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PubMed2001

Preconcentration by coprecipitation of arsenic and tin in natural waters with a Ni-pyrrolidine dithiocarbamate complex and their direct determination by solid-sampling atomic-absorption spectrometry.

A method for the determination of trace amounts of arsenic and tin in natural waters is described. Trace amounts of arsenic and tin were preconcentrated by coprecipitation with a Ni-ammonium pyrrolidine dithiocarbamate (APDC) complex. The coprecipitates obtained were directly analyzed by graphite-furnace atomic-absorption spectrometry (GFAAS) using the Ni-APDC complex solid-sampling technique. The coprecipitation conditions used for the trace amounts of arsenic and tin in natural water were investigated in detail. It was found that arsenic and tin at sub-ng mL(-1) levels were both coprecipitated quantitatively by Ni(PDC)2 in the pH range 2-3. The concentration factors by coprecipitation reached approximately 40,000 when 2 mg nickel was added as a carrier element to 500 mL of the water sample. The proposed method has been applied to the determination of trace amounts of arsenic and tin in river water and seawater reference materials, and the detection limits for arsenic and tin, which were calculated from three times of the standard deviation of the procedural blanks, are 0.02 ng mL(-1) and 0.04 ng mL(-1), respectively, for 500-mL volumes of water sample.

Arsenic↗
PubMed1999

Determination of dietary tin intake in an adult French citizen.

The tin contents in fresh food or in food stored in lacquered or unlacquered cans were determined in order to estimate the daily tin intake in a French citizen. Tin levels were 76.6 +/- 36.5 mg/kg in foods preserved in unlacquered cans, 3.2 +/- 2.3 mg/kg in foods stored in lacquered cans, and 0.03 +/- 0.03 mg/kg in fresh foods. Tin intake is essentially dependent on food stored in tin cans (98%), which only represents 5.6% of the total daily consumption of foods by a French citizen. The estimated tin intake (2.7 mg/day whether 0. 04 mg/kg of body weight) remains widely inferior to the daily tolerable dose in humans (2 mg/kg of body weight).

Adult↗
PubMed1983

Plasmacellular and granulomatous splenomegaly produced in rats by tin.

Two intravenous inoculations of metallic tin powder caused a striking, self-limited enlargement of the spleen up to five or six times its normal size. In addition to epithelioid cell granulomas in response to the foreign particles, the spleen contained extensive accumulations of plasmablasts, plasma cells, and plasma cells containing Russell bodies. The proliferative activity of the immature plasma cells was indicated by the high incidence of mitoses and cells labeled with tritiated thymidine. In contrast, the granulomas had no mitoses or labeling. A single intravenous injection of tin usually produced little or no reaction in the spleen despite an abundance of tin particles. Two intravenous injections or one intravenous and one intraperitoneal inoculation were much more effective. Experiments on route, interval, and dose suggested that the first dose of tin prepared the spleen in some manner while the second dose actually elicited the reaction. Pertussis vaccine or glucan could substitute for one of the tin injections. This new model is of interest for the study of plasma cell hyperplasia and also for revealing the pathogenic potential of metallic tin.

Animals↗
PubMed1983

The effect of stannous and stannic (tin) chloride on DNA in Chinese hamster ovary cells.

Tin(II) at concentrations up to 500 microM stannous chloride (SnCl2), produced extensive DNA damage, as detected by alkaline sucrose gradient (ASG) analysis in Chinese hamster ovary (CHO) cells treated for 1 h at 37 degrees C in serum-free minimal essential medium (MEM). However treatment of cells with tin(IV), as stannic chloride (SnCl4), produced no such DNA damage. There was no loss in colony formation 6 days after either treatment suggesting that the DNA damage induced by the tin(II) was rapidly repaired and/or that DNA synthesis proceeded on the damaged templates permitting cell division to occur. Alternatively, the type of DNA damage caused by tin(II) may not lead to a reduction in colony-forming ability. Tin(II) produced about 200 times more ASG detectable DNA damage on an equi-molar basis than did Cr(VI), a known human carcinogen. This study indicates that tin(II) may be potentially genotoxic.

Animals↗
PubMed1991

Comparison of sulphur-mode and tin-mode flame photometric detectors for the gas chromatographic determination of organotin compounds.

A comparison of sulphur-mode (393 nm) and tin-mode (610 nm) flame photometric detectors for the gas chromatographic determination of butyl- and phenyltin compounds is described. The chromatographic peaks of the butyl- and phenyltin compounds were well separated, and high sensitivity was achieved in both modes; however, the tin-mode was more specific for tin compounds than the sulphur-mode. The absolute detection limits with the sulphur-mode and the tin-mode were 3.9-7.6 pg and 2.6-5.1 pg as tin, respectively. The application of the tin-mode gas chromatographic method to the determination of organotin compounds in fish is presented. For this application, organotins are extracted (as chloride) with hydrochloric acid and n-hexane-benzene (3:2, containing 0.05% tropolone) and the extracts are pentylated by a Grignard reagent prior to gas chromatography. The absolute recoveries of butyl- and phenyltin compounds added to fish samples ranged from 68.5 to 84.4% (the coefficients of variation were less than 6.6% for all substances, n = 8). Significant amounts of three organotin compounds (di- and tributyltin and triphenyltin) in fish samples were detected by this method. This technique may have application for other organotin compounds and the monitoring of butyl- and phenyltin compounds in the environment.

Animals↗
PubMed2000

Preparation of rhenium-188-tin colloid as a radiation synovectomy agent and comparison with rhenium-188-sulfur colloid.

As a generator-produced beta-emitting radionuclide, the importance of 188Re for radionuclide therapy is increasing rapidly. We prepared 188Re-tin colloid and compared its properties with 188Re-sulfur colloid. Labeling efficiencies reached >98% for tin colloid at 2 h and 89-94% for sulfur colloid at 3 h. All the preparations were stable for 72 h in water, serum, and synovial fluid. If labeled at higher temperature, the particle size of tin colloid increased. The residual radioactivity of 188Re-sulfur colloid in disposable polypropylene syringes after injecting mice was high (62.0+/-7.0%) due to its hydrophobic nature, while that of 188Re-tin colloid was low (2.9+/-1.6%). Although both 188Re-tin colloid and 188Re-sulfur colloid might be useful for radionuclide therapy, we conclude that 188Re tin colloid is more advantageous over 188Re sulfur colloid, due to higher labeling efficiency, control of the particle size, and lower residual activity in the injection syringes.

Animals↗
PubMed1998

Protective properties of tin- and manganese-centered porphyrins against hydrogen peroxide-mediated injury in rat astroglial cells.

Tin-mesoporphyrin (tin-mp), a potent inhibitor of heme oxygenase, and manganese (III) tetrakis(1-methyl-4-pyridyl)porphyrin (MnTMPyP), a potent superoxide dismutase mimetic, reduced H2O2 toxicity in cultures of transformed rat astroglial cells if added 30 min before, or at the same time as, H2O2. Reduced toxicity was not observed if treatment was delayed for 60 min, the time by which H2O2 was essentially eliminated from cultures. Coadministration of tin-mp and MnTMPyP did not increase protection over either compound administered individually. Tin-mp, but not MnTMPyP, was stable in culture. MnCl2 was not protective, suggesting that protection by MnTMPyP was not dependent on manganous ion, a by-product of MnTMPyP breakdown. Protection by tin-mp and MnTMPyP was not associated with metalloporphyrin-mediated induction of heme oxygenase-1 or with changes in heme oxygenase-2 on western blots. Whereas protective concentrations of tin-mp did not have superoxide dismutase-mimetic properties in vitro, protective concentrations of MnTMPyP partially inhibited heme oxygenase. The data support the hypothesis that heme oxygenase inhibition is protective against acute oxidative injury.

Animals↗
PubMed2000

Tensile bond strength of resin-modified glass-ionomer cement to microabraded and silica-coated or tin-plated high noble ceramic alloy.

PURPOSE: The purpose of this study was to evaluate the influence of alloy surface microabrasion, silica coating, or microabrasion plus tin plating on the tensile bond strengths between a resin-modified glass-ionomer luting cement and a high-noble alloy. Bond strength between the microabraded alloy specimens and conventional glass-ionomer cement or resin cement were included for comparison. MATERIALS AND METHODS: One hundred twenty uniform size, disk-shaped specimens were cast in a noble metal alloy and divided into 6 groups (n = 10 pairs/group). The metal surfaces of the specimens in each group were treated and cemented as follows. Group 1: No surface treatment (as cast, control), cemented with a resin-modified glass-ionomer cement. Group 2: Microabrasion with 50-microm aluminum oxide particles, resin-modified glass-ionomer cement. Group 3: A laboratory microabrasion and silica coating system, resin-modified glass-ionomer cement. Group 4: Microabrasion and tin-plating, resin-modified glass-ionomer cement. Group 5: Microabrasion only, conventional glass-ionomer cement. Group 6: Microabrasion and tin-plating, conventional resin cement. The uniaxial tensile bond strength for each specimen pair was determined using an Instron Universal Testing Machine (Instron Corp, Canton, MA). Results were analyzed using a one-way analysis of variance (alpha = 0.05) and a Tukey post-hoc analysis. RESULTS: Mean bond strength: Group 1: 3.6 (+/- 1.5) MPa. Group 2: 4.2 (+/-0.5) MPa. Group 3: 6.7 (+/- 0.9) MPa. Group 4: 10.6 (+/- 1.8) MPa. Group 5: 1.1 (+/- 0.4) MPa. Group 6: 14.6 (+/- 2.3) MPa. Group 6 was significantly stronger than Group 4. The bond strength of specimens cemented with the resin-modified glass-ionomer cement using microabrasion and tin-plating (Group 4) was significantly stronger than all other groups except the resin cement with microabrasion and tin-plating (Group 6). CONCLUSION: Microabraded and tin-plated alloy specimens luted with the resin-modified glass-ionomer cement resulted in the greatest mean tensile strengths for the resin-modified glass-ionomer cement groups. This strength was 73% of the mean tensile strength of microabraded specimens luted with resin cement.

Aluminum Oxide↗
PubMed1979

5-aminolevulinate dehydratase activity in blood of rabbits given tin or lead.

The activity of 5-aminolevulinate dehydratase (ALAD) in rabbit blood is significantly inhibited by tin. Intravenous administration of tin (0.48 or 4.8 mumol/kg body weight) causes a decrease in the activity of the enzyme by 60% or 94% respectively. The effects of tin and lead on ALAD differ: inhibition by tin is not affected by pre-incubation at 50-60 degrees C, whereas the inhibitory effect of lead is increased by the same pretreatment. The optimum pH for rabbit blood ALAD is 6.8 in control rabbits. This optimum shifts to pH 5.8-6.0 in the blood of tin-treated rabbits, with or without pre-incubation at 60 degrees C for 5 min, while a similar shift is prevented by the same pre-incubation after lead treatment. Recovery to normal activity is faster after tin than after lead treatment.

Animals↗
PubMed1994

[Comparative study on placental transfer and maternal distribution of organic and inorganic tin following oral administration in pregnant rats].

Placental transfer and body distribution of triphenyl tin chloride (TPTC) and tin chloride (SnCl2) were investigated in pregnant rats. Pregnant wistar rats were orally administered TPTC at 0, 1.0 and 2.0 mg/rat/day during 6-10 and 14-18 days of gestation, and with SnCl2 at 0 and 20 mg/rat/day on 7, 10 and 15 days of gestation (group treated 3 times) or 6-10 and 13-16 days of gestation at 0 and 20 mg/rat/day (group treated 9 times). On day 20 of gestation in rats treated with TPTC, and day 17 in rats with SnCl2, fetuses, placentas, maternal blood and organs were obtained for analyses. Mean fetal tin levels from rats treated with 1.0 and 2.0 mg TPTC were 0.05 and 0.11 microgram/g wet weight, respectively, these values being significantly (P < 0.01) higher than in the control group. The latter was higher than the former at a significance level of 5%. No significant difference between fetal tin levels from rats treated with SnCl2 and the control group could be detected. Following oral TPTC administration, tin was present in maternal liver, kidney and brain in high concentrations. Following the oral administration of SnCl2, the tin level was highest in bone and kidney, but none could be detected in the brain.

Administration, Oral↗
PubMed1980

Uptake and retention of tin by S. mutans.

The uptake of tin by S. mutans from stannous fluoride or stannous chloride solutions was determined by atomic absorption spectroscopy. The uptake occurred rapidly, and the microorganism was shown to have a greater capacity and higher affinity to uptake of tin than of other metal ions tested. In 10 mM solutions, bound tin amounted to 17.5 per cent of the cellular dry mass. The tin uptake was independent of cell metabolism. The cell bound tin could not be washed out with water or saline, but 84 per cent was removed by ethylenediaminetetraacetic acid solutions. When pH was lowered by low 2, increasing loss of bound tin occurred. It is suggested that the binding occurs to polyanionic structural polymers in the cell wall and the cell capsule.

Binding, Competitive↗
PubMed2002

[Assessment of risk for tin mine dust in Guangxi].

OBJECTIVE: To explore the minimum observed adverse effect level(LOAEL) and intensity of pathogenesis of tin mine dust. METHODS: A cohort study design with retrospective assessment of exposure was used. Selected 4,471 male tin miners who were exposed to tin at least one year during 1960 to 1974 and were compared with 4,797 pottery dust exposed workers in the same way designed. Statistical analysis system SAS, PROC LIFETEST were used to perform the non-parameter calculation by Life Table method. RESULTS: Tin mine cohort subjects were followed up to December 31, 1994. The percentage of miners who developed silicosis was 21.7% (971/4,471). 81% of the patients had been exposed to dust before 1958. The cumulative total dust exposure(CTD) was significantly correlated with silicosis risk. The risk of silicosis was 0.012 when CTD was less than 50 mg/m-3.year-1. The risk of silicosis was increased to 0.971 when CTD was beyond 400 mg.m-3.year-1. However, the risk of silicosis was only 0.369 for dust exposed workers in pottery factories when CTD was beyond 400 mg.m-3.year-1. CONCLUSION: There was significant relationship between cumulative dust exposure and the incidence of silicosis in tin exposed workers. And silicosis induced by tin mine dust is more serious than the pottery dust.

Cohort Studies↗
PubMed1979

Complexing of reduced technetium and tin(II) by chelating phosphate compounds. II. In vitro stability of pyrophosphate and ethane-1, hydroxy-1, diphosphonate (EHDP) complexes.

The in vitro stability of 99mTc- and 113Sn-pyrophosphate and ethane-1, hydroxy-1, diphosphonate (EHDP) complexes was studied by varying the mode of preparation. The 1-hr distribution in the rat was used as an indicator for complex formation or destruction. A maximum of bone uptake and urinary excretion and a minimum of soft tissue concentration was obtained if there was an excess of phosphate in relation to tin(II) in the equilibrium. Formation of tin(II) colloid was favoured in the presence of an excess of tin(II) in the equilibrium, 99mTc colloid occurred with some delay. After dilution in neutral normal saline the chelates were more or less destroyed, as shown by a 113Sn(II) colloid formation whereas the 99mTc-phosphate complexes were transformed into a 99mTc kidney agent. At pH 11 the 113Sn(II)-phosphate complexes proved to be stable, the 99mTc-phosphate complexes were also transformed into the 99mTc kidney agent. Oxidation of all tin(II) in the equilibrium by hydrogen peroxide did not change the distribution patterns of 113Sn, 99mTc was oxidized to pertechnetate. In general complexes between tin(II) and chelating phosphate compounds proved to be more stable than those with reduced technetium. EHDP was found to form stronger complexes with tin(II) and reduced technetium than pyrophosphate.

Animals↗
PubMed1978

Uremic hyperstannum: elevated tissue tin levels associated with uremia.

Previous work has shown that the concentration of the essential trace element tin is elevated in several tissues of dialyzed uremic patients. Analysis of 80 postmortem liver samples from controls and nondialyzed uremic and dialyzed uremic patients now shows that nondialyzed uremic patients also have abnormally high tin concentrations, averaging about three times that of controls. It is concluded that these elevated tin levels are associated with uremia rather than with dialysis. Abnormally high tin levels were also found in the kidneys of uremic patients at autopsy. This may have special importance, since tin has been shown to be a powerful inducer of heme oxygenase activity in rat kidney. The urinary excretion of tin by nondialysed uremic patients was measured and found to be normal.

Adult↗
PubMedDate not supplied

Inductively coupled plasma atomic emission spectrometric determination of tin in canned food.

Various canned foods were digested sequentially with HNO3 and HCl, diluted to 100 mL, and filtered, and then tin was determined by inductively coupled plasma atomic emission spectrometry (ICP/AES). Samples of canned Satsuma mandarin, peach, apricot, pineapple, apple juice, mushroom, asparagus, evaporated milk, short-necked clam, spinach, whole tomato, meat, and salmon were evaluated. Sample preparations did not require time-consuming dilutions, because ICP/AES has wide dynamic range. The standard addition method was used to determine tin concentration. Accuracy of the method was tested by analyzing analytical standards containing tin at 2 levels (50 and 250 micrograms/g). The amounts of tin found for the 50 and 250 micrograms/g levels were 50.5 and 256 micrograms/g, respectively, and the repeatability coefficients of variation were 4.0 and 3.8%, respectively. Recovery of tin from 13 canned foods spiked at 2 levels (50 and 250 micrograms/g) ranged from 93.9 to 109.4%, with a mean of 99.2%. The quantitation limit for tin standard solution was about 0.5 microgram/g.

Food Preservation↗
PubMed1976

Tin-protein binding kinetics in normal and uremic plasma and its effect on dialysis fluxes.

A high affinity of plasma protein for tin has been demonstrated by ultrafiltration studies. At physiologic concentrations, UF/P remained below 1%, consistent with more than 99% binding. Binding of tin was nearly complete despite a decrease in plasma protein concentration to 3.5 Gm% and an increase in plasma tin by 80 mg/L. This binding inhibits efflux of tin from plasma during dialysis while influx occurs readily. This may be a mechanism for accumulation of tin in patients undergoing maintenance hemodialysis. A mechanism for tin chelation could be clinically beneficial in the syndrome of dialysis dementia.

Blood Proteins↗
PubMed1977

The chloride transport induced by triaklyl-tin compound across erythrocyte membrane.

The effect of tripropyl-tin chloride on anion permeability was studied using red cells previously treated with a covalent binding inhibitor 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) to inhibit completely and irreversibly the natural anion transport system. It was demonstrated that the tin compound can mediate chloride-hydroxide and chloride-chloride exchanges across the "impermeabilised" erythrocyte membrane. In the non hemolytic range, the rate of exchange increased with the concentration of the tin compound in a non linear fashion, and no saturation effect was seen. The temperature profile of the chloride self exchange induced by tripropyl-tin was studied and the apparent activation energy found was 29 Kcal/mol. The tripropyl-tin chloride cannot mediate a chloride-bicarbonate exchange. Because of this discriminatory effect between hydroxide and bicarbonate, the tin compound can be useful in certain experimental conditions as seen for the study of the anion "carrier" of the red cell membrane ("cousin, J.L., Motais, R. and Sola, F. (1975) J. Physiol. Lond. 253, 385-399).

Bicarbonates↗
PubMed1993

Tin protoporphyrin prolongs the biochemical remission produced by heme arginate in acute hepatic porphyria.

BACKGROUND: In acute porphyria, repletion of intrahepatic heme, with exogenously administered heme, suppresses the overproduction of delta-aminolaevulinic acid (ALA) and porphobilinogen (PBG). The effect of reducing heme breakdown has been assessed by administering tin protoporphyrin, a competitive inhibitor of heme oxygenase. METHODS: The effect of tin protoporphyrin, 1 mumol/kg, and heme arginate, 3 mg/kg, individually and combined was compared with placebo in patients with an acute porphyric crisis. The treatments were given by intravenous infusion on three successive mornings. Thirty-four attacks were studied in 8 patients (9 placebo, 10 heme arginate alone, 4 tin protoporphyrin alone, and 11 combination treatments). RESULTS: Placebo and tin protoporphyrin alone had little effect on ALA and PBG excretion. Following heme arginate alone or combined with tin protoporphyrin, there was a marked and similar suppression of both ALA and PBG excretion (P < 0.005 for each, compared with pretreatment values). However, on the 5th day after discontinuing treatment, the excretion of ALA and PBG were both lower following combination therapy than following heme arginate alone (P < 0.005 and P < 0.01, respectively). CONCLUSIONS: These findings suggest that inhibition of heme oxygenase by tin protoporphyrin prolongs the biochemical remission induced by heme arginate in the porphyric crisis.

Acute Disease↗