65Zn Levels Research Articles

Study of radioactive impurities in neutron transmutation doped germanium

A program to develop low temperature (mK) sensors with neutron transmutation doped Ge for rare event studies with a cryogenic bolometer has been initiated. For this purpose, semiconductor grade Ge wafers are irradiated with thermal neutron flux from Dhruva reactor at Bhabha Atomic Research Centre (BARC), Mumbai. Spectroscopic studies of irradiated samples have revealed that the environment of the capsule used for irradiating the sample leads to significant levels of 65Zn, 110mAg and 182Ta impurities, which can be reduced by chemical etching of approximately ~50μm thick surface layer. From measurements of the etched samples in the low background counting setup, activity due to trace impurities of 123Sb in bulk Ge is estimated to be ~1Bq/g after irradiation. These estimates indicate that in order to use the NTD Ge sensors for rare event studies, a cooldown period of ~2 years would be necessary to reduce the radioactive background to ≤1mBq/g.

Bioavailability, distribution and clearance of tracheally-instilled and gavaged uncoated or silica-coated zinc oxide nanoparticles.

BackgroundNanoparticle pharmacokinetics and biological effects are influenced by several factors. We assessed the effects of amorphous SiO2 coating on the pharmacokinetics of zinc oxide nanoparticles (ZnO NPs) following intratracheal (IT) instillation and gavage in rats.MethodsUncoated and SiO2-coated ZnO NPs were neutron-activated and IT-instilled at 1 mg/kg or gavaged at 5 mg/kg. Rats were followed over 28 days post-IT, and over 7 days post-gavage. Tissue samples were analyzed for 65Zn radioactivity. Pulmonary responses to instilled NPs were also evaluated at 24 hours.ResultsSiO2-coated ZnO elicited significantly higher inflammatory responses than uncoated NPs. Pulmonary clearance of both 65ZnO NPs was biphasic with a rapid initial t1/2 (0.2 - 0.3 hours), and a slower terminal t1/2 of 1.2 days (SiO2-coated ZnO) and 1.7 days (ZnO). Both NPs were almost completely cleared by day 7 (>98%). With IT-instilled 65ZnO NPs, significantly more 65Zn was found in skeletal muscle, liver, skin, kidneys, cecum and blood on day 2 in uncoated than SiO2-coated NPs. By 28 days, extrapulmonary levels of 65Zn from both NPs significantly decreased. However, 65Zn levels in skeletal muscle, skin and blood remained higher from uncoated NPs. Interestingly, 65Zn levels in bone marrow and thoracic lymph nodes were higher from coated 65ZnO NPs. More 65Zn was excreted in the urine from rats instilled with SiO2-coated 65ZnO NPs. After 7 days post-gavage, only 7.4% (uncoated) and 6.7% (coated) of 65Zn dose were measured in all tissues combined. As with instilled NPs, after gavage significantly more 65Zn was measured in skeletal muscle from uncoated NPs and less in thoracic lymph nodes. More 65Zn was excreted in the urine and feces with coated than uncoated 65ZnO NPs. However, over 95% of the total dose of both NPs was eliminated in the feces by day 7.ConclusionsAlthough SiO2-coated ZnO NPs were more inflammogenic, the overall lung clearance rate was not affected. However, SiO2 coating altered the tissue distribution of 65Zn in some extrapulmonary tissues. For both IT instillation and gavage administration, SiO2 coating enhanced transport of 65Zn to thoracic lymph nodes and decreased transport to the skeletal muscle.

Assessment of gamma emitting radionuclides in the aquatic ecosystem of Kakrapar Atomic Power Station and evaluation of radiological doses to aquatic plants

During operation and maintenance of Pressurised Heavy Water Reactors (PHWRs) at Kakrapar Atomic Power Station (KAPS), low level radioactive liquid waste is generated and released to the aquatic ecosystem (Moticher lake). The silt and aquatic weed (Hydrilla verticillata) samples collected from different locations in Moticher lake were analysed for 137Cs, 134Cs, 65Zn, 60Co, 54Mn and 40K during 2007–2008. A wide variation in activity levels of 137Cs, 134Cs, 65Zn, 60Co, 54Mn and 40K in silt and weed samples were observed in aquatic system of KAPS. The activity buildup in the silt is confined to a small area in the Moticher lake. The activity levels were found to be insignificant at 1 km away from discharge point (upstream and downstream). An attempt was made to evaluate the radiological dose to aquatic weed (Hydrilla verticillata), which was found to be well within the dose limit prescribed by US DOE. The total radiological dose due to the naturally occurring radionuclide (40K) is comparatively higher than that of other reactor released gamma emitting radionuclides.

4-Hydroxynonenal disrupts zinc export in primary rat cortical cells

Accumulating evidence implicates oxidative stress in the pathogenesis of several neurodegenerative disorders including Alzheimer's disease (AD). Increased lipid peroxidation, decreased levels of polyunsaturated fatty acids, and increased levels of 4-hydroxynonenal (HNE) have been demonstrated in AD brain. Proteins responsible for zinc export are localized on the plasma membrane and may be vulnerable to damage from lipid peroxidation. To test this hypothesis, cultured primary rat cortical neurons were incubated with 65Zn for 1 h and then treated with HNE (0–35 μM) for 4 h. Levels of 65Zn in aliquots of medium were measured at 1, 2, 4 h following treatment with HNE and intracellular 65Zn measured after 4 h using liquid scintillation counting. The amount of 65Zn in medium did not differ significantly. However, a statistically significant ( p < 0.05) increase of 65Zn was observed inside cortical neurons after treatment with 20 μM HNE for 4 hours. These data suggest that HNE may impair a protein essential for zinc export leading to increased levels of intracellular zinc.

Do earthworms mobilize fixed zinc from ingested soil?

A wide range of organisms inhabit the soil and has to deal with soil-bound metals. The bioavailable fraction of metals may be estimated explicitly using the isotopic dilution technique. In the present paper, we evaluated the isotopic exchange technique for assessing the bioavailability of soil Zn (using 65Zn) to earthworms. To validate the technique, the worms were first exposed to various 65Zn levels, and errors due to soil entrained in the gut were evaluated. This exposure indicated no effect of gamma-radiation on growth (wet weight gain) of the organisms and that depuration of the earthworms minimized errors in labile pools determined by isotopic dilution. Our study further showed that the earthworms accessed 55-65% of the total Zn in the soil. The labile pool for the earthworms Eisenia andrei was similar to that for the plant Lactuca sativa, indicating that earthworms and plants to a large extent access the same fraction of soil Zn. Hence, the isotopic dilution technique has the potential to assess biologically available pool of Zn in soils. As lettuce is not known to significantly mobilize nonlabile metals in soil, this study indicates that Zn uptake by E. andrei is predominantly via the exchangeable pools (possibly the soil pore water) rather than dissolution of Zn held within soil particles or within soil organic matter or other food sources.

The Role of Zinc Binding in the Biological Activity of Botulinum Toxin

Botulinum toxin is a zinc-dependent endoprotease that acts on vulnerable cells to cleave polypeptides that are essential for exocytosis. To exert this poisoning effect, the toxin must proceed through a complex sequence of events that involves binding, productive internalization, and intracellular expression of catalytic activity. Results presented in this study show that soluble chelators rapidly strip Zn(2+) from its binding site in botulinum toxin, and this stripping of cation results in the loss of catalytic activity in cell-free or broken cell preparations. Stripped toxin is still active against intact neuromuscular junctions, presumably because internalized toxin binds cytosolic Zn(2+). In contrast to soluble chelators, immobilized chelators have no effect on bound Zn(2+), nor do they alter toxin activity. The latter finding is because of the fact that the spontaneous loss of Zn(2+) from its coordination site in botulinum toxin is relatively slow. When exogenous Zn(2+) is added to toxin that has been stripped by soluble chelators, the molecule rebinds cation and regains catalytic and neuromuscular blocking activity. Exogenous Zn(2+) can restore toxin activity either when the toxin is free in solution on the cell exterior or when it has been internalized and is in the cytosol. The fact that stripped toxin can reach the cytosol means that the loss of bound Zn(2+) does not produce conformational changes that block internalization. Similarly, the fact that stripped toxin in the cytosol can be reactivated by ambient Zn(2+) or exogenous Zn(2+) means that productive internalization does not produce conformational changes that block rebinding of cation.

Calcium control of zinc uptake in rainbow trout

Water hardness is known to control the uptake and toxicity of zinc and other metals through either chemical competition, biological acclimation, or both processes. The dominant process controlling zinc uptake has not been previously elucidated, nor has the effect of calcium been investigated independently of other cations. We determined zinc uptake by rainbow trout acclimated and exposed to four calcium treatments: (1) low calcium (6.5 mg Ca/l; 160 μM) acclimation and low calcium exposure (LL); (2) low acclimation and high calcium (131 mg Ca/l; 3300 μM) exposure (LH); (3) high acclimation and low exposure (HL); and (4) high acclimation and high exposure (HH). Trout were exposed to sublethal zinc (100 μg 65Zn/l; 1.5 μM) for 24 h, and whole body and gill 65Zn levels were determined. Zinc uptake was approximately linear during the 24 h exposure period and uptake was calcium dependent. 65Zn uptake by trout was 22 μg/kg per h in the LL treatment and 4.5 μg/kg per h in the HH treatment. 65Zn uptake by trout in the LH and HL treatments was 13 and 10 μg/kg per h, respectively. 65Zn uptake in gills was also significantly reduced by calcium acclimation or exposure. Trout in the LH and HH treatments had five fold lower 65Zn concentrations than LL treatment fish. The results of this study demonstrate that calcium reduces zinc uptake through both biological acclimation and chemical processes, and that the protective effects of calcium are approximately additive.

Ethanol Decreases Zinc Transfer to the Fetus in Normal but Not Metallothionein‐Null Mice

Ethanol causes significant teratogenicity in normal (MT+/+) but not metallothionein-null (MT-/-) fetuses. Impaired maternal fetal zinc (Zn) transfer is indicated, because ethanol significantly reduces plasma Zn concentrations in MT+/+ dams while increasing concentrations in MT-/- dams. In this study we examined maternal-fetal Zn homeostasis in response to ethanol in MT+/+ and MT-/- mice and the origins of the increase in plasma Zn in MT-/- mice. Mice were treated with saline or ethanol (0.015 ml/g intraperitoneally at 0 and 4 hr) on day 12 of gestation. An additional subcutaneous injection of 65Zn tracer was administered after the second ethanol injection before mice were killed 3 hr later. Maternal liver MT levels were not different between ethanol and saline MT+/+ mice. Both liver Zn and 65Zn levels were higher in MT+/+ mice. Plasma Zn concentrations were higher in MT-/- mice, with MT-/- ethanol-treated mice having levels greater than those of MT-/- saline-treated controls. MT+/+ ethanol-treated fetuses exhibited lower 65Zn transfer and whole Zn concentrations compared with MT+/+ and MT-/- saline and MT-/- ethanol fetuses. So we could examine changes in plasma Zn after ethanol treatment, MT+/+ and MT-/- mice were injected with 65Zn 3 days before they received ethanol treatment. Muscle and skin showed a decrease in 65Zn retention in both genotypes over 3 hr. There was a trend toward greater 65Zn release from skin and muscle at an earlier time in MT-/- mice: 24% vs. 2% decrease (MT-/- vs. MT+/+) for muscle and 28% vs. 15% decrease (MT-/- vs. MT+/+) for skin at 2 hr. The results show (a) that ethanol interferes with the transfer of Zn to the fetus, and that this is MT dependent, and (b) that the increase in plasma Zn seen in MT-/- mice after ethanol administration is a result of Zn release from the skin and muscle, in the absence of hepatic Zn sequestration.

Ethanol Decreases Zinc Transfer to the Fetus in Normal but Not Metallothionein-Null Mice

Background: Ethanol causes significant teratogenicity in normal (MT+/+) but not metallothionein-null (MT−/−) fetuses. Impaired maternal fetal zinc (Zn) transfer is indicated, because ethanol significantly reduces plasma Zn concentrations in MT+/+ dams while increasing concentrations in MT−/− dams. In this study we examined maternal-fetal Zn homeostasis in response to ethanol in MT+/+ and MT−/− mice and the origins of the increase in plasma Zn in MT−/− mice. Methods and Results: Mice were treated with saline or ethanol (0.015 ml/g intraperitoneally at 0 and 4 hr) on day 12 of gestation. An additional subcutaneous injection of 65Zn tracer was administered after the second ethanol injection before mice were killed 3 hr later. Maternal liver MT levels were not different between ethanol and saline MT+/+ mice. Both liver Zn and 65Zn levels were higher in MT+/+ mice. Plasma Zn concentrations were higher in MT−/− mice, with MT−/− ethanol-treated mice having levels greater than those of MT−/− saline-treated controls. MT+/+ ethanol-treated fetuses exhibited lower 65Zn transfer and whole Zn concentrations compared with MT+/+ and MT−/− saline and MT−/− ethanol fetuses. So we could examine changes in plasma Zn after ethanol treatment, MT+/+ and MT−/− mice were injected with 65Zn 3 days before they received ethanol treatment. Muscle and skin showed a decrease in 65Zn retention in both genotypes over 3 hr. There was a trend toward greater 65Zn release from skin and muscle at an earlier time in MT−/− mice: 24% vs. 2% decrease (MT−/− vs. MT+/+) for muscle and 28% vs. 15% decrease (MT−/− vs. MT+/+) for skin at 2 hr. Conclusions: The results show (a) that ethanol interferes with the transfer of Zn to the fetus, and that this is MT dependent, and (b) that the increase in plasma Zn seen in MT−/− mice after ethanol administration is a result of Zn release from the skin and muscle, in the absence of hepatic Zn sequestration.

Hepatic Zinc Response via Metallothionein Induction after Tumor Transplantation

Based on previous findings that liver zinc and metallothionein (MT) levels increase after tumor transplantation, zinc metabolism in tumor-bearing mice was studied to clarify the role of zinc–MT in host defense systems. Zinc in the hepatic cytosolic MT fraction did not increase in tumor-bearing mice fed a zinc-deficient diet, suggesting that dietary zinc is necessary for apo-MT induction in the liver after tumor transplantation and is then incorporated into the apo-MT. When 65ZnCl2 was intravenously injected, liver 65Zn levels in the tumor-bearing mice were higher than those in control mice for 72 h after the injection. Pancreatic and blood 65Zn levels in tumor-bearing mice were lower than those in controls for 24 h (pancreas) and 6 h (blood) after the injection. These findings indicate that the hepatic zinc response via MT induction influences zinc metabolism in the body after tumor transplantation. Moreover, 65Zn uptake in the liver of MT-deficient tumor-bearing mice was lower than that in control tumor-bearing mice 1 h after injection. 65Zn uptake in the tumor and blood 65Zn levels in the MT-deficient tumor-bearing mice were higher than those in the control tumor-bearing mice. Tumor weight increased more in MT-deficient mice than in control mice. The formation of zinc–MT in the liver of tumor-bearing mice might decrease blood zinc availability for tumors and other tissues, such as the pancreas.

The role of the pancreas in intestinal zinc secretion in metallothionein-null mice.

The distribution and excretion of endogenous Zn, including the role of the pancreas, were examined in fasted MT+/+ and MT-/- mice. At 3 and 6 h after receiving 65Zn tracer by subcutaneous injection, 65Zn levels were compared in tissues of MT+/+ and MT-/- mice. 65Zn levels were significantly higher in the liver and pancreas of the MT+/+ mice, whereas in the MT-/- mice, 65Zn levels were significantly higher in muscle, skin, and most of the gastrointestinal tract other than the stomach and upper small intestine. In MT-/- mice, 3% of the injected 65Zn was recovered in the luminal contents of the small intestine over 3-6 h, compared with <1.5% in the MT+/+ mice. A loading dose of Zn (150 microg, s.c.) sufficient to raise the plasma Zn concentration by fourfold to fivefold in both MT+/+ and MT-/- mice resulted in similar increases in pancreatic Zn levels in each genotype, although more Zn appeared in the lower small intestine of MT-/- mice. Pancreatectomy decreased the level of 65Zn in the small intestine of MT-/- but not MT+/+ mice. Longer-term studies over 4 days demonstrated few differences in tissue 65Zn between MT+/+ and MT-/- mice, with the exception of the pancreas, where 65Zn retention after fasting in MT-/- mice was half that of MT+/+ mice. MT-/- mice also had significantly lower Zn concentrations in the pancreas. Fecal excretion of 65Zn in MT-/- mice was greater than that of MT+/+ mice in the first 24 h (24.7 vs. 18.2% of injected dose; p < 0.05). Besides metallothionein (MT), there were no significant differences in the molecular weight distribution of Zn binding ligands in the lumen of the small intestine between MT+/+ and MT-/- mice. Mice lacking MT I and II lose more endogenous Zn into the gut because of a relative failure of the pancreas to retain Zn. However, increased Zn secretion via the small intestinal mucosa may also contribute to intestinal Zn loss in MT-/- mice.

Metallothionein-Null Mice Absorb Less Zn from an Egg-White Diet, but a Similar Amount from Solutions, although with Altered Intertissue Zn Distribution

The influence of metallothionein (MT) on Zn transfer into non-gut tissues was investigated in MT-null (MT−/−) and normal (MT+/+) mice 4 h after oral gavage of aqueous 65ZnSO4solution at doses of 154, 385, 770 and 1540 nmol Zn per mouse. Zn transfer was not significantly different between MT+/+ and MT−/− mice and was directly proportional to the oral dose (slope = 0.127, r = 0.991; 0.146, r = 0.994, respectively). Blood 65Zn and plasma Zn concentrations increased progressively in MT−/− mice at doses >154 nmol Zn, reaching levels of 2.4% of oral dose and 60 μmol/L, respectively, at the 1540 nmol Zn dose. The corresponding values for MT+/+ mice were approximately half, 1.0% and 29 μmol/L. Intergenotypic differences were found in tissue distribution of 65Zn within the body; MT−/− mice had higher 65Zn levels in muscle, skin, heart and brain, whereas MT+/+ mice retained progressively more Zn in the liver, in conjunction with a linear increase in hepatic MT up to the highest Zn dose. MT induction in the small intestine reached its maximum at an oral dose of 385 nmol Zn and did not differ at higher doses. Absorption of a 770 nmol 65Zn dose from a solid egg-white diet was only one fourth (MT+/+) and one eighth (MT−/−) of the Zn absorption from the same dose of 65Zn in aqueous solution. MT+/+ mice had greater (P < 0.05) Zn absorption from the egg-white diet than did MT−/− mice, indicating that gut MT confers an absorptive advantage, but only when Zn is incorporated into solid food.

Zinc levels in the rat fetal liver are not determined by transport across the placental microvillar membrane or the fetal liver plasma membrane.

During pregnancy, zinc (Zn) levels in the rat fetal liver increase markedly. Why they do so or how the increase is regulated is unknown. We firstly investigated whether the increase occurs as a result of increased Zn transfer across the placenta and then tested whether the regulation occurred at the level of the microvillar membrane of the placenta or the fetal liver plasma membrane. Rats at different stages of gestation were injected with 7.5 microCi 65Zn in 100 microliters rat serum and killed after 1 h. 65Zn levels in the fetus remained constant at equivalent to the amount in 50 microliters maternal plasma per fetus until Day 18; at this time they increased to equivalent to 1.33 ml and then continued to increase until term. We isolated placental microvillar vesicles from placentas at each stage of gestation, characterized them, and measured Zn uptake. Zn uptake rates did not change during pregnancy. Similarly, we isolated vesicles from fetal liver plasma membrane and measured Zn uptake. Again, the uptake properties did not change during pregnancy. The data suggest that some other step in the transport process is rate limiting and that the increase in Zn levels in the fetal liver that occurs during pregnancy is possibly a result, rather than a cause, of metallothionein induction.

Altered Zn status by α-hederin in the pregnant rat and its relationship to adverse developmental outcome

The hypothesis that an acute-phase reaction in the pregnant animal causes a systemic redistribution of Zn, resulting in a transient but developmentally adverse Zn deficiency in the embryo, was tested by treating pregnant rats during organogenesis with α-hederin, an agent reported to induce substantial metallothionein (MT) synthesis in rat liver, and determining hepatic MT concentration, hepatic and plasma Zn concentration, and systemic distribution of a pulse of 65Zn after treatment. Developmental toxicity was assessed by evaluating morphologic development in term fetuses. A single dose of α-hederin, injected sc at dosages of 3 to 300 μmol/kg, caused an acute phase response, indicated by decreased Fe and Zn, and increases Cu, α 1-acid glycoprotein, and ceruloplasmin concentration in plasma, along with a dosage-related increase in maternal hepatic MT concentration. The maximum induction of MT was 11 to 15-fold greater than control and occurred at dosages of 30 μmol/kg and higher, and MT concentration reached its peak 12 to 24 h after treatment. Zn concentration in liver and liver cytosol increased along with MT, reaching a maximum level at dosages of 30 μmol/kg and higher. Plasma Zn concentration decreased after α-hederin treatment to a level approximately 75% of control at a dosage of 30 μmol/kg and 50% of control at 300 μmol/kg. Therefore, hepatic MT induction was associated with most, but not all, of the decrease in plasma Zn concentration. Zn distribution was evaluated by giving an oral pulse of 65Zn 8 h after treatment with 0, 30, or 300 μmol/kg α-hederin on gestation day 11, and measuring 65Zn levels 18 h after treatment. The fraction of 65Zn distributed to the liver of treated rats (either dosage) was twice that of control, but distribution of 65Zn to other maternal tissues was decreased. 65Zn accumulation by conceptuses was significantly decreased, attributable to decreased accumulation in decidua, but not in visceral yolk sacs or embryos; however, at this stage of development the decidua accounts for a greater quantity of Zn than either of the other products of conception and may serve as the Zn-storing tissue for the conceptus. Both 30 and 300 μmol/kg increased resorption incidence, and 300 μmol/kg also decreased fetal weight and increased the incidence of abnormal fetuses. Serum collected from rats two hours after α-hederin treatment (i.e., before the onset of MT synthesis) supported rat embryo development in vitro, whereas serum collected 18 h after treatment did not. Adding Zn to this serum restored normal embryonic development. These data are consistent with the hypothesis that systemic changes in Zn status, brought about by a hepatic acute phase response, including a substantial induction of hepatic MT, may be a mechanism for maternally mediated abnormal development.

Effects of cadmium, copper and metallothionein synthesis inhibiting and stimulating compounds on zinc uptake and accumulation in rat hepatoma HTC cells

Experiments were carried out to investigate the uptake and accumulation of Zn in rat hepatoma HTC cells, as affected by interfering metals (Cd, Cu), metallothionein synthesis inhibiting compounds (Actinomycin D, cycloheximide) and metallothionein synthesis stimulating compounds (dexamethasone, dibu-cAMP). Cell viability was tested under all experimental conditions by the measurement of LDH leakage, K + uptake and total cell protein. Determinations of Zn were performed by AAS (total Zn) or by γ-ray spectrometry ( 65Zn). Metallothionein analysis was carried out by Cd-saturation tests. The results indicate that cellular responses in rat hepatoma HTC cells with respect to the uptake and accumulation of 65Zn are fully comparable with literature data existing for 65Zn accumulation in rat hepatocytes, under all experimental conditions applied. Cu 2+ and dibutyryl-cAMP did not significantly affect rates of 65Zn accumulation. Cd 2+, Actinomycin D and cycloheximide reduced 65Zn uptake, but dexamethasone additions resulted in increased 65Zn accumulation in the cells. Effects on 65Zn were shown both in cytosolic and in the membranes/organelles cell fractions. HPLC chromatography in control cells suggested that newly accumulated cytosolic 65Zn was predominantly MT-associated. Dexamethasone-induced 65Zn accumulation could not be related to elevated cellular MT levels, nor were the total cytosolic Zn levels significantly affected. Non-specific attenuations in MT levels (Actinomycin D, cycloheximide and dibu-cAMP) yielded linear relations between cytosolic 65Zn and MT levels, without any change in cytosolic Zn (AAS). Combined addition of Cd and dexamethasone yielded elevated MT levels, but severely reduced total cytosolic Zn and 65Zn concentrations. The results further indicate the non-Zn-specific nature of dexamethasone-action and suggest the relatively easy Zn-complexing and Zn-release of MT. The simultaneous determinations of total cytosolic zinc and cytosolic 65Zn levels showed that the application and sole measurement of radiotracers may yield only one-sided views of what is actually present or occurring in the cells.

Border-Row Sprays for Control of the Plum Curculio in Apple Orchards: Behavioral Study

In spring 1987, 215 65Zn-labeled adult plum curculios, Conotrachelus nenuphar (Herbst), were released, just after they emerged from overwintering, at a single site located at the southern edge of a woodlot bordering an unsprayed apple orchard in southern Quebec. At petal fall, between the second and third day of release, a border-row spray of insecticide was applied to the two perimeter rows of apple trees in front of the release site. Dispersal of the population was compared with another group of 254 curculios released simultaneously in the center of the 1.7-ha orchard. In 1988 and 1989, the borderrow spray was applied to the entire orchard perimeter. Plum curculio damage at harvest was assessed and compared with that found in a nearby unsprayed apple orchard. Labeling had no significant effect on field mortality and behavior. Insects released at the edge of the woodlot moved toward the orchard. Mortality was three times higher for insects dispersing through the sprayed rows than for those dispersing in the center of the orchard. Among insects that were recaptured in the orchard and at its edge, 83% were found either dead under the sprayed trees (59%) or alive along the outside edge of the sprayed rows (24%). The remaining curculios (17%) were found alive within the orchard. Plum curculio damage at harvest decreased from 1987 (52%) to 1989 (2.4%), whereas in a nearby unsprayed apple orchard, it averaged 70% (minimum 43%, maximum 88%). A single petal fall border spray was moderately effective in protecting fruit, but the combination of a pink spray and a petal fall border spray provided economically acceptable control. Reinfestation after the petal fall spray appeared to be the main cause of plum curculio damage at harvest. Toads, Bufo americanus americanus Holbrook, were found with high levels of 65Zn. Ways to improve the efficiency of plum curculio control by border-row spraying are discussed.

Effects of histidine on tissue zinc distribution in rats.

Histidine has been reported to affect body zinc status by increasing urinary zinc excretion. The effects of experimental histidinemia on distribution of 65Zn in anesthetized rats were studied. Infusion of L-histidine at a rate sufficient to raise plasma concentrations to approximately 2 mM for 6 h starting 48 h after a single intraperitoneal 65Zn injection did not alter 65Zn activities in a variety of tissues when compared with anesthetized uninfused animals. However, plasma 65Zn and erythrocyte 65Zn were decreased, and liver 65Zn was increased. If 65Zn was injected intravenously during histidine infusion, net accumulation of zinc by some tissues was increased, but uptake by others was reduced relative to uninfused animals. In all cases, however, uptake expressed relative to plasma 65Zn levels was increased when allowance was made for the more rapid fall in plasma 65Zn during histidine infusion. Similar infusions of D-histidine produced quantitatively similar effects. Since enzymatic mechanisms and amino acid carriers would be expected to show stereoselectivity, such processes are unlikely to be involved in the zinc distribution changes described. The possibility of zinc transport by a hitherto unidentified carrier is discussed. These experiments confirm that histidinemia can affect zinc status, but any associated changes in urinary zinc excretion do not seem adequate to account for the tissue changes found.

Translocation and function of zinc in roots

Abstract Wheat seedlings were grown with entire or split root systems in nutrient solutions with variable levels of Zn. Entire root systems with 1 μM Zn progressively lowered solution pH for 16 days (D16); roots without Zn lowered pH identically until D13 after which it increased. Shoot growth of seedlings without Zn was depressed from D14. Split root systems had each half root in a separate solution (A and B) with either the same Zn concentration (nil or 1 μM = Zn00 or Zn++) or 0.05, 0.1, or 1 μM Zn in A and none in B (Zn+0). To solution A, 45Ca was added on D7 and 65Zn on D23; no Ca was found in solution B at any time. On D24, Zn00 plants were Zn deficient with dry matter (DM) depressed in shoots and enhanced in roots; Zn concentrations in the youngest emerged leaf blade (YEB) and root B were low (13 and 12 μg/g DM). Zn+0 plants had the same DM as ZN++ plants; their Zn concentrations in YEB and root B were relatively high (more than 19 and 21 μg/g DM). From 65Zn levels in root B, the rate of Zn transloc...

Effect of Dietary Picolinic Acid on the Metabolism of Exogenous and Endogenous Zinc in the Rat

The excretion of 65Zn was compared by metabolic balance studies in adult male rats fed purified diets containing 0.8 mmol Zn/kg diet, with and without 40 mmol picolinic acid per kilogram diet, after single intragastric (i.g.) and intraperitoneal (i.p.) doses of the isotope. In a third experiment picolinic acid was introduced for 3 d into the diet of rats prelabeled with 65Zn. The urinary excretion of total zinc was increased by the ingestion of picolinic acid in all three experiments. The urinary and fecal outputs of 65Zn were both consistently greater in picolinic acid-fed rats than in the corresponding control animals. This was particularly marked after i.p. injection of the tracer, and the specific activities of urine and feces from the treated rats were both increased. When picolinic acid was introduced into the diet of prelabeled rats there was a delay of 24 h in the urinary response and 48 h in the fecal response. The residual 65Zn levels were reduced in several tissues from the picolinic acid-fed rats, especially after i.p. administration of the isotope. These observations indicate that dietary picolinic acid increases the turnover of endogenous zinc in addition to enhancing the absorption and excretion of ingested metal, and this has implications for its use in cases of zinc deficiency.

A whole body counting technique using ultralow doses of 59Fe and 65Zn in absorption and retention studies in humans

A whole body counting technique is described which allows monitoring of gamma ray emission rates from body levels of 59Fe and 65Zn in the same range as emission rates of gamma rays from naturally occurring 40K in the total body. Consequently absorption/retention studies were performed with doses of 0.1 microCi. Experimental results from studies using corn intrinsically labeled with 65Zn and wheat intrinsically labeled with 59Fe are presented and illustrate how absorption of 59Fe as low as 4% and retention of 65Zn up to 418 days were measured in humans.