Effect of zinc on biological half-lives of 65Zn in whole body and liver and on distribution of 65Zn in different organs of rats following nickel toxicity

This study was designed to determine the effect of zinc on the biological half-lives of ⁶⁵Zn in whole body and liver and on distribution of ⁶⁵Zn in different organs of rats following nickel toxicity. Sprague-Dawley (SD) rats received either nickel in the form NiSO₄·6H₂O at a dose of 800 mg/L in drinking water, zinc in the form of ZnSO₄·7H₂O at a dose of 227 mg/L in drinking water, and nickel plus zinc or drinking water alone for a total duration of 8 wk. All of the rats were injected with a tracer dose of 0.37 MBq ⁶⁵Zn at the end of the treatment period. The effects of different treatments were studied on biological half-lives of ⁶⁵Zn in whole body and liver and on the distribution of ⁶⁵Zn in different organs of rats. In the present study, we have noted that nickel treatment to normal rats caused a significant decrease in the slow component (Tb₂) in liver, which improved following zinc supplementation. Nickel administration to normal-diet-fed animals caused significant lowering in the percentage uptake of ⁶⁵Zn values in the brain, liver, and intestine. However, the administration of zinc to nickel-treated rats improved the status of ⁶⁵Zn in different organs. The Tb₂ in the liver and the percentage uptake of ⁶⁵Zn values elevated following zinc supplementation to nickel-treated rats.     

65Zinc uptake from blood into brain and other tissues in the rat

Zinc is essential for normal growth, development and brain function although little is known about brain zinc homeostasis. Therefore, in this investigation we have studied⁶⁵Zn uptake from blood into brain and other tissues and have measured the blood-brain barrier permeability to⁶⁵Zn in the anaesthetized rat in vivo. Adult male Wistar within the weight range 500–600 g were used.⁶⁵ZnCl₂ and [¹²⁵I]albumin, the latter serving as a vascular marker, were injected in a bolus of normal saline I.V. Sequential arterial blood samples were taken during experiments that lasted between 5 min and 5 hr. At termination, samples from the liver, spleen, pancreas, lung, heart, muscle, kidney, bone, testis, ileum, blood cells, csf, and whole brain were taken and analysed for radio-isotope activity. Data have been analysed by Graphical Analysis which suggests⁶⁵Zn uptake from blood by all tissues sampled was unidirectional during this experimental period except brain, where at circulation times<30 min,⁶⁵Zn fluxes were bidirectional. In addition to the blood space, the brain appears to contain a rapidly exchanging compartment(s) for⁶⁵Zn of about 4 ml/100g which is not csf.     

Supplementation of zinc mitigates the altered uptake and turnover of <Superscript>65</Superscript>Zn in liver and whole body of diabetic rats

Diabetes is a life threatening disease and its onset is linked with both environmental and genetic factors. Zinc metabolism gets altered during diabetes and results in many complications. The present study was designed to elucidate the effects of zinc supplementation on the biokinetics of ⁶⁵Zn in whole body, liver and its biodistribution in diabetic rats. The animals were divided into four groups viz; normal control; diabetic (single intraperitoneal injection of alloxan 150 mg/kg body weight); zinc treated (227 mg/l in drinking water); and diabetic + zinc treated. To carry out biokinetics study, each rat was injected intraperitoneally with 0.74 MBq radioactivity of ⁶⁵Zn following 4 weeks of different treatments and the radioactivity was determined by using a suitably shielded scintillation counter. Alloxan induced diabetic rats showed a significant decrease in both the fast (Tb₁) and slow (Tb₂) components of biological half-life of ⁶⁵Zn which, however, were normalized in whole body (P > 0.05) following zinc supplementation. In case of liver, Tb₂ component was brought back to the normal but Tb₁ component was not increased significantly. The present study indicates that the paucity of zinc in the tissues of the diabetic animals was due to decreased retention of tissue zinc as evidenced by increased serum Zn, hyperzincuria and increased rate of uptake of ⁶⁵Zn by the liver. Zinc supplementation caused a significant improvement in the retention of zinc in the tissues and is therefore likely to be of benefit in the treatment of diabetes.     

Zinc-selenium interaction in the rat

Retention, dynamics of⁷⁵Se and⁶⁵Zn distribution, and elimination were studied in rats after separate or joint single doses of these metals. White female Wistar rats were divided into four groups (fifteen rats each). Group I received Na₂ ⁷⁵SeO₃ (0.1 mg Se/kg i.g.), group II received Na₂ ⁷⁵SeO₃+ZnCl₂ (5 mg Zn/kg s.c.), group III received⁶⁵ZnCl₂, and group IV received⁶⁵ZnCl₂+Na₂SeO₃. The zinc and selenium contents in the tissues were estimated during 120 h after administration; excretion in urine and feces of animals was determined throughout the experiment. Combined administration of zinc and selenium resulted in an enhanced selenium retention in the brain, spleen, kidneys, blood, lungs, and heart. A selenium-induced increase in the concentration of zinc was noted in the bowels, blood, liver, kidneys, spleen, brain, and lungs. The effects of the zinc/selenium interaction were visible especially in the lowered level of excretion of these elements. Zinc induced a decrease in the excretion of selenium in urine, with no concomitant changes in the excretion in feces. However, a visible decrease in the excretion of zinc in the feces was observed in the presence of selenium. The present results indicate an occurrence of clear-cut interaction effects between zinc and selenium administered simultaneously in the rat.     

Equivalent uptake of organic and inorganic zinc by monkey kidney fibroblasts, human intestinal epithelial cells, or perfused mouse intestine

Zinc (Zn) is recognized as an essential nutrient, and is added as a supplement to animal and human diets. There are claims that zinc methionine (ZnMet) forms a stable complex that is preferentially transported into tissues, and this has contributed to uncertainty about conflicting reports on the bioavailability of various Zn compounds. This study evaluated the cellular and intestinal uptake of inorganic and organic forms of Zn. Steady-state uptake of⁶⁵Zn by human intestine epithelial cells, and monkey kidney fibroblasts was not significantly different with zinc chloride (ZnCl₂), ZnMet, or zinc propionate (ZnProp) (P > 0.05). Uptake of⁶⁵Zn from zinc chelated with EDTA was significantly lower (P < 0.01). In live mice,⁶⁵Zn uptake by perfused intestine and deposition in intestine and liver showed no significant difference between ZnCl₂ and ZnMet. Equimolar [⁶⁵Zn]methionine and zinc[³⁵S]methionine were prepared according to a patented method that yields “ complexed” Zn. Cellular uptake of the radiolabeled methionine was <0.1% of the radiolabeled Zn from these complexes, indicating separate uptake of the Zn and methionine. Gel filtration did not distinguish between⁶⁵Zn in ZnCl₂, ZnProp, or reagent ZnMet, though feed-grade ZnMet containing >10% protein did give a higher-mol-wt form of⁶⁵Zn. Results of this study show equivalent uptake of Zn from inorganic and organic compounds, and support recent feed trials on Zn bioavailability.     

Radiation dose rates of differentiated thyroid cancer patients after <Superscript>131</Superscript>I therapy

Postoperative ¹³¹I treatment for differentiated thyroid cancer (DTC) can create a radiation hazard for nearby persons. The present prospective study aimed to investigate radiation dose rates in ¹³¹I-treated DTC patients to provide references for radiation protection. A total of 141 ¹³¹I-treated DTC patients were enrolled, and grouped into a singular treatment (ST) group and a repeated treatment (RT) group. The radiation dose rate of ¹³¹I-treated patients was measured. The rate of achieving discharge compliance and restricted contact time were analyzed based on Chinese regulations. Multivariate logistic regression analysis was used to analyze the independent factors associated with the clearance of radioiodine. The rate of achieving discharge compliance (¹³¹I retention <?400 MBq) was 79.8 and 93.7% at day 2 (D2) for the ST and RT groups, respectively, and reached 100% at D7 and D4, respectively. The restricted contact time with ¹³¹I-treated patients at 0.5 m for medical staff, caregivers, family members, and the general public ranged from 4 to 7 days. Multivariate logistic regression analysis showed that the 24-h iodine uptake rate was the only significant factor associated with radioiodine clearance. For the radiation safety of ¹³¹I-treated DTC patients, the present results can provide radiometric data for radiation protection.     

Zinc uptake across the apical membrane of freshwater rainbow trout intestine is mediated by high affinity, low affinity, and histidine-facilitated pathways

Zinc is both a vital nutrient and an important toxicant to aquatic biota. In order to understand the interplay between nutrition and toxicity, it will be important to determine the mechanisms and the factors that regulate zinc uptake. The mechanism of apical intestinal Zn(II) uptake in freshwater rainbow trout and its potential modification by the complexing amino acid histidine was investigated using brush-border membrane vesicles (BBMVs). Following characterisation of the BBMV preparation, zinc uptake in the absence of histidine was both time- and concentration-dependent and consisted of two components. A saturable phase of uptake was described by an affinity constant of 57±17 μM and a transport capacity of 1867±296 nmol mg membrane protein⁻¹ min⁻¹. At higher zinc levels (>500 μM) a linear, diffusive component of uptake was evident. Zinc transport was also temperature-dependent, with Q₁₀ values suggesting zinc uptake was a carrier-mediated process. Zinc uptake by vesicles in the presence of histidine was correlated to a mono-histidine species (Zn(His)⁺) at all Zn(II) concentrations examined.     

Physiological and morphological traits associated with zinc efficiency in Exacum

Interspecific hybrids of Exacum exhibit variation in the expression of zinc efficiency. This research investigated the genetic basis for this variation and evaluated a series of physiological and morphological traits for their association with zinc efficiency. Chi-square analyses of self-pollinated progeny from both zinc-efficient and zinc-inefficient parents indicate a significant genetic component. One hundred percent of the progeny from the inefficient parent were classified as inefficient, while the progeny from the efficient parent segregated 32% inefficient to 68% efficient. Six plants from each phenotypic class (efficient and inefficient) of the efficient parent were utilized in analyses of plant traits. Statistically significant associations were identified between the zinc-efficient phenotype and mol Zn uptake mg^-1 root, root-to-shoot ratio, specific root length, mol Zn uptake cm^-2 root surface area, and Zn uptake cm^-1 root length. No association was identified between zinc-efficient phenotype and root diameter, transpiration rate, or H⁺ production. Zinc uptake cm^-1 root length had the greatest association with the zinc-efficiency phenotype and was able to discriminate the two phenotypic classes. We suggest that Zn uptake cm^-1 root length is the most significant factor explaining the variation between the zinc-efficient and zinc-inefficient phenotypes in Exacum.     

Cultured human skin fibroblasts absorb65Zn

The radioactive isotope⁶⁵Zn was used to study the incorporation of zinc by cultured human skin fibroblasts. The development of the method for studying cell uptake of⁶⁵Zn in a minimal synthetic medium is presented. Kinetics carried out on control cultures up to 240 min indicated that zinc uptake occurred in three phases, the first being the most rapid. Temperature and pH affect zinc uptake, in favor of an active transport process. In addition, the rate of incorporation is considerably decreased during the first phases after adding potassium cyanide, during the last phases after adding sodium iodoacetate, and during all the phases if dithioerythritol is used. A hypothesis is therefore proposed according to which several types of mechanisms would be involved in zinc uptake by fibroblasts. At least a part of these mechanisms is energy-dependent.     

The uptake of zinc by erythrocytes under near-physiological conditions

The in vitro uptake of zinc by erythrocytes was measured under near-physiological conditions, using⁶⁵Zn as a radioactive tracer. Because of the presence of serum albumin—a strong zinc ligand—a low concentration of medium free zinc was maintained. Under these conditions a high-affinity carrier for zinc transport over the cell membrane was identified. With human erythrocytes, a Michaelis constant (K _m ) of 0.2 nM with respect to free medium zinc was measured and aV _max of 4.5 nmoles Zn transported per h/g dry wt. TheK _m for medium Zn increases when the size of the internal erythrocytic Zn pool is augmented, whereasV _max remains virtually unchanged. A model to explain this phenomenon is proposed. It is suggested that this phenomenon could underlie observations, confirmed here, that the in vitro uptake of Zn by animal erythrocytes depends on the Zn status of the animal.     

Zinc supplementation ameliorates glycoprotein components and oxidative stress changes in the lung of streptozotocin diabetic rats

Zinc (Zn) is a component of numerous enzymes that function in a wide range of biological process, including growth, development, immunity and intermediary metabolism. Zn may play a role in chronic states such as cardiovascular disease and diabetes mellitus. Zn acts as cofactor and for many enzymes and proteins and has antioxidant, antiinflammatory and antiapoptotic effects. Taking into consideration that lung is a possible target organ for diabetic complications, the aim of this study was to investigate the protective role of zinc on the glycoprotein content and antioxidant enzyme activities of streptozotocin (STZ) induced diabetic rat tissues. Female Swiss albino rats were divided into four groups. Group I, control; Group II, control + zinc sulfate; Group III, STZ-diabetic; Group IV, diabetic + zinc sulfate. Diabetes was induced by intraperitoneal injection of STZ (65 mg/kg body weight). Zinc sulfate was given daily by gavage at a dose of 100 mg/kg body weight every day for 60 days to groups II and IV. At the last day of the experiment, rats were sacrificed, lung tissues were taken. Also, glycoprotein components, tissue factor (TF) activity, protein carbonyl (PC), advanced oxidative protein products (AOPP), hydroxyproline, and enzyme activities in lung tissues were determined. Glycoprotein components, TF activity, lipid peroxidation, non enzymatic glycation, PC, AOPP, hydroxyl proline, lactate dehydrogenase, catalase, superoxide dismutase, myeloperoxidase, xanthine oxidase, adenosine deaminase and prolidase significantly increased in lung tissues of diabetic rats. Also, glutathione levels, paraoxonase, arylesterase, carbonic anhydrase, and Na⁺/K⁺- ATPase activities were decreased. Administration of zinc significantly reversed these effects. Thus, the study indicates that zinc possesses a significantly beneficial effect on the glycoprotein components and oxidant/antioxidant enzyme activities.     

Uptake and turnover of65Zn in subcellular fractions of brain of rat under normal and zinc-deficient conditions

After a single injection,⁶⁵Zn is slowly taken up by the brain of the rat to a maximum after 7 d, followed by a turnover phase, with a half-time of about 3 wk. In the brain of rats on a zinc-deficient diet, the⁶⁵Zn content in the brain continued to increase up to 30 d after the injection. The uptake and turnover phases in six different subcellular fractions of the brain showed a pattern similar to that of the whole brain in both the control and zinc-deficient rats. There was no internal redistribution of⁶⁵Zn in the brain under conditions of progressive zinc deficiency. The results are discussed in a model for zinc homeostasis in the brain.     

Blood-brain exchange routes and distribution of65Zn in rat brain

Zinc is essential for normal development and function of the CNS although much is to be learned about brain Zn homeostasis. In these experiments adult male Wistar rats within the weight range 500–600 g were used. Ventriculo-cisternal perfusion was performed to allow the measurement of⁶⁵Zn fluxes between blood and csf across the choroid plexuses. Blood-brain or blood-cerebrospinal fluid barrier permeability to⁶⁵Zn has been determined by graphical analysis in experiments that lasted between 5 and 180 minutes. Cerebral capillary permeability to⁶⁵Zn was found to be low with a K_in of about 5×10^–4ml/min/g. Choroid plexus permeability to⁶⁵Zn was about 12 fold greater, although Zn influx to brain via this route was <5% that across cerebral capillaries. The autoradiographic distribution of⁶⁵Zn in brain showed regional variation with lowest levels in white matter and high levels in the dentate gyrus and hippocampus.     

Effect of excess dietary histidine on rate of turnover of65Zn in brain of rat

The effect of the chronic administration of histidine on the brain zinc level was examined in growing, male Wistar rats. Using a purified diet, the minimum zinc requirement for normal growth and normal plasma and tissue zinc levels was found to be around 10 ppm. Given this zinc content; the diet was supplemented with 5% and 8% histidine, respectively, or with 10% glycine (as control). Brain zinc was analyzed by measuring the rate of turnover of⁶⁵Zn from 2–4 weeks after a single injection of the tracer. Feeding the diet supplemented with 5% histidine caused a small decrease in the plasma zinc concentration and a slight increase in the rate of turnover of⁶⁵Zn in the cerebrum and the cerebellum as compared to the control group. The animals fed the diet supplemented with 8% histidine became severely zinc deficient (as evidenced by a 50% reduction in the plasma zinc content), however, the rate of turnover of⁶⁵Zn in all brain regions examined was significantly decreased as compared to the control group. The results indicate that histidine has no specific complexing action on the brain zinc.     

Effects of increased pCO2 on zinc uptake and calcification in the tropical coral Stylophora pistillata

Zinc (Zn) is an essential element for corals. We investigated the effects of ocean acidification on zinc incorporation, photosynthesis, and gross calcification in the scleractinian coral Stylophora pistillata. Colonies were maintained at normal pH_T (8.1) and at two low-pH conditions (7.8 and 7.5) for 5 weeks. Corals were exposed to ⁶⁵Zn dissolved in seawater to assess uptake rates. After 5 weeks, corals raised at pH_T (8.1) exhibited higher ⁶⁵Zn activity in the coral tissue and skeleton, compared with corals raised at a lower pH. Photosynthesis, photosynthetic efficiency, and gross calcification, measured by ⁴⁵Ca incorporation, were however unchanged even at the lowest pH.     

Role of MMP-2 in PKCδ-mediated inhibition of Na+ dependent Ca2+ uptake in microsomes of pulmonary smooth muscle: Involvement of a pertussis toxin sensitive protein

Treatment of bovine pulmonary artery smooth muscle with the O₂^•− generating system hypoxanthine plus xanthine oxidase stimulated MMP-2 activity and PKC activity; and inhibited Na⁺ dependent Ca²⁺ uptake in the microsomes. Pretreatment of the smooth muscle with SOD (the O₂^•− scavenger) and TIMP-2 (MMP-2 inhibitor) prevented the increase in MMP-2 activity and PKC activity, and reversed the inhibition of Na⁺ dependent Ca²⁺ uptake in the microsomes. Pretreatment with calphostin C (a general PKC inhibitor) and rottlerin (a PKCδ inhibitor) prevented the increase in PKC activity and reversed O₂^•− caused inhibition of Na⁺ dependent Ca²⁺ uptake without causing any change in MMP-2 activity in the microsomes of the smooth muscle. Treatment of the smooth muscle with the O₂^•− generating system revealed, respectively, 36 kDa RACK-1 and 78 kDa PKCδ immunoreactive protein profile along with an additional 38 kDa immunoreactive fragment in the microsomes. The 38 kDa band appeared to be the proteolytic fragment of the 78 kDa PKCδ since pretreatment with TIMP-2 abolished the increase in the 38 kDa immunoreactive fragment. Co-immunoprecipitation of PKCδ and RACK-1 demonstrated O₂^•− dependent increase in PKCδ-RACK-1 interaction in the microsomes. Immunoblot assay elicited an immunoreactive band of 41 kDa G_iα in the microsomes. Treatment of the smooth muscle tissue with the O₂^•− generating system causes phosphorylation of G_iα in the microsomes and pretreatment with TIMP-2 and rottlerin prevented the phosphorylation. Pretreatment of the smooth muscle tissue with pertussis toxin reversed O₂^•− caused inhibition of Na⁺ dependent Ca²⁺ uptake without affecting the protease activity and PKC activity in the microsomes. We suggest the existence of a pertussis toxin sensitive G protein mediated mechanism for inhibition of Na⁺ dependent Ca²⁺ uptake in microsomes of bovine pulmonary artery smooth muscle under O₂^•− triggered condition, which is regulated by PKCδ dependent phosphorylation and sensitive to TIMP-2 for its inhibition. (Mol Cell Biochem xxx: 107–117, 2005)     

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 of⁶⁵Zn in anesthetized rats were studied. Infusion ofl-histidine at a rate sufficient to raise plasma concentrations to approximately 2mm for 6h starting 48 h after a single intraperitoneal⁶⁵Zn injection did not alter⁶⁵Zn activities in a variety of tissues when compared with anesthetized uninfused animals. However, plasma⁶⁵Zn and erythrocyte⁶⁵Zn were decreased, and liver⁶⁵Zn was increased. If⁶⁵Zn 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 plasma⁶⁵Zn levels was increased when allowance was made for the more rapid fall in plasma⁶⁵Zn during histidine infusion. Similar infusions ofd-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.     

Influence of Zinc on the Biokinetics of 65Zn in Brain and Whole Body and Its Bio-distribution in Aluminium-Intoxicated Rats

The present study was designed to understand the influence of zinc (Zn) if any, on the biokinetics of ⁶⁵Zn in brain as well as whole body and its bio-distribution following aluminium (Al) treatment to rats. Male Sprague–Dawley rats weighing 140–160 g were divided into four different groups viz: normal control, aluminium treated (100 mg/kg b.wt./day via oral gavage), zinc treated (227 mg/L in drinking water) and combined aluminium and zinc treated. All the treatments were carried out for a total duration of 8 weeks. Al treatment showed a significant increase in fast component (Tb₁) but revealed a significant decrease in slow component (Tb₂) of biological half-life in brain as well as in whole body. However, Zn supplementation to Al-treated rats reversed the trend in both brain and whole body, which indicates a significant decrease in Tb₁ component while the Tb₂ component was significantly increased. Further, Al treatment showed an increased percent uptake value of ⁶⁵Zn in cerebrum, cerebellum, heart, liver and lungs whereas a decrease in uptake was found only in blood. On the other hand, there was a significant decline in ⁶⁵Zn activity in nuclear and mitochondrial fractions of brain of Al-treated rats. However, Zn treatment reversed the altered ⁶⁵Zn uptake values in different organs as well as in various subcellular fractions. The study demonstrates that Zn shall prove to be effective in regulating the biokinetics of ⁶⁵Zn in brain and whole body and its distribution at the tissue and subcellular levels in Al-treated rats.     

Uptake and translocation of zinc absorbed through roots and fruiting organs in peanuts

Peanut plants (Arachis hypogaea L.) are known to absorb Ca, P and S through the fruiting organs, but information on Zn uptake pattern is lacking. Therefore, a green-house experiment was conducted to study the uptake and translocation of Zn when applied in the rooting and fruiting zones of peanut plants. To locate the pathway and distribution of radioactive Zn, autoradiographs of plants were also taken.Zinc uptake data and autoradiographs indicated that a substantial amount of⁶⁵Zn was absorbed through the fruiting organs (auxillary system). Of the total⁶⁵Zn in the whole plant, 55.2 per cent was absorbed through roots and remaining 44.8 per cent through fruiting organs. Zinc was translocated to all the plant parts regardless of its absorption through roots or fruiting organs. The highest zinc concentration was recorded in the kernels, followed by leaves, stem and the shell.Contribution from the Department of Soils, Haryana Agric. Univ., Hissar-India.     

Uptake and transport of foliar applied zinc (65Zn) in bread and durum wheat cultivars differing in zinc efficiency

Using two bread wheat (Triticum aestivum) and two durum wheat (Triticum durum) cultivars differing in zinc (Zn) efficiency, uptake and translocation of foliar-applied ⁶⁵Zn were studied to characterize the role of Zn nutritional status of plants on the extent of phloem mobility of Zn and to determine the relationship between phloem mobility of Zn and Zn efficiency of the used wheat cultivars. Irrespective of leaf age and Zn nutritional status of plants, all cultivars showed similar Zn uptake rates with application of ⁶⁵ZnSO₄ to leaf strips in a short-term experiment. Also with supply of ⁶⁵ZnSO₄ by immersing the tip (3 cm) of the oldest leaf of intact plants, no differences in Zn uptake were observed among and within both wheat species. Further, Zn nutritional status did not affect total uptake of foliar applied Zn. However, Zn-deficient plants translocated more ⁶⁵Zn from the treated leaf to the roots and remainder parts of shoots. In Zn-deficient plants about 40% of the total absorbed ⁶⁵Zn was translocated from the treated leaf to the roots and remainder parts of shoots within 8 days while in Zn-sufficient plants the proportion of the translocated ⁶⁵Zn of the total absorbed ⁶⁵Zn was about 25%. Although differences in Zn efficiency existed between the cultivars did not affect the translocation and distribution of ⁶⁵Zn between roots and shoots. Bread wheats compared to durum wheats, tended to accumulate more ⁶⁵Zn in shoots and less ⁶⁵Zn in roots, particularly under Zn-deficient conditions. The results indicate that differences in expression of Zn efficiency between and within durum and bread wheats are not related to translocation or distribution of foliar-applied ⁶⁵Zn within plants. Differential compartementation of Zn at the cellular levels is discussed as a possible factor determining genotypic variation in Zn efficiency within wheat.