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Phthalic acid dermatitis caused by an organostannic compound, tributyl tin phthalate.

We report a case of primary irritant contact dermatitis caused by an organostannic insecticide, tributyl tin phthalate, which has been thought to be stable and safe. A factory worker has been in contact with raw tributyl tin phthalate on one leg. Soon after taking a hot-water bath, he developed severely painful erythema on this leg. Patch tests and chemical analysis revealed that hot water hydrolyzed tributyl tin phthalate and produced concentrated phthalic acid. Since phthalic acid, a weak acid, was then concentrated, an acute irritant reaction appeared in this patient.

Accidents, Occupational↗

Formation of novel anionic gold-tin cluster compounds.

A straightforward procedure for the formation of mixed metal Au/Sn clusters is presented: reaction of the heteroborate [SnB11H11]2- with phosphine gold electrophiles gave the clusters [Bu3NH]3[{(Et3P)Au(SnB11H11)}3] and [Bu3MeN]4[{(dppm)Au2(SnB11H11)2}2], which were characterised by X-ray diffraction.

Journal Article↗

Tin-halide compounds. IV1. tert-butyltrichlorotin (IV).

The molecules of the title compound, [Sn(C(4)H(9))Cl(3)], adopt an eclipsed conformation with respect to the C and Cl atoms, and possess crystallographic C(s) symmetry. The molecular structure and geometric parameters are comparable with those of related organotin trihalides.

Journal Article↗

Comprehensive-trace level determination of methyltin compounds in aqueous samples by cryogenic purge-and-trap gas chromatography with flame photometric detection.

A comprehensive method was developed for the sensitive and fast determination of trace levels of methyltin compounds in aqueous samples. Tin compounds in aqueous solution at pH 5 were converted to the corresponding volatile hydrides: CH3SnH3, (CH3)2SnH2, and (CH3)3SnH, by reaction with potassium borohydride. A CP-4010 purge and trap injector (PTI) was used to purge analyte species from water directly. The volatile derivatives were base-line separated on a capillary column in an Angilent-6890 gas chromatograph by a suitable temperature program and were detected by a flame photometric detector (FPD). The detection limits were 18 ng L-1 for monomethyltin, 12 ng L-1 for dimethyltin, and 3 ng L-1 for trimethyltin, respectively. This method was successfully applied to the determination of methyltin compounds in different aqueous samples.

Chemical Industry↗

The relation of the neurotoxicity of organic tin and lead compounds to neurotubule disaggregation.

The effect of organic lead and tin compounds upon the integrity of cerebral neurotubules has been studies in vitro and in vivo, using 3H-colchicine binding as an index of tubulin aggregation. Triethyl tin, trimethyl lead and triethyl lead chlorides at concentrations above 5 X 10(-5)M, all prevented the polymerization of tubulin. Inorganic lead had a similar effect. Trimethyl tin had a much lesser capacity to prevent such polymerization. Rats received a single dose of each organometal, by subcutaneous injection and the capacity of hippocampal soluble protein to bind 3H colchicine was assessed. At organometal doses sufficient to cause morphological damage and behavioral change, no significant differences of colchicine binding capacity were apparent.

Animals↗

The development and in-vivo behavior of tin containing radiopharmaceuticals--I. Chemistry, preparation, and biodistribution in small animals.

Tin is an essential ingredient of most technetium-99m radiopharmaceutical preparations but its in-vivo distribution and long-term fate are not well understood. Tin-117m (t1/2 14d; gamma 159 keV, 86%) is an ideal tracer for studying biological behavior of tin compounds as well as for developing clinically-useful radiopharmaceuticals. This work describes the preparation and in-vivo distribution in mice of a number of tin-117m labeled compounds with commonly used ligands. High bone uptake of most compounds studied as well as the unexpectedly high bone uptake of Sn4+-DTPA indicates a high bone affinity of tin bound to chemically diverse ligands. Various compounds show subtle but significant differences in blood clearance, excretion, and soft-tissue uptake. Differences among Sn2+ and Sn4+ compounds with the same ligand are particularly noteworthy. For stannic chelates, higher bone uptake, faster blood clearance, and reduced soft-tissue concentration were observed. It appears that tin compounds bind to bone predominantly through the tin atom and that the differences in biodistribution depend on factors such as the net charge on the complex, the oxidation state of tin, and hydrolytic and kinetic stabilities of the complexes. The results indicate that the favorable half-life and decay characteristics of tin-117m in various stannic compounds, especially stannic-DTPA, make it potentially useful as an agent for skeletal scintigraphy and radiotherapy of bone tumors.

Animals↗

Irritant dermatitis from tri-N-butyl tin oxide in paint.

Organo-tin compounds are known irritants. Tributyl tin oxide is a common biocide in some marine and other paints. An outbreak of irritant contact dermatitis in painters exposed to paints containing tributyl tin oxide is reported.

Adult↗

The action of 5-coordinate triorganotin compounds on rat liver mitochondria.

5-Coordinate tin compounds influence mitochondrial function in the same three ways as triorganotin compounds: (1) they inhibit the energy conservation system like oligomycin, (2) they cause a Cl-/OH- exchange across mitochondrial membranes and (3) at high concentrations they cause large scale swelling. Unlike other triorganotin compounds they inhibit (1) at much lower concentrations than (2) and are as effective as oligomycin. Thhe implications of these findings for the mechanism of reaction of organotins with proteins, enzymes and mitochondria are discussed.

Adenosine Triphosphate↗

Reactions of the heavier group 14 element alkyne analogues Ar'EEAr' (Ar' = C6H3-2,6(C6H3-2,6-Pri2)2; E = Ge, Sn) with unsaturated molecules: probing the character of the EE multiple bonds.

Reactions of the alkyne analogues Ar'EEAr' (Ar' = C6H3-2,6(C6H3-2,6-Pr(i)2)2; E = Ge (1); Sn (2)) with unsaturated molecules are described. Reaction of 1 and 2 with azobenzene afforded the new hydrazine derivatives Ar'E{(Ph)NN(Ph)}EAr' (E = Ge (3); Sn (4)). Treatment of 1 with Me3SiN3 gave the cyclic singlet diradicaloid Ar'Ge{mu2-(NSiMe3)}2GeAr' (5), whereas 2 afforded the monoimide bridged Ar'Sn{mu2-N(SiMe3)}SnAr' (6). Reaction of 1 with t-BuNC or PhCN yielded the adduct Ar'GeGe(CNBu(t))Ar' (7) or the ring compound (8). In contrast, the tin compound 2 did not react with either t-BuNC or PhCN. Treatment of 1 with N2CH(SiMe3) generated Ar'Ge{mu2-CH(SiMe3)}{mu2:eta2-N2CH(SiMe3)}{mu2-N2CH(SiMe3)}GeAr' (9) which contains ligands in three different bridging modes and no Ge-Ge bonding. Reaction of 1 with an excess of N(2)O gave a germanium peroxo species Ar'(HO)Ge(mu2-O)(mu2:eta2-O2)Ge(OH)Ar' (10) which features a ring. Oxidation of 1 by tetracyanoethylene (TCNE) led to cleavage of the Ge-Ge bond and formation of a large multiring system of formula Ar'Ge3+{(TCNE)2-}3{(GeAr')+}3. The digermyne 1 also reacted with 1 equiv of PhCPh to give the 1,2-digermacyclobutadiene 12, which has a ring, and with Me(3)SiCCH or PhCC-CCPh to activate a flanking C6H3-2,6-Pr(i)2 ring and give the tricyclic products 13 and 14. The "distannyne" 2 did not react with these acetylenes. Overall, the experiments showed that 1 is highly reactive toward unsaturated molecules, whereas the corresponding tin congener 2 is much less reactive. A possible explanation of the reactivity differences in terms of the extent of the singlet diradical character of the Ge-Ge and Sn-Sn bonds is discussed.

Journal Article↗

Speciation of inorganic and organotin compounds in biological samples by liquid chromatography with inductively coupled plasma mass spectrometric detection.

This paper describes the effect of inorganic tin chloride on the separation of trimethyl-, tributyl- and triphenyltin-chlorides by reversed-phase ion-pair high-performance liquid chromatography with detection by inductively coupled plasma mass spectrometry. The detection limits are 1.6 pg, 1.5 pg and 2.3 pg as tin for trimethyltin, tributyltin and triphenyltin, respectively. The relative standard deviation for ten injections of 20 ng of the tin compounds was less than 5%. Inorganic tin was held strongly on the columns used, to a greater extent on the silica column compared to the polymer column. Extraction and determination of tributyltin and triphenyltin as chlorides in fish tissue (certified reference material) and tuna fish (grocery store) were performed. The recovery study from fish tissue showed an efficiency of over 90% for both tributyltin and triphenyltin and over 60% recovery for spiked tuna.

Animals↗

General toxicology of tin and its organic compounds.

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.

Animals↗

The effect of tin chloride on the structure and function of DNA in human white blood cells.

Tin compounds are being used increasingly in the home, in industry and in medicine. There have been relatively few studies on the long term biological effects of this metal, although acute effects have been documented. In this report we describe experiments which show that tin(II), as stannous chloride, is readily taken up by human white blood cells (WBC) and can cause damage to DNA. Damage was detected in WBC after exposure to 10-50 microM tin(II) for 30 min at either 0 degree or 37 degrees C. The amount of damage observed was more extensive than that produced by exposure of cells to equimolar amounts of chromium(VI), a known carcinogen and DNA damaging agent. Additional indication of cellular damage is that exposure of human lymphocytes or mouse splenocytes to tin(II) interfered with their ability to be stimulated by the polyvalent mitogen concanavalin A (Con A). By contrast, tin(IV) was not taken up by cells, did not cause DNA damage nor did it inhibit stimulation of DNA synthesis in cells that were exposed to Con A.

Biological Transport↗

[Recent progress in the study of analytical methods, toxicity, metabolism and health effects of organotin compounds].

Over the years, a variety of uses has been found of organic tin compounds as fungicides, as stabilizers in plastics and for other industrial uses. The purpose of this article is to summarize and review the results so far obtained as to the analytical method for organotins in biological samples, the toxicity, metabolism, and biochemical and health effects of organotin compounds. 1) Many methods have been developed for analysis of organotin compounds by spectrophotometry, polarography, gas- or liquid-chromatography, etc. These methods, however, are mainly for analysis of organotins in standard solutions or in water, and are not suitable for organotin compounds in biological samples. Recently, we have developed several methods for analysis of various kinds of organotin compounds in biological samples. These methods are able simultaneously to separate and determine trace amounts (at nanogram order) of organotin compounds and their metabolites in the same biological samples. 2) Acute toxicity of organotin compounds which appeared on the literature are summarized. Trialkyl and triaryl compounds seem to be more toxic than the tetra-, di-, or mono-compounds of the same chain length. With an increase in the number of C atoms the toxicity of alkyl compounds decreases. Aryltin compounds are less toxic than alkyltin compounds. 3) Intestinal absorption sites for tetra-alkyltins are jejunum and duodenum, and those for trialkyltins are ileum and jejunum. A considerable amount of orally administered tetra- and trialkyltins of low molecular weights are absorbed, but only very little of the other organotin compounds seems to be absorbed from the gastrointestinal tract. Absorbed organotin compounds rapidly undergo dealkylation by the microsomal mono-oxygenase system dependent on cytochrome P-450 in the liver, brain or other organs, and the compounds and their metabolites distribute to the whole body, ultimately being excreted into urine, bile and faeces. The biological half life of organotin compounds in mammals is usually short, a half of the amount of tributyl- and triphenyl-tins deposited in the body disappearing in several days. A part of organotin compounds excreted into bile is demonstrated to have been absorbed from the intestine and to circulate in the body via enterohepatic circulation. 4) Specific effects of organotin compounds on the biological systems and health include disturbance of the structure and function of the central nervous system (interstitial edema of white matter), inhibited oxidative phosphorylation in mitochondria of cells, atrophy of the thymus and thymus dependent lymphoid tissues resulting in the dysfunction of T cells for immunity, inhibited enzyme activity, lesions in the liver and bile ducts etc., although some specificity is observed among species of animals and organotin compounds. Recently we found that a single oral administration of triphenyltin fluoride to rabbits induces transient diabetes and diabetic lipemia by inhibiting insulin secretion from morphologically normal pancreatic B-cells...

Animals↗

Cell detachment and growth of fibroblasts as parameters for cytotoxicity of inorganic metal salts in vitro.

Eight inorganic metal compounds (AlCl3, Al(OH)3 gel, Al(OH)3 salt, SnCl2, ZnSO4, K2Cr2O7, CdCl2, HgCl2) were tested for their cytotoxic effect on an established hamster fibroblast line (BHK-21/C13) in vitro using a cell detachment assay and two different growth assays, the cloning efficiency and the cell number after 2 days subconfluent culture as parameters. The test conditions for these assays were optimized, including incubation period, application of test substance, growth conditions and data analysis. Aluminum, zinc and tin compounds showed low cytotoxic effects when compared to potassium, cadmium and mercuric compounds. Potassium dichromate was highly toxic in both growth assays (0.0001-0.01 mM, with a clear dependency on the incubation time), whereas it proved to be only slightly toxic in the detachment assay (0.1-5 mM). Cadmium and mercuric chlorides were the most toxic compounds in the growth (0.00001-0.001 mM) and the cell detachment assays (0.01-0.1 mM). Variable incubation periods barely affected the cytotoxicity of mercuric chloride. Ranking of these cytotoxicity data was found to be identical to the ranking of LD50 values (oral, rat) as well as to the ranking according to threshold limit values for human workroom environment, and of human eye irritation data.

Aluminum↗

Organometal-induced antinociception: a time- and dose-response comparison of triethyl and trimethyl lead and tin.

Recent reports have demonstrated that organolead and -tin compounds can alter behavioral reactivity to noxious stimuli. To further define the dose response and temporal characteristics of these neurobehavioral effects, male Fischer 344 rats were injected sc with either one-fourth, one-half, or three-fourths the acute LD50 of triethyl lead (TEL), triethyl tin (TET), trimethyl lead (TML), trimethyl tin (TMT), or distilled water and tested on a 57.5 degrees C hot plate 1, 7, 14, 21, and 28 days after dosing. All four organometals altered hot plate latencies, but the magnitude and time course of these effects differed among the compounds. TEL produced a dose-related increase in latencies which was maximal 1 and 7 days postdosing and had dissipated by 28 days. In contrast, the group administered TML (3/4 LD50) exhibited a late developing antinocioception which became evident 14 days after dosing and persisted throughout the period of testing. The intermediate dose of TMT (1/2 LD50) also produced a delayed increase in response times which was observed 21 and 28 days post-treatment. The 3/4 LD50 dose of TMT produced increased hot plate latencies on all post-treatment test days except Day 14. TET (1/2 LD50) produced increased hot plate latencies 1, 7, 14, and 21 days postdosing and also induced a reversible ataxia and akinesia. Higher doses of TET proved lethal to 80% of the animals and lower doses failed to alter response times in the hot plate. These data demonstrate that trialkyl lead and tin compounds can produce time- and dose-related increases in hot plate latencies.

Animals↗