Tin rod, 50mm, diameter 6.0mm, 99.999+%; CAS Number: 7440-31-5; EC Number: 231-141-8; Synonyms: Tin,SN007930; find -GF17787404 MSDS, related peer-reviewed papers, technical documents, similar products & more at Sigma-Aldrich

Tin rod, 50mm, diameter 6.0mm, 99.999+ 7440-31-5

The newer essential trace elements, chromium, tin, nickel, vanadium and silicon.

[Tin in the environment].

Inorganic tin salts are poorly absorbed and rapidly excreted in the faeces; as a result they have a low toxicity. Only about 5 per cent is absorbed from the gastrointestinal tract, widely distributed in the body, then excreted by the kidney. Some tin is deposited in lung and bone. Some tin salts can cause renal necrosis after parenteral doses. Mutagenic studies on metallic tin and its compounds have been negative. Long-term animal carcinogenic studies have shown fewer malignant tumours in animals exposed to tin than in controls. Human volunteers developed mild signs of toxicity with tin, given in fruit juices, at a concentration of 1400 mg per litre. The WHO 1973 permissible limit for tin in tinned food is 250 micrograms per kg. The adult daily intake of tin was about 17 mg per day in 1940, but it has now decreased to about 3.5 mg, due to improvements in technique of tinning with enamel overcoat and crimped lids to minimize exposure to tin and lead solder. This level is well below the level of 5-7 mg per kg body weight shown to give rise to toxic symptoms. Tin deficiency has not been described in man. Amounts in excess of 130 mg per day have been shown to accumulate in liver and kidneys. Many of the organotin compounds are toxic; the most toxic being trimethyltin and triethyltin, which are well absorbed from the gastrointestinal tract. Most of the other alkyl and aryltin compounds are poorly absorbed from the gastrointestinal tract, and are therefore less toxic when given orally than when given parenterally. The main results of toxicity are skin and eye irritation; cholangitis of the lower biliary tract, and later hepatotoxicity; and neurotoxicity, which has been shown to be due to intramyelin oedema induced by triethyltin, and neuronal necrosis caused by trimethyltin. Many of the organotin compounds affect mitochondrial oxidative phosphorylation and alter membranes, but the contribution of these biochemical and membrane effects in the cause of intramyelin oedema and neuronal necrosis has not been fully clarified. Widespread degeneration results, especially with trimethyltin. Peripheral neuropathy has not been reported as occurring with either inorganic or organic tin in humans. Certain dialkyltin compounds have been shown to cause adverse effects on cell-mediated immunity, specifically on the T cell lymphocyte. Experimental studies have failed to reveal any evidence of carcinogenicity, mutagenicity, or teratogenicity. Recent studies suggest that tin compounds exhibit some antitumour activity and may have a future role in cancer diagnosis and chemotherapy, and in controlling hyperbilirubinaemia.

Toxicity of tin and its compounds.

We set out to investigate potential differences and similarities between the selective forces acting upon the coding and noncoding regions of five different sets of genes defined according to functional and evolutionary criteria: 1) two reference gene sets presenting accelerated and slow rates of protein evolution (the Complement and Actin pathways); 2) a set of genes with evidence of accelerated evolution in at least one of their introns; and 3) two gene sets related to neurological function (Parkinson's and Alzheimer's diseases). To that effect, we combine human-chimpanzee divergence patterns with polymorphism data obtained from target resequencing 20 central chimpanzees, our closest relatives with largest long-term effective population size. By using the distribution of fitness effect-alpha extension of the McDonald-Kreitman test, we reproduce inferences of rates of evolution previously based only on divergence data on both coding and intronic sequences and also obtain inferences for other classes of genomic elements (untranslated regions, promoters, and conserved noncoding sequences). Our results suggest that 1) the distribution of fitness effect-alpha method successfully helps distinguishing different scenarios of accelerated divergence (adaptation or relaxed selective constraints) and 2) the adaptive history of coding and noncoding sequences within the gene sets analyzed is decoupled.

Analysis of Five Gene Sets in Chimpanzees Suggests Decoupling between the Action of Selection on Protein-Coding and on Noncoding Elements.

A tolerable limit for tin concentration in canned food of 250 ppm (Fritsch et al., 1977) is generally accepted. However, biochemical effects attributable to tin have been observed even after oral administration of 1 and 3 mg Sn/kg body wt (Yamaguchi et al., 1980). These doses reflect 10 and 30 ppm tin in the diet. The experiments of de Groot (1973) showed that hemoglobin concentrations in the blood of rats decreased significantly feeding a diet containing 150 ppm tin. The absorption of iron was diminished after simultaneous administration of 0.8 mumol Sn(II) and iron, reflecting a tin dose of 95 ppm tin, by injection into jejunal loops of rats (Schäfer and Forth, 1983). In general, however, canned food usually plays a secondary role in daily nutrition. Fortunately, concentrations of about 2000 ppm tin as reported by Warburton et al. (1962) and Barker and Runte (1972) are not found in canned food, but values between 50 and 500 ppm are not unusual (Piscator, 1979). If a large amount of canned food is eaten daily over a long period, disturbances of gastric acid secretion and a reduction in iron absorption or heme metabolism cannot be excluded. The storage of food, especially acid foods, in opened cans should be avoided as this practice increases the amount of tin in the food when it is consumed.

Tin--a toxic heavy metal? A review of the literature.

The toxicology of tin is almost entirely the toxicology of the organic compounds of tin, for the metal itself and its inorganic compounds appear to be nearly harmless for practical purposes. Furthermore, the neurotoxicity of organotin is essentially that of trimethyltin and triethyltin.

General toxicology of tin and its organic compounds.

This article reviews the literature related to the bioavailability of tin, inorganic tin compounds, and organotin compounds. On the one hand, the toxicity of metallic tin and inorganic tin compounds is low. In aqueous systems, the potential bioavailability of tin seems to depend on the concentration of the truly dissolved ion species. Some studies suggest that tin is an essential trace element for humans. However, organotin compounds have been proven to be of toxicological relevance. Triorganotin compounds are particularly toxic explaining their wide use as biocides (e.g., in antifouling paints or pesticides). Persistence of organotin compounds is governed by moderate to fast aerobic biotic degradation processes, slow anaerobic biotic degradation, slow abiotic degradation by photolysis, and fast, but reversible, adsorption/desorption processes. Organotin compounds are ubiquitously distributed in aquatic organisms. Bioconcentration in organisms and ecotoxicity are dependent on the bioavailable fraction. The bioavailability is highest at neutral and slightly alkaline pH and is reduced in the presence of dissolved organic carbon. The biomagnification of organotin compounds via the food chain is of minor importance compared with the bioconcentration from the water phase.

Case study: bioavailability of tin and tin compounds.

Are nickel, vanadium, silicon, fluorine, and tin essential for man? A review.

Mutagens and potential mutagens in the biosphere. II. Metals--mercury, lead, cadmium and tin.

Tinplate is light gauge, steel sheet or strip, coated on both sides with commercially pure tin and has been used for well over a hundred years as a robust form of food packaging. Altogether, about 25,000 million food cans are produced and filled in Europe per annum, about 20% of these having plain internal (unlacquered) tin-coated steel bodies. Worldwide, the total for food packaging is approximately 80,000 million cans. Tinplate is also extensively used for the production of beverage cans. Europe produces and fills over 15,000 million tinplate beverage cans per annum all of which are internally lacquered. The use of tinplate for food and beverage packaging, will result in some tin dissolving into the food content, particularly when plain uncoated internal surfaces are used. The Provisional Tolerable Weekly Intake for tin is 14 mg/kg body weight and recommended maximum permissible levels of tin in food are typically 250 mg/kg (200 mg/kg UK) for solid foods and 150 mg/kg for beverages. However, the question arises as to whether evidence exists that such elevated levels of tin in food in any way constitute a risk to human health. This review considers the factors affecting the dissolution of tin, the reported measurements/surveys of actual levels of tin in canned foods and the studies and reports of acute (short term) toxicity relating to the ingestion of elevated levels of tin in food products. Chronic studies are mentioned, but are not covered in detail, since the review is mainly concerned with possible effects from the ingestion of single high doses. From published data, there appears to be a small amount of evidence suggesting that consumption of food or beverages containing tin at concentrations at or below 200 ppm has caused adverse gastrointestinal effects in an unknown but possibly small proportion of those exposed. However, the evidence supporting this assertion is derived from reports of adverse effects which offer data that are limited, incomplete or of uncertain veracity. Clinical studies provide greater confidence regarding the effects of exposure concentration and dose, but few relevant studies have been made. Adverse gastrointestinal effects were observed in limited clinical studies at concentrations of 700 ppm or above, although no adverse gastrointestinal effects were also reported in two studies at higher concentrations. Overall, therefore, the published data do not present a particularly comprehensive profile on the toxic hazard to man of acute exposure to divalent inorganic tin. A food survey suggested that the contents of almost 4% of plain internal tinplate food cans contain over 150 mg/kg of tin and over 2.5 million such cans are consumed every year in the UK alone. Despite this, in the last 25 years, there have been no reports of acute effects attributable to tin contamination in the range 100-200 ppm. These facts strongly suggest that there is little evidence for an association between the consumption of food containing tin at concentrations up to 200 ppm and significant acute adverse gastrointestinal effects. Clearly though, only further clinical studies will generate unequivocal evidence that current legislative limits provide safe levels for adults in the general population.

Tin in canned food: a review and understanding of occurrence and effect.

Commonly used methods of analysis for tin in foods.

Methods for both total and form-variable tin analysis in biological media are reviewed. While total tin analysis was common in the past, and in some cases still is, better understanding of the toxicology and toxicokinetics of organotins in biological systems requires knowledge of specific tin forms present. Both chromatographic and non-chromatographic methods for chemical speciation of organotins in various media have been described, the former appearing to offer the most promising approaches. High performance liquid chromatography (HPLC) in tandem with tin-specific metal detection presently appears to offer the most promise.

The analysis of total and form-variable tin in various media.

General aspects of tin-free antifouling paints.

Experimental studies over the last decade have suggested an association between thymus immune and homeostatic function and exogenous tin. It has been hypothesized that the thymus gland synthesizes and secretes one or more tin bearing factors that enhance immune defenses against malignancy and retard the gradual loss of immune capacity with senescence. This review conciliates data from several divergent areas of research in order to explore the rationale for the above concepts.

Tin and the thymus gland: a review.

Applications of tin-containing intermediates to carbohydrate chemistry.

Tin generates a wide variety of biological activities deriving from its chemical character. In this article, the biological activities of tin compounds are reviewed with a focus on the connection with immunity. The table of contents is as follows: Introduction, 1. Inorganic Tin and Immunity, 2. Organic Tin and Immunity, 2.1. Immunotoxicity, 2.1.1. Immunosuppression, 2.1.2. Thymus atrophy, 2.1.3. Changes in the membrane surface antigens of T cells, 2.2. Antitumor activity, 2.3. Anti-inflammatory action, 2.4. Tolerance manifestation of thymus atrophy, 3. Cellular and Biochemical Aspects of the Activity Manifestation, 3.1. Intracellular distribution of organotins 3.2. Effects on structure and function of Golgi apparatus and endoplasmic reticulum, 3.3. Effects on physical properties of phospholipid membrane, 3.4. Suppressive effects on cell proliferation system, 3.5. Consideration, Conclusion. To sum up this article, tin compounds (especially organotin compounds) act mainly on cellular immune systems and the mechanism appears to be due to their hydrophobicity-dependent intracellular distribution and their action on the phospholipid metabolism including the inhibition of intracellular phospholipid transport between organelles through an impairment of the structure and functions of the Golgi apparatus and the endoplasmic reticulum (ER), and the consequent inhibition of the membrane-mediated signal transduction system leading to DNA synthesis via phospholipid turnover and Ca2+ mobilization.

[Biological activity of tin and immunity].

Inorganic tin: chemistry, disposition and role in nuclear medicine diagnostic skeletal imaging agents.

Functional variations in the mannose-binding lectin (MBL2) gene causing low levels of serum MBL are associated with susceptibility to numerous infectious diseases. We investigated whether there is genetic association of MBL2 variant alleles with cutaneous leishmaniasis (CL) caused by Leishmania guyanensis. We used PCR-restriction fragment length polymorphism to genotype six MBL2 variants, three in the promoter region and three in the exon 1. An association was noted between the single nucleotide polymorphism -221X/Y of the MBL2 gene and CL (P=2.9 × 10(-6); odds ratio (OR)=1.9 (1.4-2.5) consistent with the hypothesis that the -221X allele confers high risk to development of CL among L. guyanensis-infected individuals. Furthermore, L. guyanensis-infected individuals bearing the codon 57 allele C had a higher risk of developing CL (P=5 × 10(-5); OR=1.9 (1.4-2.6)). The low MBL expressor haplotype LXPB was also associated to CL (P=6 × 10(-4)). This study raises the possibility that functional polymorphisms in MBL2 gene play a role in clinical outcome of Leishmania infection.

Functional variations in MBL2 gene are associated with cutaneous leishmaniasis in the Amazonas state of Brazil.

Hyperactivation of the hypothalamic-pituitary-adrenal axis is a common finding in major depression; this may lead to increased levels of cortisol, which are known to cause oxidative stress imbalance and apoptotic neuronal cell death, particularly in the hippocampus, a key region implicated in mood regulation. Agmatine, an endogenous metabolite of L-arginine, has been proposed for the treatment of major depression. Corticosterone induced apoptotic cell death and increased ROS production in cultured hippocampal neuronal cells, effects that were abolished in a concentration- and time-dependent manner by agmatine. Interestingly, the combination of sub-effective concentrations of agmatine with fluoxetine or imipramine afforded synergic protection. The neuroprotective effect of agmatine was abolished by yohimbine (α2-adrenoceptor antagonist), ketanserin (5-HT2A receptor antagonist), LY294002 (PI3K inhibitor), PD98059 (MEK1/2 inhibitor), SnPP (HO-1 inhibitor), and cycloheximide (protein synthesis inhibitor). Agmatine increased Akt and ERK phosphorylation and induced the transcription factor Nrf2 and the proteins HO-1 and GCLc; induction of these proteins was prevented by yohimbine, ketanserin, LY294002, and PD98059. In conclusion, agmatine affords neuroprotection against corticosterone effects by a mechanism that implicates Nrf2 induction via α2-adrenergic and 5-HT2A receptors, Akt and ERK pathways, and HO-1 and GCLc expression.

Agmatine induces Nrf2 and protects against corticosterone effects in hippocampal neuronal cell line.

Organotin compounds (OTCs) are among the most toxic substances ever introduced to the environment by man. They are common pollutants in marine ecosystems, but are also present in the terrestrial environment, accumulated mainly in sewage sludge and landfill leachates. In investigations of the degradation and methylation processes of OTC in environmental samples, the use of enriched isotopic tracers represents a powerful analytical tool. Sn-enriched OTC are also necessary in application of the isotope dilution mass spectrometry technique for their accurate quantification. Since Sn-enriched monobutyltin (MBT), dibutyltin (DBT) and tributyltin (TBT) are not commercially available as single species, "in house" synthesis of individual butyltin-enriched species is necessary. In the present work, the preparation of the most toxic butyltin, namely TBT, was performed via a simple synthetic path, starting with bromination of metallic Sn, followed by butylation with butyl lithium. The tetrabutyltin (TeBT) formed was transformed to tributyltin chloride (TBTCl) using concentrated hydrochloric acid (HCl). The purity of the synthesized TBT was verified by speciation analysis using the techniques of gas chromatography coupled to inductively coupled plasma mass spectrometry (GC-ICP-MS) and nuclear magnetic resonance (NMR). The results showed that TBT had a purity of more than 97%. The remaining 3% corresponded to DBT. TBT was quantified by reverse isotope dilution GC-ICP-MS. The synthesis yield was around 60%. The advantage of this procedure over those previously reported lies in its possibility to be applied on a micro-scale (starting with 10mg of metallic Sn). This feature is of crucial importance, since enriched metallic Sn is extremely expensive. The procedure is simple and repeatable, and was successfully applied for the preparation of (117)Sn-enriched TBTCl from (117)Sn-enriched metal.

Tin

rod, 50mm, diameter 6.0mm, 99.999+%

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