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PubMed2001

The effect of prenatal indium chloride exposure on chondrogenic ossification.

Daily indium chloride doses of control (0) or 400 mg/kg were administered orally to pregnant Sprague-Dawley (SD) rats by gavage, on d 20 of gestation. Indium concentration was determined in the maternal and fetal blood, livers, kidneys, skulls, and femurs by atomic absorption spectrometry. Further groups of pregnant rats were treated with control (0) or 400 mg/kg indium chloride orally, during the whole gestation period. The fetuses were examined on d 21 of gestation, using histological and histochemical methods. Four hours after the administration indium concentration was found to be significant in the blood, liver, and kidneys of the dams. Twenty-four hours later it increased in the blood but not in the liver and kidney. Fetal indium concentrations were 40-50% of the maternal levels due to a barrier of the placenta. In the skull and the femur, indium was already detectable at 4 h after the administration, and by the end of 24 h, metal concentration was several times higher than that at 4 h, indicating accumulation. Furthermore, it was found that the birefringency of collagen detectable by picrosirius red staining in polarized light around the chondrocytes disappeared and became irregular. In the matrix of the epiphyseal cartilage, the regular, birefringent network demonstrable by Rivanol reaction became irregular and hardly recognizable. In the cytoplasm of the chondrocytes, the diffuse, evenly distributed positive Ricinus communis agglutinin reaction became irregular or disappeared. Similar but much weaker changes were observed with concanavalin A and wheat germ agglutinin stainings. It was concluded that the missing femur and micromelia diagnosed by alizarin staining is the consequence of a specific toxic effect of indium that inhibits chondrogenic ossification. No similar histochemical changes were observed in the bones of the skull developing by desmogenic ossification, despite the presence of indium. Data indicate that the mechanisms of the effects of indium causing retardation and/or malformation differ in the bones developing through desmogenic or chondrogenic ossification.

Animals↗
PubMed1990

Pharmacokinetics of indium-111-labeled antimyosin monoclonal antibody in murine experimental viral myocarditis.

The pharmacokinetics of indium-111-labeled antimyosin monoclonal antibody Fab were investigated with use of murine experimental viral myocarditis as a model. The biodistribution of indium-111-labeled antimyosin antibody Fab on days 3, 5, 7, 14, 21 and 28 after encephalomyocarditis virus inoculation demonstrated that myocardial uptake increased significantly on days 5, 7 and 14 (maximum on day 7) in infected versus uninfected mice (p less than 0.001). In vivo kinetics in infected mice on day 7 demonstrated that the heart to blood ratio reached a maximum 48 h after the intravenous administration of indium-111-labeled antimyosin Fab, which was considered to be the optimal time for scintigraphy. The scintigraphic images obtained with indium-111-labeled antimyosin Fab demonstrated positive uptake in the cardiac lesion in infected mice. The pathologic study demonstrated that myocardial uptake correlated well with pathologic grades of myocardial necrosis. High performance liquid chromatography revealed the presence of an antigen-antibody complex in the circulation of infected mice after the injection of indium-111-labeled antimyosin Fab. This antigen bound to indium-111-labeled antimyosin Fab in the circulation might be whole myosin and this complex may decrease myocardial uptake and increase liver uptake. It is concluded that indium-111-labeled antimyosin monoclonal antibody Fab accumulates selectively in damaged heart tissue in mice with acute myocarditis and that indium-111-labeled antimyosin Fab scintigraphy may be a useful method for the visualization of acute myocarditis.

Animals↗
PubMedDate not supplied

Effect of admixed indium on the clinical success of amalgam restorations.

The purpose of this study was to clinically evaluate two formulations of a dispersed-phase, high-copper dental amalgam alloy (Indisperse), which contained admixed indium. One alloy tested contained 5% indium, and the second alloy contained 10% indium. A similar alloy without indium, Dispersalloy, was also placed for comparison. Over the course of the five-year study, there were no differences clinically or statistically regarding texture and luster. The margins of the restorations containing indium incurred slightly less fracture than the non-indium-containing restorations; however, these differences were not clinically significant. It can be concluded that the admixture of 5-10% indium as well as the increased ratio of eutectic spheres to lathe-cut particles found in the indium alloys enhance the clinical performance of amalgam restorations.

Dental Amalgam↗
PubMed1996

Effects of indium and iron ions on in vitro calcium phosphate precipitation and crystallinity.

The elution characteristics of indium and iron ions from six kinds of dental casting alloys were studied in vitro. A certain amount of indium (0.01-1.70 mg/cm2) was solubilized from the surface of only one prosthetic semiprecious brand (Miro Bright) in either 1% lactic acid or 0.05% hydrochloric acid solutions. The elution of iron was below the detection limit or < 0.01 mg/cm2. We also studied the stimulatory effects of indium and ferric ions on the calcium phosphate precipitation in the absence and presence of an inhibitor (phosvitin, a phosphoprotein purified from egg yolks). Indium and ferric ions promoted the reaction, and their stimulatory effects were stronger than the inhibitory effects of phosvitin (250 micrograms/ml). These facts suggest that indium, but not iron, could be eluted into the mouth, and that the eluted indium may stimulate the formation of oral calcium phosphate precipitates, counteracting the inhibition by saliva-derived phosphoproteins. The effects of these metal ions on calcium phosphate precipitates were also studied using both X-ray diffractometry and infrared spectrophotometry. It was shown that both indium and ferric ions decreased the grade of crystallinity of the calcium phosphate precipitates (hydroxyapatite).

Chelating Agents↗
PubMed1994

Enzyme immunoassay to determine heavy metals using antibodies to specific metal-EDTA complexes: optimization and validation of an immunoassay for soluble indium.

An immunoassay that measures soluble indium at concentrations from 0.005 ppb to 320 ppm is described. The assay utilized a monoclonal antibody that binds specifically to indium-EDTA complexes in an antigen-inhibition format. The sensitivity of the assay could be modulated by changing the nature of the soluble inhibiting antigen. The range of the assay was from 0.6 to 320 ppm, 0.1 to 120 ppm, or 0.005 to 2000 ppb when indium-EDTA, indium-(p-nitrobenzyl)-EDTA, or indium-EDTA-bovine serum albumin, respectively was used as the soluble inhibiting antigen. The assay reliably monitored indium concentration in the presence of a 100-fold excess of manganese, magnesium, or copper ions and the quantitation of indium by immunoassay correlated closely with the values obtained using atomic absorption spectroscopy. This technology could be employed in immunoassays for other metals that are priority pollutants.

Antibodies, Monoclonal↗
PubMed2003

Indium-111-Octreotide scintigraphy in differentiated thyroid carcinoma metastases that do not respond to treatment with high-dose I-131.

AIM: Differentiated thyroid cancer is characterized by a very good prognosis in the majority of the patients. The therapy of choice is surgery followed by ablation with Iodine-131 (I-131). However, some patients have metastases that have lost the capability of concentrating I-131, even when it is given in therapeutic doses. In the present study, we describe the value of Indium-111 Octreotide (Octreoscan) in differentiated thyroid cancer patients with increased Tg levels who failed to demonstrate a response to treatment with high-dose I-131. METHOD: Fifteen consecutive patients with progressive differentiated thyroid cancer (ten female, five male) (mean age: 59 years, range 13-81 years; eight papillary, six follicular, and one Hürthle cell carcinoma) were studied. Progression was based on increasing Tg levels and was confirmed by radiological evaluation. Whole body scintigraphy (WBS) was performed after the administration of 200 MBq of Indium-111-Octreotide. The images were assessed by two experienced observers and compared with post-treatment I-131 WBS. RESULTS: In seven out of 15 patients distant metastases were already present at initial stage, whereas in ten patients the primary tumor stage was T3 or T4 indicating that the majority of the patients had advanced disease. In two out of five patients with a positive I-131 WBS, Indium-111-Octreotide was false negative. In nine out of ten patients with a negative I-131 WBS, Indium-111-Octreotide demonstrated multiple metastases. In those patients with a positive SSR-scintigraphy, metastases were found in the lungs ( n=14), bone ( n=7), mediastinum ( n=3), liver ( n=2), brains ( n=1), and cutis ( n=1). Overall, three out of 15 patients had a negative Indium-111-Octreotide result revealing a sensitivity of 80%. CONCLUSION: Our findings demonstrate the diagnostic value of Indium-111-Octreotide in differentiated thyroid cancer that fails to respond to I-131 treatment. It opens the possibility for additional treatment with high doses of Indium-111-Octreotide or its analogs in a majority of the patients.

Adolescent↗
PubMed1987

Imaging of cardiac allograft rejection in dogs using indium-111 monoclonal antimyosin Fab.

The acute rejection of cardiac allografts is currently diagnosed by the presence of myocyte necrosis on endomyocardial biopsy. We evaluated the efficacy of noninvasive scintigraphic imaging with indium-111-labeled anticardiac myosin Fab fragments (indium-111 antimyosin) to detect and quantify cardiac allograft rejection. Six dogs that had intrathoracic heterotopic cardiac allograft transplantation were injected with indium-111 antimyosin and planar and single photon emission computed tomographic (SPECT) images were obtained in various stages of acute and subacute rejection. Four dogs had an allograft older than 8 months and had been on long-term immunosuppressive therapy; two dogs had an allograft less than 2 weeks old and were not on immunosuppressive therapy. Count ratios comparing heterotopic with native hearts were calculated from both SPECT images and in vitro scans of excised and sectioned hearts and were compared with the degree of rejection scored by an independent histopathologic review. Indium-111 antimyosin uptake was not visible in planar or SPECT images of native hearts. Faint diffuse uptake was apparent in cardiac allografts during long-term immunosuppression and intense radioactivity was present in hearts with electrocardiographic evidence of rejection. The heterotopic to native heart count ratios in SPECT images correlated significantly with the count ratios in the excised hearts (r = 0.93) and with the histopathologic rejection score (r = 0.97). The distribution of indium-111 antimyosin activity in right and left ventricles corresponded to areas of histopathologic abnormalities. Immunoperoxidase studies showed deposition of indium-111 antimyosin only in areas of myocyte necrosis. The results demonstrate that indium-111 antimyosin imaging can noninvasively detect the presence, location and severity of canine cardiac allograft rejection.

Animals↗
PubMed1990

Indium-111 labelled granulocyte scanning to detect inflammation in the lungs of patients with chronic sputum expectoration.

Thirty eight patients with chronic sputum expectoration underwent indium-111 labelled granulocyte lung scanning and measurement of whole body loss of indium-111 labelled granulocytes. Twenty four patients had radiologically proved bronchiectasis and 14 had mucus hypersecretion without radiological evidence of bronchiectasis. None was having an acute exacerbation at the time of the scan. The median 24 hour volume of sputum expectorated was 17 (range 2-175) ml. The 24 hour volume of purulent sputum was 5 (0-142) ml; six patients expectorated mucoid sputum only. Twenty one of the 38 patients had a positive granulocyte lung scan. All nine patients expectorating more than 20 ml purulent sputum in 24 hours had positive lung scans and all had lost more than 19% of the indium-111 from the body after five to seven days. Of the six patients with mucoid sputum, only one had a positive scan and these subjects lost only 6-11% of the indium-111 in five to seven days. The percentage loss of indium-111 from the body correlated with 24 hour purulent sputum volume (r = 0.41, n = 38, p less than 0.001) and total elastolytic activity in 24 hour sputum (r = 0.54, n = 14, p less than 0.01). The loss of indium-111 was not related to the extent of bronchiectasis when purulent sputum volume was allowed for. Indium-111 labelled granulocyte scanning provides a sensitive and objective method for detecting inflammation in the lungs and should help to improve understanding of chronic bronchial sepsis and possibly treatment in selected cases.

Adult↗
PubMed1992

Clinical evaluation of high-copper dental amalgams with and without admixed indium.

High-copper amalgam alloys containing 5% and 10% admixed indium, shown in previous studies to have improved properties and acceptable biological behavior, were evaluated in a clinical study designed to examine factors relating to clinical success. One hundred and seventy-five Class I and Class II amalgam restorations were placed in 25 patients. Each patient received all three dispersed-phase amalgams tested: without indium (Dispersalloy), with 5% indium (Indisperse 5), with 10% indium (Indisperse 10). After 30 months, 22 patients were recalled and 146 restorations evaluated. The margins of the indium-containing amalgam restorations incurred slightly less marginal breakdown, an effect that could be attributed to the addition of admixed indium and to the increase in silver-copper eutectic spheres which is found in these alloys. These amalgams also demonstrated a slightly darker appearance, and were slightly rougher than the non-indium-containing amalgam. These differences were minor; at 30 months, all restorations were well within the clinically acceptable range for each parameter evaluated.

Analysis of Variance↗
PubMed1987

Indium 111-labeled white blood cell scans after vascular prosthetic reconstruction.

The clinical value of indium 111-labeled white blood cell (WBC) scanning done after vascular graft procedures was investigated to differentiate noninfectious postoperative inflammation associated with graft incorporation from early prosthetic graft infection. Indium 111-labeled WBC scans were initially obtained in 30 patients before discharge from the hospital and during the subsequent follow-up period (334 days). Fourteen of 30 patients (47%) had normal predischarge scans that included all 10 patients who had grafts confined to the abdomen and 4 of 20 patients (20%) who had grafts arising or terminating at the femoral arteries (p less than 0.05). Sixteen of 30 patients (53%) discharged with abnormal initial indium 111 WBC scans underwent serial scanning until the scan normalized or a graft complication developed. All of the 16 patients had grafts involving the groin region. Abnormal indium 111 uptake in the femoral region continued for a mean 114 days without the development of prosthetic graft infections. The sensitivity of indium 111-labeled WBC scans for detecting wound complications was 100%, whereas the specificity was 50%. Thus, the accuracy of the test was only 53%. We conclude that (1) abnormal indium 111 WBC scans are common after graft operations involving the groin region but are unusual after vascular procedures confined to the abdomen, and (2) in the absence of clinical suspicion, the indium 111-labeled WBC scan does not reliably predict prosthetic graft infection because of the low specificity of the test in the early postoperative period.

Aged↗
PubMed1989

Indium selectively increases the cytochrome P-450 dependent O-dealkylation of coumarin derivatives in male mice.

Indium pretreatment of rats and mice has been reported to decrease the concentration of cytochrome P-450, thereby reducing the activity of some cytochrome P-450 dependent enzymatic reactions. The present study reveals that pretreatment of C57Bl/6JHan mice of both sexes with one s.c. dose of 120 mg of In2(SO4)3.5 H2O per kg of body weight decreases the concentration of cytochrome P-450 to about 65% of control levels. Neither cytochrome b5 nor NADPH-cytochrome P-450 reductase is affected. Hepatic microsomal ethoxyresorufin O-deethylase activity declines to about 75% of control values. In contrast, with coumarin substrates, a sex dependence in the direction of change is observed: in female mice indium decreases the activity to about 75%, whereas in males it enhances the activity to 140%. Moreover, with 7-(methoxy-14C)coumarin as substrate, indium-pretreated male mice exhale about 180% and females about 65% of 14CO2 compared to the corresponding controls. A close correlation between the in vivo and in vitro effects of indium on the metabolism of the coumarin derivatives is suggested. After isolation and purification of cytochrome P-450, SDS-PAGE indicates in indium-pretreated male mice an intensification of a 48.5 kDa protein band which is decreased in females. Immunological studies using antibodies raised against control female cytochrome P-450 show cross reactivity among all microsomes used in these experiments. High percentages of inhibition occur in microsomes with high molecular activity towards coumarin derivatives. The in vitro kinetics of antibody-inhibited O-deethylation of 7-ethoxycoumarin seems to obey a non- or partial-competitive type of inhibition. Indium pretreatment of mice produces sex-dependent effects on the metabolism of coumarin derivatives.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1992

Diagnosis of right ventricular acute myocardial infarction by dual isotope thallium-201 and indium-111 antimyosin SPECT imaging.

To assess the diagnostic value of indium-111 antimyosin for detecting right ventricular (RV) wall acute infarction, 30 patients with electrocardiographic-documented left ventricular inferior (posterior) wall acute myocardial infarction underwent simultaneous dual isotope indium-111 antimyosin and thallium-201 single-photon emission computed tomography (SPECT) within 2 days of admission. RV necrosis was defined as uptake of indium-111 antimyosin anterior and to the right of septal thallium uptake. Twenty-nine of the 30 patients (97%) had indium-111 antimyosin uptake in the inferior, posterior or lateral walls of the left ventricle and 14 of 30 (47%) had additional RV antimyosin uptake. Three different patterns of RV uptake of indium-111 antimyosin were observed: crescent-shaped, focal and apical. Twenty-seven patients underwent gated blood pool scanning before hospital discharge. Twelve of the 14 patients with RV antimyosin uptake had gated blood pool scintigraphy and 7 of 12 had RV dysfunction; 5 had normal RV function. Except for 1 patient who had questionable RV antimyosin uptake and had RV dysfunction, no patient without RV antimyosin uptake had RV dysfunction. In summary, right and left ventricular necrosis can be detected on tomographic images of indium-111 antimyosin uptake in patients with inferior infarctions when simultaneous uptake of a perfusion tracer, thallium-201, is imaged and used as an aid to reconstruction and anatomic localization.

Adult↗
PubMed1989

The potential unreliability of indium 111 oxine labeling in studies of endothelial cell kinetics.

The current widespread use of indium 111 oxine for labeling endothelial cells to study their interaction with various bioprosthetic flow surfaces presupposes a high retention of the radioisotope within the cell and a lack of significant adherence of any marker released from the cell to the surface under study. We measured the loss of indium 111 from freshly harvested, canine, venous endothelial cells, and their viability in cell culture, for varying intervals up to 24 hours. At prescribed intervals, aliquots of the radiolabeled endothelial cell suspension were centrifuged, and the supernatant was separated from the cell pellet. The relative radioactivity of each was measured in a gamma well counter and the spontaneous loss of marker from the endothelial cells was calculated. Spontaneous loss of indium 111 was 7.8% +/- 1.9% at 1 hour and 47.6% +/- 1.8% at 24 hours. Loss of activity was virtually constant between 14 and 24 hours. Endothelial cell viability was 80% at 24 hours. We next studied the in vitro affinity of indium 111 oxine and indium 111 transferrin for untreated expanded polytetrafluoroethylene vascular grafts and for similar grafts treated with two surfactants commonly used to increase the "wetability" of expanded polytetrafluoroethylene, a nonionic sufectant (Nonidet) and tridodecylmethylammonium chloride, and with two glycoproteins, fibronectin and basement membrane gel. A minimum of three graft segments were studied in each group. The affinity of graft material for indium 111, in both its oxine and transferrin complex, was significantly increased by treating the graft with a wetting agent, and it was further increased by the addition of a glycoprotein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Hemodynamic effect of indium chloride in pregnant rats.

Daily indium chloride doses of control (0) or 200 mg/kg were administered orally to pregnant Sprague-Dawley (SD) rats by gavage, on d 6-15 of gestation. On d 16 of gestation hemodynamic tests were performed; Arterial blood pressure, cardiac output (CO), and volume organ blood flow were determined with radioactive microspheres using the reference sample method (McDevitt & Nies, 1976). Indium chloride increased the cardiac index (CI), but did not change arterial blood pressure and total peripheral resistance (TPR). Indium decreased the organ fractions of the cardiac output to kidneys, ovaries, uterus, and placenta, while those to brain, lungs, and liver were not affected. In the placenta the blood flow was reduced significantly while the vascular resistance increased. The blood flow and vascular resistance did not change in the rest of the organs studied. The changes in arterial blood pressure, CO, Cl, TPR, organ fraction of cardiac output, blood flow, and vascular resistance in most of the organs displayed normal responsiveness to noradrenaline (NA) infusion. The reduction of uterine and placenta fractions and placental blood flow, produced by NA infusion were significantly greater in control than in the indium-treated group. Data indicate that the hemodynamic changes induced by indium are detrimental to the fetus. Indium chloride exposure modifies the maternal effect of noradrenaline such that there is maternal survival at the expense of fetal mortality.

Abnormalities, Drug-Induced↗
PubMed1996

Cell survival after Auger electron emission from stable intracellular indium exposed to monochromatic synchrotron radiation.

The biological effect of Auger electrons emitted from indium in V79 cells was investigated. K-shell vacancies were induced by synchrotron x-rays. Two energies, 100 eV above and below the K-edge of indium, were used. The cell survival for controls was similar to that which has been reported by others, with D37 = 4.4 Gy. Indium-oxine-labelled cells exhibited a survival clearly below that of the controls, D37 = 3.2 Gy, but no significant difference in survival between irradiations above and below the K-edge could be observed. The explanation is, inter alia, that the number of photons interacting with indium atoms incorporated into the cell, is small compared with the number of photons interacting with other atoms in the cell. The toxicity of indium oxine made it impossible to incorporate a sufficient number of indium atoms into the cells to observe a difference in this study. However, monoenergetic irradiation above and below the K-edge, provides a technique for the investigation of basic biological effects of Auger processes.

Animals↗
PubMed2000

Comparative developmental toxicity study of indium in rats and mice.

The developmental toxicity of indium was examined in both rats and mice using comparable experimental protocols. Pregnant rats received a single intravenous administration of indium trichloride (InCl(3)) at 0.4 mg In/kg, on day 9, 10, or 11 of pregnancy and their fetuses were examined on day 20. Pregnant mice were treated in the same manner at 0.8 or 1.6 mg In/kg on day 7, 8, or 9 of pregnancy and their fetuses were examined on day 18. In rats, indium caused fetal weight decrease and fetal gross malformations, such as brachyury, kinked tail, cleft palate, and oligodactyly, most severely by the administration on day 10. In mice, however, indium did not cause fetal gross malformations, although it caused fetal weight decrease at 0.8 mg In/kg or more and fetal death at 1.6 mg In/kg, most severely by the administration on day 8. It was concluded from these results that rats and mice were susceptible to the embryotoxicity of indium at similar developmental stages in the early organogenetic period, but mice were less susceptible to the teratogenicity of indium than rats in terms of gross malformation. Toxicokinetic factors may be involved in this different susceptibility. Teratogenesis Carcinog. Mutagen. 20:219-227, 2000.

Abnormalities, Drug-Induced↗
PubMed1989

Effects of transferrin-indium on cellular proliferation of a human leukemia cell line.

In previous studies, we have demonstrated that transferrin-gallium inhibits cellular proliferation by a mechanism whereby cellular iron utilization is impaired. Since indium, a similar class 3A metal, has not been well studied, we examined its effects on cellular iron uptake and cellular proliferation. In these studies, we provide evidence that indium, when bound to transferrin, has a 50-fold higher effect on inhibition of cellular proliferation than indium added as indium salt. Cells exposed to relatively low concentrations of transferrin-indium exhibit markedly increased transferrin receptor expression but, as with transferrin-gallium, these cells incorporate an inappropriately low amount of iron, suggesting that there is a defect in the release of internalized iron from transferrin. In further studies, we utilize a monoclonal antibody against transferrin receptor that inhibits transferrin-mediated iron uptake. This antibody exhibits a dose-related inhibition of cellular proliferation, and when both transferrin-indium and monoclonal antibody are added to media, there is a more than additive effect on inhibition of cellular proliferation.

Antibodies, Monoclonal↗
PubMed1987

Comparison of several indium-111 ligands in labeling blood cells: effect of diethylpyrocarbonate and CO2.

The effect of oxine sulfate, oxine sulfonate, tropolone, and Merc (2 mercaptopyridine-1-oxide) were compared with oxine, with respect to their capability of labeling blood cells when complexed to indium-111 (111In). Indium-111 oxine sulfate performed similarly to [111In]oxine with regard to cell labeling capability. Indium-111 oxine sulfonate had no labeling ability. Indium-111 tropolone and Merc were not superior to [111In]oxine as cell labeling agents. Carbon dioxide (CO2) and a CO2 generating compound, diethyl pyrocarbonate, dramatically improved the cell labeling ability in plasma of [111In]tropolone and Merc. In the case of oxine, this improvement was less distinct. Theoretical aspects of the CO2 cell labeling stimulating effect are discussed in terms of intra- and extracellular transferrin and lactoferrin iron (indium) binding capacity. Indium-111 tropolone behaved favorably with respect to inhibition of leukocyte migration, compared with oxine and Merc. Combined with the property of easy cell labeling and good solubility in water, also in the complexed state, tropolone must be regarded as the most suitable cell labeling ligand.

Animals↗