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At least 19 recordsLinked to original sources
PubMed1991

Tin compounds inhibit the plasma cell response to metallic tin. Transfer of inhibition by parabiosis.

Injection of metallic tin powder causes intense proliferation of plasma cells in draining lymph nodes of Lewis rats. Pretreatment orally with soluble tin salts prevents this response to subsequently injected metallic tin. In the present work, pretreatment with tin salts by parenteral injection was just as effective as addition to the drinking water. This new approach made the following experiments possible. Poorly soluble tin compounds were found to be inhibitory when injected parenterally. Tin salts injected parenterally into one of two rats joined in parabiotic union prevented the plasma cell response to metallic tin in both parabionts. The transfer of the inhibitory effect via the cross-circulating blood represents significant progress toward understanding the mechanisms involved. The evidence suggests the possibility that tin salts elicit an intermediary substance or process that is responsible for inhibition of the plasma cell response to metallic tin.

Animals↗
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↗
PubMed2000

[Tin compounds in pharmacy and nutrition].

The occurrence of tin in plants, animals and humans is discussed, in relation to its abundance in the lithosphere and hydrosphere and the range of the different tin(II) and tin(IV) complexes formed. A reasoned consideration of its essentiality for living species is provided. It is concluded that tin is beneficial, even if not yet proved to be an essential element. After reference to the chemistry of tin compounds, there is a detailed discussion of their toxicity in animals and humans. Feasible routes for tin intake and uptake into humans are described. The past and current use of tin pharmaceuticals is reviewed and the areas for which they are currently permitted for use in humans as dentifrices and mouth washes, as radio-pharmaceuticals and for the treatment of jaundiced newborns are described. A detailed review of tin-containing antitumour agents as representative tin pharmaceuticals is also given. Finally, a list of tin-containing drugs and drug candidates is also shown.

Animal Nutritional Physiological Phenomena↗
PubMed1985

[Resistance to organic tin compounds mediated by plasmids of bacteria of Pseudomonas genus].

Resistance to organic tin compounds of P. aeruginosa and E. coli carrying antibiotic resistance plasmids and to P. putida containing biodegradation plasmids was studied. It was shown that 5 resistance plasmids and the biodegradation CAM plasmid of Pseudomonas increased 3-4 times the strain resistance to triethylstannylsuccinylimide and triethylstannylmaleinimide. All these plasmids belong to the P-2 incompatibility group and also determine the bacterial resistance to potassium tellurite. Isolation and investigation of the mutant plasmids loosing simultaneously the capacity for determination of resistance to potassium tellurite and organic tin compounds suggest that resistance to these compounds in the investigated plasmids is determined by the same genetic system.

Drug Resistance, Microbial↗
PubMed1998

Synthesis and biological activity of gold and tin compounds in ovarian cancer cells.

We have investigated the patterns of in vitro cytotoxicity, induced by six newly synthesized gold and tin compounds, in three human ovarian cancer cell lines (SW 626, IGROV 1 and OVCAR-3). Four gold compounds, i.e. gold(I)lupinylsulfide hydrochloride [1] (containing a naked gold atom), triethylphosphinogold(I)lupinylsulfide hydrochloride [2], triphenyl-phosphinogold(I)lupinylsulfide hydrochloride [3] and 1 ,2-bis(diphenylphosphino)ethane bis[gold(I)lupinylsulfide] dihydrochloride [4] (all containing a gold atom coordinated with different phosphines), were prepared. Moreover, the triethylphosphinogold(I)(2-diethylamino)ethylsulfide hydrochloride [5] in which the simple diethylaminoethylthiol replaced the bulky lupinylthiol was synthesized. The tin compound, triethyltin(IV)lupinylsulfide hydrochlorlde [6], was also studied. Comparative tests with cisplatin, the most widely used antitumor agent in ovarian cancer, were carried out in biological Investigations. In vitro cytotoxicity, by MTT assay, showed that compound [4] and compound [6] exhibited interesting antiproliferative activity in all the three cell lines (mean IC50=1.3 and 0.7 microM, respectively) compared to cisplatin (mean IC50=4.8 microM). In addition, the PA-1 cell line, more sensitive to cisplatin (IC50=0.6 microM), was included as a comparison in the study. Cell count assays confirmed the cytotoxic properties of compounds [4] and [6] against the four cell lines, reporting higher growth Inhibition potency than cisplatin, with IC50 values in the sub-micromolar range.

Antineoplastic Agents↗
PubMed2000

Effect of inorganic and organic tin compounds on ACh- and voltage-activated Na currents.

1. Inorganic tin and organotin compounds, occurring in aquatic ecosystems, are toxic and can cause behavioral abnormalities in living organisms. To determine the possible neuronal basis of these actions, the effects of both forms of Sn were studied on identified neurones of the mollusk, Lymnaea stagnalis L. 2. SnCl2 caused a dose-dependent decrease in the acetylcholine (Ach)-induced inward current. The effective threshold concentration, measured by a two microelectrode voltage clamp technique, was 0.1 microM, and the maximal effect occurred at 5 microM SnCl2. The depression of the inward current was greater after a 10 min preapplication (20%) than after 3 min treatment (7%). 3. The next series of experiments compared the actions of inorganic or organic tin compounds. In whole cell clamp experiments both (CH3)2SnCl2 and (CH3)3SnCl, like inorganic Sn, decreased the amplitude of Ach-induced current. Increasing the duration of the preapplication time resulted in an increase in the effect, but the action was not reversible. SnCl2 treatment caused a concentration-dependent alteration (initial potentiation followed by depression) of the amplitude of I(Na(V)) over the whole voltage range and slightly shifted the I-V curves to the left. In contrast, trimethyl tin decreased the amplitude of I(Na(V)) only at high concentration (100 microM). The activation time course of I(Na) was increased (tau = 0.43 ms in control and 0.55 ms in Sn), but Sn did not alter the inactivation parameters (tau = 3.43 and 3.41 ms). 4. These results support earlier findings that agonist- and voltage-activated channels are direct targets of toxic metals. We conclude that tin in both inorganic and organic forms acts at neuronal membranes to modulate synaptic transmission through direct actions on agonist-activated ion channels, and suggest that these actions may be the basis of the altered behavior of animals in tin-polluted environments.

Animals↗
PubMed2000

Solid-state and high-resolution liquid 119Sn NMR spectroscopy of some monomeric, two-coordinate low-valent tin compounds: very large chemical shift anisotropies.

High-resolution liquid- and solid-state 119Sn NMR spectroscopy was used to study the bonding environment in the series of monomeric, two-coordinate Sn(II) compounds of formula Sn(X)C6H3-2,6-Trip2 (X = Cl, Cr(eta 5-C5H5)(CO)3, t-Bu, Sn(Me)2C6H3-2,6-Trip2; Trip = C6H2-2,4,6-i-Pr3). The trends in the principal components of the chemical shift tensor extracted from the solid-state NMR data were consistent with the structures determined by X-ray crystallography. Furthermore, the spectra for the first three compounds displayed the largest 119Sn NMR chemical shift anisotropies (up to 3798 ppm) of any tin compound for which data are currently available. Relaxation time based calculations for the dimetallic compound 2,6-Trip2H3C6Sn-Sn(Me)2C6H3-2,6-Trip2 suggests that the chemical shift anisotropy for the two-coordinate tin center may be as much as ca. 7098 ppm, which is as broad as the 1 MHz bandwidth of the NMR spectrometer.

Journal Article↗
PubMed1982

Effects of organotin compounds on maximal electroshock seizure (MES) responsiveness in mice. I. TRI(n-alkyl)tin compounds.

Male mice (25-30 g) were injected (ip) with 0, 3.5 X 10(-6), or 17.5 X 10(-6) mol trimethyltin bromide (TMT), triethyltin bromide (TET), tri-n-propyltin chloride (TPT), or tri-n-butyltin bromide (TBT) per kg. Additional groups of mice were also injected (ip) with either 0 or 17.5 X 10(-6) mol sodium bromide (NaBr) or 17.5 X 10(-6) mol stannic bromide (SnBr4) per kg. The mice were tested with maximal electroshock seizure (MES) at 0.5, 4, 21-24, and 96 h following exposure to the organotin compounds. Mice exposed to TMT, TET, TPT, or TBT exhibited dose-dependent decreases in MES severity as evaluated by seizure-grade distributions and duration of tonic seizure phases. The tri-n-alkyltin compounds exhibited a structure-activity relationship in their ability to decreased maximal responsiveness to the MES test. In order of decreasing ability they were: TMT greater than TET greater than TPT greater than TBT. Administration of NaBr and SnBr4 did not alter MES responsiveness, indicating the essential role of the alkyl moieties of the tri-n-alkyltin compounds in producing alterations in central nervous system function.

Animals↗