zinc concentration were elevated in most tissues sampled; they were high in testis and kidney and very high in liver. The results strongly indicate that the operative trauma and/or acute inflammatory conditions in the wounds in animals not treated with zinc tape initiate a movement of zinc from serum, some tissues and the content of the intestine to the liver. In the zinc tape treated group the increase in liver zinc was supplied mostly by the zinc tape. It is assumed that these large increases in zinc concentration in the liver are the result of the incorporation of zinc into certain zinc containing proteins which are produced in response to the inflammatory process in the wound. An increase was also found in the copper concentration in the liver of zinc tape treated animals and a decrease in the iron concentration in the liver of both groups of operated animals compared to controls.

Absorption↗

PubMed2003

Exchangeable zinc pool size in infants is related to key variables of zinc homeostasis.

The exchangeable zinc pool (EZP) is the sum of the combined pools that exchange with zinc in the plasma within 48-72 h and is thought to be critical for zinc-dependent biological processes. The size of the EZP in adults has been found to be positively related to dietary zinc intake, daily absorbed zinc and fecal excretion of endogenous zinc. In this study, we examine data on EZP size in relation to variables of zinc homeostasis in normal infants on different feeding regimens. Data from 45 male infants who participated in one of four different studies contribute to the analysis. The feeding regimens include exclusive breastfeeding (n = 9; age, 2-5 mo); breastfeeding plus modest supplementation with cow's milk-based formula (n = 16; age, 3-4 mo); exclusive formula feeding (n = 4; age, 3-4 mo) and exclusive breastfeeding plus complementary foods (n =16; age, 7 mo). Fractional absorption was determined by fecal monitoring after oral administration of zinc-stable isotopes. Urine enrichment 4-8 d posttracer was used to determine endogenous fecal zinc (7-mo-old infants excepted) and EZP size. Univariate correlations and multivariate regression analyses were performed between EZP and age, weight, dietary zinc intake, fractional absorption, total absorbed zinc and endogenous fecal zinc. Results include no significant relationship between EZP size and age, body weight or fractional absorption but a positive relationship with daily absorbed zinc and endogenous fecal zinc excretion. We conclude that the amount of absorbed zinc is not tightly regulated, and that endogenous fecal zinc is dependent on and responsive to the zinc status of the organism.

Homeostasis↗

PubMed1990

Effect of marginal maternal zinc intake on zinc absorption and growth of 3-month-old infant rhesus monkeys.

One compensatory mechanism for marginal zinc intake may be through an enhanced absorption of zinc. Such a compensatory mechanism could be of value to the neonate, as poor zinc nutriture during early life has severe consequences on growth and development. We studied the uptake of zinc by 3-month-old infant rhesus monkeys born to dams fed control diets (100 micrograms of zinc per gram of diet or zinc-restricted diets (4 micrograms of zinc per gram of diet). Zinc uptake/retention was studied by feeding 3-month-old infant monkeys that had fasted an infant formula containing zinc 65 by gavage. Whole body radioactivity was counted immediately after intubation and on days 10 and 17 after intubation. Regardless of dietary group, 65 zinc retention was high, ranging from 33% to 71% of the dose fed to the monkeys. There were no significant differences between the two dietary groups in the percentage of zinc retention at days 10 and 17. Independent of the dietary group, there was no correlation between plasma zinc and zinc absorption. A positive correlation was found between weight gain and zinc retention in the marginal zinc infants, while a negative correlation between weight gain and zinc retention was observed in the control infants. These observations suggest that the mechanisms underlying growth may be different in infants born to dams fed control vs marginal zinc diets.

Animals↗

PubMed2001

Zinc homeostasis in the brain of adult rats fed zinc-deficient diet.

Zinc concentration and (65)Zn uptake in the brain of rats fed zinc-deficient diet for 12 weeks were examined, based on a previous finding of the impairment of learning behavior by the zinc deprivation. Zinc concentrations in the brain, except for the hippocampal formation, did not decrease significantly in zinc-deficient rats, whereas zinc concentration in the liver of the zinc-deficient rats was approximately half that of control rats. When zinc-deficient rats were subjected to brain autoradiography with (65)Zn, (65)Zn concentration in any brain region of zinc-deficient rats was significantly higher than in control rats 6 days after injection of (65)ZnCl(2). The increase rate of (65)Zn concentration in the brain by the zinc deprivation was approximately 150%, and was similar to those in the liver and serum, suggesting that dietary zinc deprivation may cause a scarcity of zinc in the brain, in addition to the peripheral tissues such as the liver. These results indicate that the adult brain is responsive to dietary zinc deprivation. In the brain of zinc-deficient rats, the increase rate of (65)Zn concentration in the hippocampal formation seemed to be low compared to those in other brain regions. The hippocampal formation may be the most responsive to dietary zinc deprivation in the adult brain. The present finding demonstrates that zinc homeostasis in the brain is altered by chronically dietary zinc deprivation.

Animal Feed↗

PubMed2003

Human ZIP1 is a major zinc uptake transporter for the accumulation of zinc in prostate cells.

The prostate gland of humans and other animals accumulates a level of zinc that is 3-10 times greater than that found in other tissues. Associated with this ability to accumulate zinc is a rapid zinc uptake process in human prostate cells, which we previously identified as the hZIP1 zinc transporter. We now provide additional evidence that hZIP1 is an important operational transporter that allows for the transport and accumulation of zinc. The studies reveal that hZIP1 (SLC39A1) but not hZIP2 (SLC39A2) is expressed in the zinc-accumulating human prostate cell lines, LNCaP and PC-3. Transfected PC-3 cells that overexpress hZIP1 exhibit increased uptake and accumulation of zinc. The V(max) for zinc uptake was increased with no change in K(m). Along with the increased intracellular accumulation of zinc, the overexpression of hZIP1 also results in the inhibition of growth of PC-3 cells. Down-regulation of hZIP1 by treatment of PC-3 cells with hZIP1 antisense oligonucleotide resulted in a decreased zinc uptake. Uptake of zinc from zinc chelated with citrate was as rapid as from free zinc ions; however, the cells did not take up zinc chelated with EDTA. The cellular uptake of zinc is not dependent upon an available pool of free Zn(2+) ions. Instead, the mechanism of transport appears to involve the transport of zinc from low molecular weight ligands that exist in circulation as relatively loosely bound complexes with zinc.

Carrier Proteins↗

PubMed2004

ZnT-1 expression in astroglial cells protects against zinc toxicity and slows the accumulation of intracellular zinc.

Zinc ions are emerging as an important factor in the etiology of neurodegenerative disorders and in brain damage resulting from ischemia or seizure activity. High intracellular levels of zinc are toxic not only to neurons but also to astrocytes, the major population of glial cells in the brain. In the present study, the role of ZnT-1 in reducing zinc-dependent cell damage in astrocytes was assessed. Zinc-dependent cell damage was apparent within 2 h of exposure to zinc, and occurred within a narrow range of approximately 200 microM. Pretreatment with sublethal concentrations of zinc rendered astrocytes less sensitive to toxic zinc levels, indicating that preconditioning protects astrocytes from zinc toxicity. Fluorescence cell imaging revealed a steep reduction in intracellular zinc accumulation for the zinc-pretreated cells mediated by L-type calcium channels. Heterologous expression of ZnT-1 had similar effects; intracellular zinc accumulation was slowed down and the sensitivity of astrocytes to toxic zinc levels was reduced, indicating that this is specifically mediated by ZnT-1 expression. Immunohistochemical analysis demonstrated endogenous ZnT-1 expression in cultured astroglia, microglia, and oligodendrocytes. Pretreatment with zinc induced a 4-fold increase in the expression of the putative zinc transporter ZnT-1 in astroglia as shown by immunoblot analysis. The elevated ZnT-1 expression following zinc priming or after heterologous expression of ZnT-1 may explain the reduced zinc accumulation and the subsequent reduction in sensitivity toward toxic zinc levels. Induction of ZnT-1 may play a protective role when mild episodes of stroke or seizures are followed by a massive brain insult.

Animals↗

PubMed2005

Increased abundance of labile intracellular zinc during cell proliferation was due to increased retention of extracellular zinc in 3T3 cells.

Platelet-derived growth factor (PDGF)-, epidermal growth factor (EGF)- and insulin-like growth factor I (IGF-I)-stimulated cell proliferation in 3T3 cells was accompanied by increased abundance of labile intracellular pool of zinc (LIPZ). However, the origin and regulation of this cell proliferation-associated increase in the abundance of LIPZ are unknown. Cellular zinc homeostasis involves zinc transporters and metallothionein. The objectives of this study were to determine whether cell proliferation-associated increase in the abundance of LIPZ was a result of an increased zinc uptake and to assess the involvement of zinc transporters and metallothionein in this cell proliferation-associated increase in the abundance of LIPZ in 3T3 fibroblasts. Zinc transporters assessed included both zinc importer (Zip1) and zinc exporters (ZnT1, ZnT2 and ZnT4). Growth factors increased the abundance of LIPZ while total cellular zinc concentration remained unaffected, demonstrating that LIPZ was responsive to the increased needs for zinc during growth factor-stimulated cell proliferation. Growth factors also increased net zinc retention as indicated by higher 65zinc radioactivity and elevated mRNA levels of Zip1, ZnT1 and ZnT4. Although zinc is essential to cell proliferation, excessive cellular zinc accumulation causes cytotoxicity. Collectively, these observations suggest that increase in the abundance of LIPZ during growth factor-stimulated cell proliferation was due to increased net retention of extracellular zinc, which was apparently achieved through a coordinated up-regulation of the expression of transporters involved in both zinc influx and efflux to ensure adequate supply of zinc to sustain cell proliferation, yet to prevent potential zinc cytotoxicity in 3T3 cells.

3T3 Cells↗

PubMed1977

Zinc absorption through skin: correction of zinc deficiency in the rat.

The therapeutic effect of topical administration of zinc was tested in pregnant rats consuming a diet deficient in the element. Four groups of rats were fed a zinc-deficient diet for 24 hr. Half of the animals were treated during this period with a topical application of oil saturated with zinc chloride, for the full 24 hr in one group, and for the last 8 hr in the other. In the two remaining groups, oil without zinc chloride was applied under the same conditions as described above, and in all cases oral ingestion of the supplement was prevented. At the end of the 24-hr period, the animals were killed and plasma zinc was determined. An additional group of animals consuming a diet adequate in zinc was killed without any treatment to provide control values of normal plasma zinc. Rats consuming the deficient diet and without topical zinc supplementation had plasma zinc values significantly lower than all other groups after 24 hr. Animals receiving zinc supplementation for 8 hr had plasma levels similar to those of the control group fed an adequate zinc diet and significantly higher than those of rats that received no zinc application to the skin. In animals in which zinc was applied for 24 hr, plasma zinc values were significantly higher than in any other group, including normal controls. The results indicate that percutaneous transport of zinc may be of sufficient magnitude to be clinically significant and that topical application of this element may be useful in cases of dietary zinc deficiency or diseases producing a zinc deficiency state.

Animals↗