Distribution Of 65Zn Research Articles

Effects of ingested nanomaterials on tissue distribution of co-ingested zinc and iron in normal and zinc-deficient mice

Cellulose nanofibers (CNF) reduced serum triglyceride levels in rats when co-administered with heavy cream by gavage. Do CNF and other nanomaterials (NMs) alter the tissue distribution and retention of co-administered metal ions? We evaluated whether 5 different NMs affected tissue distribution of co-ingested 65Zn++ and 59Fe+++ in zinc-replete versus zinc-deficient mice. Male C57BL/6J mice were fed either zinc-replete or zinc-deficient diets for 3 weeks, followed by gavage with NM suspensions in water containing both 65ZnCl2 and 59FeCl3. Urine and feces were measured for 48 h post-gavage. Mice were euthanized and samples of 22 tissues were collected and analyzed for 65Zn and 59Fe in a gamma counter. Our data show that zinc deficiency alters the tissue distribution of 65Zn but not of 59Fe, indicating that zinc and iron homeostasis are regulated by distinct mechanisms. Among the tested NMs, soluble starch-coated chitosan nanoparticles, cellulose nanocrystals, and TiO2 reduced Zn and Fe tissue retention in zinc-deficient but not in zinc-replete animals.

Accumulation, distribution and redistribution of 109Cd and 65Zn in wheat (Triticum aestivum L.) and bean (Phaseolus vulgaris L.) plants on nutrient media with elevated zinc or cadmium

Accumulation, distribution and redistribution of 109Cd and 65Zn in wheat (Triticum aestivum L.) and bean (Phaseolus vulgaris L.) plants on nutrient media with elevated zinc or cadmium

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.

Selective uptake, distribution, and redistribution of 109Cd, 57Co, 65Zn, 63Ni, and 134Cs via xylem and phloem in the heavy metal hyperaccumulator Solanum nigrum L

The focus of this article was to explore the translocation of (109)Cd, (57)Co, (65)Zn, (63)Ni, and (134)Cs via xylem and phloem in the newly found hyperaccumulator Solanum nigrum L. Two experiments with the uptake via the roots and transport of (109)Cd, (57)Co, and (65)Zn labeled by roots, and the redistribution of (109)Cd, (65)Zn, (57)Co, (63)Ni, and (134)Cs using flap label in S. nigrum in a hydroponic culture with a standard nutrient solution were conducted. The results showed that (109)Cd added for 24h to the nutrient medium of young plants was rapidly taken up, transferred to the shoot, and accumulated in the cotyledons and the oldest leaves but was not efficiently redistributed within the shoot afterward leading to a rather low content in the fruits. In contrast, (57)Co was more slowly taken up and released to the shoot, but afterward, this element was redistributed from older leaves to younger leaves and maturing fruits. (65)Zn was rapidly taken up and transferred to the shoot (mainly to the youngest leaves and not to the cotyledons). Afterward, this radionuclide was redistributed within the shoot to the youngest organs and finally accumulated in the maturing fruits. After flap labeling, all five heavy metals tested ((109)Cd, (57)Co, (65)Zn, (63)Ni, (134)Cs) were exported from the labeled leaf and redistributed within the plant. The accumulation in the fruits was most pronounced for (63)Ni and (65)Zn, while a relatively high percentage of (57)Co was finally found in the roots. (134)Cs was roughly in the middle of them. The transport of (109)Cd differed from that previously reported for wheat or lupin and might be important for the potential of S. nigrum to hyperaccumulate cadmium.

Regulatory Role of Zinc on the Biokinetics and Biodistribution of 65Zn During the Initiation of Experimentally Induced Colon Cancer

The present study was conducted to evaluate the kinetics of zinc utilization during the formation of colon carcinoma in an animal model of colon carcinogenesis. The rats were segregated into 4 groups: untreated control, 1,2 dimethylhydrazine (DMH) treated, zinc treated, and DMH+zinc treated. Colon carcinogenesis was initiated through weekly subcutaneous injections of DMH (30 mg/kg body weight) for 8 wk. Zinc (in the form of zinc sulphate) was supplemented at a dose level of 227mg/L in drinking water, ad libitum for the entire duration of study. Whole body 65Zn kinetics followed two-compartment kinetics, with Tb1 representing the initial fast component of the biological half-life and Tb2, the slower component. The Tb1 component showed a significant elevation while the Tb2 component was significantly diminished in DMH-treated rats, which, however, got normalized following zinc supplementation. The biodistribution and subcellular distribution of 65Zn was significantly affected in DMH-treated rats when compared to normal control rats. However, zinc significantly reversed the altered 65Zn uptake in different organs and various fractions of colon. The present study for the first time demonstrated a faster mobilization of zinc during initiation of experimentally induced colon carcinoma and provides a physiological basis for the role of zinc in colon tumorigenesis.

Polaprezinc, a zinc compound, is distributed to the lingual epithelium and increases its zinc concentration in zinc-deficient rats

Aims To clarify the mechanism underlying the effect of polaprezinc on hypogeusia, we investigated the uptake of polaprezinc by the tongue in rats. Main methods Rats were fed a zinc-sufficient (Zn(+)) or zinc-deficient (Zn(−)) diet. After 4 weeks on the Zn(−) diet, polaprezinc (1, 3, or 10 mg/kg) or [ 65Zn] polaprezinc (10 mg/kg) was administered orally once a day. The zinc concentration or the 65Zn radioactivity of the tongue was measured by inductively-coupled plasma mass spectrometry or gamma counting, respectively. In addition, the distribution of 65Zn in the tongue was analyzed by microautoradiography and the proliferative activity of taste bud cells was measured from the uptake of 5-bromo-2′-deoxyuridine. Key findings The zinc concentration of the lingual epithelium, but not the whole tongue, was markedly decreased in Zn(−) rats compared with Zn(+) rats. After administration of polaprezinc to Zn(−) rats at doses of 1, 3, and 10 mg/kg, the zinc concentration in the lingual epithelium increased significantly from 85 ± 4 to 105 ± 7 ( p < 0.05), 120 ± 3 ( p < 0.001), and 124 ± 3 ( p < 0.001) µg/g, respectively. After administration of [ 65Zn] polaprezinc, the 65Zn radioactivity of the tongue and serum were higher in Zn(−) rats than in Zn(+) rats. 65Zn was mainly detected in the epithelium on microautoradiograms of the tongue in Zn(−) rats. In addition, polaprezinc (3 and 10 mg/kg) improved the reduced proliferation of taste bud cells due to zinc deficiency. Significance Polaprezinc is distributed to the lingual epithelium and restores its zinc concentration in Zn(−) rats resulting in improvement of cellular functions, especially proliferation.

Biokinetics and dose estimation of 65Zn in the salivary gland and male reproductive organs

ICRP is revising its recommendations for radiological protection and has added salivary and secretory glands as new target organs. However, little information is available on the distributions of radionuclides in the salivary gland, secretory glands and male reproductive organs. This study deals with the distribution of 65Zn in the salivary gland and male reproductive organs as a function of time after a single intravenous and oral administration. For the study, 64 Wistar strain male rats, eight weeks of age were used. The rats were periodically sacrificed, the liver, kidney, spleen, pancreas, thymus, salivary gland, testis, epididymitis and prostate gland sampled and the radioactivity of these organs measured with an NaI scintillation counter. The relative concentration of 65Zn was highest in the prostate gland. We estimated the radiation dose in humans using rat data for the salivary and secretory glands as well as reproductive organs after intake of 65Zn.

Effect of Zinc on Biological Half-Lives of &lt;SUP&gt;65&lt;/SUP&gt;Zn in Whole Body and Liver and on Distribution of &lt;SUP&gt;65&lt;/SUP&gt;Zn 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.

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.

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.

Repeated administration of alpha-hederin results in alterations in maternal zinc status and adverse developmental outcome in the rat.

The administration of alpha-hederin, an inducer of metallothionein, results in a secondary zinc deficiency that may be an important maternally mediated mechanism of developmental toxicity. Previous studies have shown adverse developmental outcome with a single administration of alpha-hederin to rats on gestation day (GD) 8 or 11. The objective of this study was to determine whether dosing of alpha-hederin throughout organogenesis would result in a sustained elevation of maternal hepatic metallothionein and subsequent developmental abnormalities. Rats were administered dosage levels of 0 (vehicle only), 20, or 30 mumol/kg from GD 6-15. Maternal hepatic metallothionein levels were 10-fold higher on GD 16 in the treatment groups than the controls. Consequently, liver zinc concentrations increased 60% and 54%, whereas plasma levels decreased 23% and 33% in the 20 and 30 mumol/kg treatment groups, respectively. At GD 20, mean fetal weights of the treatment litters were 11% less than control litters. The administration of alpha-hederin resulted in a threefold increase in the number of offspring that exhibited developmental abnormalities, including visceral and skeletal malformations. Following an oral pulse of 65Zn subsequent to treatment with 0 or 20 mumol/kg of alpha-hederin, the distribution of 65Zn to the liver of treated dams was twice that of controls, whereas the radiolabeled zinc apportioned to the decidua and uterus decreased by 44%. Furthermore, the 65Zn detected in the embryos from treated dams was 70% lower than in embryos from control dams. In conclusion, low doses of a metallothionein inducer administered to the dam from GD 6-15 resulted in a sustained elevation of hepatic metallothionein and a subsequent redistribution of zinc leading to a decrease in the zinc available to the embryo and ultimately to adverse development of the offspring. Repeated dosing throughout organogenesis, as required in regulated safety assessment testing, increased the severity of the effects previously observed with single large dosages of the toxicant administered during midgestation.

Zinc distribution in the brain of Nagase analbuminemic rat and enlargement of the ventricular system

65ZnCl 2 was intravenously injected into Nagase analbuminemic rats (NAR), which have a genetical mutation affecting albumin mRNA processing and lack serum albumin, to test the hypothesis that albumin is necessary for zinc (Zn) transport into the brain. One hour after injection, 65Zn was largely concentrated in the choroid plexus of NAR as well as normal parental Sprague–Dawley rats (SDR). Six days after injection, in both groups, the 65Zn concentration in the choroid plexus decreased, with increases in other brain regions. The finding that there was no significant difference in brain distribution of 65Zn between NAR and SDR suggests that Zn transport into the brain and its distribution through the blood–cerebrospinal fluid barrier as well as the blood–brain barrier are not dependent on serum albumin. A most interesting observation was that the cerebral ventricles were considerably enlarged in NAR.

Zinc transport in the rat olfactory system

To study zinc (Zn) mobility in the rat olfactory tract, brain distribution of 65Zn after injection into the olfactory bulb or amygdaloid nuclei was analyzed by autoradiography. Twenty-four hours after 65Zn injection into the olfactory bulb, 65Zn was distributed in the ipsilateral piriform cortex, amygdaloid nuclei and the anterior commissure. Moreover, in the case of injection of a higher level of 65Zn into the olfactory bulb, 65Zn was distributed in the ipsilateral entorhinal cortex in addition to the above regions. Twenty-four hours after 65Zn injection into the amygdaloid nuclei, 65Zn was distributed in the ipsilateral piriform and entorhinal cortex. These results suggest that Zn is intraneuronally transported along the olfactory tract. Zn may be taken up by the piriform neurons after release from the secondary olfactory neuron terminals and transported to the entorhinal area.

Biokinetics and dosimetry of chromium, cobalt, hydrogen, iron and zinc radionuclides in male reproductive tissues of the rat

. Following intravenous administration to male rats, the uptake and retention by reproductive tissues of chromium-51, cobalt-57, iron-59, zinc-65 and tritium has been studied for up to 28 days. Chromium-51, 57Co, 59Fe and 3H were not or only transiently accumulated in gonads or accessory sex glands at concentrations greater than whole body concentrations. However, 65Zn was concentrated in the dorsolateral region of the prostate gland and autoradiography showed preferential uptake by epithelial cells and lumen of glands. When combined with other information available from the literature, this data would suggest that current models adequately describe the biokinetics of chromium, cobalt, iron and tritium in the prostate and testes and zinc in the testes. Uptake of zinc by the prostate would appear to be best described by an average value of 0.1% and a conservative value of 0.5%. Allowing for greater uptake of zinc (0.5%) by the prostate, after inhalation of 65Zn in a soluble form, increases prostate dose by about 3 fold compared to current models. The pessimistic assumptions of a higher relative biological effectiveness (20) for all Auger emissions from 65Zn in cell nuclei and a heterogeneous distribution of 65Zn to sensitive cells in the prostate increases prostate dose by a further factor of 9. Even on the basis of these cautious estimates, occupational exposures to radioisotopes of these elements do not explain the excess of prostate cancer reported amongst some nuclear workers.

Differential transport of Zn, Me and sucrose along the longitudinal axis of developing wheat grains

The hypothesis that Zn and Mn are transported within the grain in a similar manner to sucrose was investigated in the developing wheat grain. Detached ears were cultured in solution containing 65Zn, 54Mn and [14C]‐sucrose for 10 to 120 min at 18–22 days post‐anthesis. At different times the grain was cut transversely into 1‐mm sections and the radioactivity in each section determined The embryo region was damaged in some grains to investigate the effect of reduced accumulation rate on the transport of 65Za, 54Mn and [14C]‐sucrose to the embryo. The distribution of 65Zn. 54Mn and [14C]‐sucrose between the endosperm cavity sap. endosperm, embryo and pericarp in grains labelled for 2.5 and 6 h at 18–22 days post‐anthesis was also determined. [14C]‐su‐crose was initially high in the first, embryo‐containing section of the grain but decreased progressively to the distal end of the grain. The amount of 65Zn along the longitudinal axis of the grain was distributed evenly in each 1‐mm section, whilst 54Mn accumulated exponentially in the first proximal 1‐mm section of the grain and was distributed evenly in the remaining sections. Damaging the embryo had no effect on 65Zn and 54Mn transport to the section containing the embryo. The pericarp contained almost all of the grain 65Za and 54Mn, with small amounts found in the embryo, endosperm and endosperm cavity sap. Increasing amounts of [14C]‐sucrose were found in the endosperm as time progressed. The rate of accumulation of 65Zn, 54Mn and [14C]‐sucrose was much higher in the embiyo than the endosperm: the difference between the embryo and endosperm was especially large for 65Zn and 54Mn. It is suggested that 65Zn and 54Mn are not transported within the grain in the same way as [14C]‐sucrose. [14C]‐sucrose moves laterally out of the vascular system of the crease into the endosperm cavity and is subsequently taken up and stored in the endosperm. In contrast, 65Zn and 54Mn appear to be retained within the vascular system of the crease and may be transported more slowly to grain parts such as the embryo and pericarp tissue.

Biological half-lives of zinc and manganese in rat brain

The brains of rats injected intravenously with 65ZnCl 2 or 54MnCl 2 were subjected to high-resolution autoradiography. The distribution of 65Zn and 54Mn in each brain region gradually decreased from 6 days to 42 days for 65Zn and from 15 days to 60 days for 54Mn after the injection. The biological half-lives of Zn in each region studied were in the range of 16–43 days; the longest was observed in the amygdaloid nuclei. The regions where the long biological half-life was observed were consistent with the ones with the high density of Zn-containing neuron terminals reported previously. The biological half-lives of Mn in each region determined were 51–74 days; the longest were those in the hypothalamic nuclei and thalamus.

Decreased zinc absorption in guinea pig models of acute and chronic ileitis

The biochemical defects underlying decreased Zn absorption in inflammatory bowel disease have not been identified. In vitro studies have suggested that reactive oxygen species (e.g., hypochlorous acid and superoxide), produced by phagocytic cells during the inflammatory response, mobilize Zn from metallothionein (MT) and other proteins that bind Zn via sulfhydryl groups. We avaluated the in vivo effects of intestinal inflammation on Zn absorption and Zn binding to intestinal MT and cysteine-rich intestinal protein (CRIP), possible components of a carrier-mediated intestinal Zn transport system. Guinea pig models of acute (NaOCl luminal perfusion) and chronic (2,4,6-trinitrobenzene sulfonic acid [TNBS] injection) ileitis were used. The rate of 65Zn absorption from the isolated ileum and the molecular distribution of 65Zn in mucosal cytosol determined by size-exclusion HPLC were measured after 1 hr of perfusion in the acute model and after 7 days in the chronic model. Zinc absorption was significantly lower in guinea pigs with either chronic or acute inflammation. In both models, decreased binding of 65Zn to MT and CRIP was also observed. The results indicate that decreased Zn absorption during intestinal inflammation may be mediated by the effects of oxidants on the transport activity of intestinal proteins that bind Zn via sulfhydryl groups.

Role of Metallothionein and Cysteine-Rich Intestinal Protein in the Regulation of Zinc Absorption by Diabetic Rats

Hyperzincuria and low Zn absorption in diabetic animals and humans have prompted speculation that diabetics are more susceptible to Zn deficiency. There is little information, however, describing the effects of diabetes on the biochemical mechanisms of intestinal Zn transport. We evaluated Zn absorption in streptozotocin-induced diabetic rats based on a model of Zn transport in which cysteine-rich intestinal protein serves as an intracellular carrier that is inhibited by metallothionein (MT). Apparent absorption and retention of Zn and Cu in rats fed a purified diet were measured in a balance study 15-17 d after induction of diabetes. The rate of 65Zn absorption from isolated intestinal segments, molecular distribution of 65Zn in mucosal cytosol, and tissue MT levels were measured on d 20-22. Food consumption, and thus Zn and Cu intake, by diabetic rats was twice that of controls. Although fractional absorption (percent) of Zn and Cu was lower in the diabetic rats, net absorption (micrograms/100 g body weight/d) was higher. The higher net absorption in the diabetic group was offset, however, by higher urinary excretion, so that Zn and Cu retention was similar in both groups of animals. Low fractional absorption is attributable to the down-regulation of intestinal Zn transport, as indicated by the lower rate of 65Zn absorption from isolated intestinal segments in the diabetic rats. Down-regulation of intestinal transport is in turn attributable to higher concentrations of intestinal MT, which resulted in more 65Zn in the mucosal cytosol bound to MT, an inhibitor of Zn transport, and less to cysteine-rich intestinal protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential hepatic response of 65Zn distribution between mice bearing experimental tumor and inflammation

Discriminative detection of tumor and inflammation was tried by radio-imaging of hepatic uptake of 65Zn. This closely related to the level of metallothionein (MT) and reflected the extent of tumor growth in mice and rats transplanted with experimental tumor. The elevation of 65Zn distribution in liver of experimental tumor-bearing mice was inhibited by treatment with Zn-deficient diet, while stimulated by dexamethasone. This stimulation occurred 2 days after tumor transplantation, at which time 67Ga-citrate could not image the tumor. On the other hand, hepatic distribution of 65Zn was also elevated in mice by inducing experimental abscess, although the effect of both treatments on this elevation was different from the case of tumor; the elevation was inhibited by treatment with dexamethasone. These results suggest that radio-imaging of hepatic Zn uptake with a short-life gamma emitting isotope such as 69mZn with use of dexamethasone, if required, may be useful for a preliminary test to detect early-stage malignant disease.

Effect of hypoxia and exercise on the distribution of 65Zn in rat muscles

The aim of this study was to determine the influence of hypoxia and exercise in 65Zn distribution in various rat muscles. A total of 80 male wistar rats weighing 250 ± 10 g were randomly separated into eight groups: four groups in air, two at rest, and the other two after exercise; four groups in hypoxia (3 days exposure), two at rest, and the other two after exercise. Two groups ( n = 10) in air and two other groups under hypoxia were injected with 65Zn. The 65Zn uptake by blood, pH, and PaO 2 decreased significantly during hypoxia. The Zn concentration increased significantly in serum, diaphragm, gastrocnemius, and heart Zn after exercise in air. After hypoxia, at rest, Zn increased in serum and in diaphragm. After chronic hypoxia, at rest, radioactivity of 65Zn increased in heart, gastrocnemius, and bone, and it was similar in air condition after exercise with respect to rest. In both cases (air and hypoxia), the uptake of 65Zn by the tissues was higher at rest. After exercise in hypoxia, endogenous Zn decreased in heart and in diaphragm.