Effects of some organotin compounds on tissue amine levels in rats.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
The effects of triethyltin on Ca2+ mobilization in human PC3 prostate cancer cells have been explored. Triethyltin increased [Ca2+]i at concentrations larger than 3 microM with an EC50 of 30 microM. Within 5 min, the [Ca2+]i signal was composed of a gradual rise and a sustained phase. The [Ca2+]i signal was reduced by half by removing extracellular Ca2+. The triethyltin-induced [Ca2+]i increases were inhibited by 40% by 10 microM nifedipine, nimodipine and nicardipine, but were not affected by 10 microM of verapamil or diltiazem. In Ca2+-free medium, pretreatment with thapsigargin (1 microM), an endoplasmic reticulum Ca+ pump inhibitor, reduced 200 microM triethyltin-induced Ca+ increases by 50%. Pretreatment with U73122 (2 microM) to inhibit phospholipase C did not alter 200 microM triethyltin-induced [Ca2+]i increases. Incubation with triethyltin at a concentration that did not increase [Ca2+]i (1 microM) in Ca2+-containing medium for 3 min potentiated ATP (10 microM)- or bradykinin (1 microLM)-induced [Ca2+]i increases by 41 +/- 3% and 51 +/- 2%, respectively. Collectively, this study shows that the environmental toxicant triethyltin altered Ca2+ handling in PC3 prostate cancer cells in a concentration-dependent manner: at higher concentrations it increased basal [Ca2+]i; and at lower concentrations it potentiated agonists-induced [Ca2+]i increases.
The current status of global marine pollution by TBT (tributyltin), TPT (triphenyltin) and polychlorinated biphenyls (PCBs) was examined by determining their concentrations in squid livers. TBT and TPT concentrations in squid livers were higher in coastal waters than in open oceans. The highest values of TBT and TPT of 279 and 519 ng g(-1), respectively, were detected off Japan. TBT concentrations were higher in the northern hemisphere than those of the southern hemisphere organisms. TPT was not detected in squid livers collected in the southern hemisphere. The variation in TBT and TPT concentrations between the northern and the southern hemisphere was greater than those recognized for PCBs distribution in the world oceans. This global distribution pattern of TBT, TPT and PCB seemed to reflect their usage (amount, period and manner of utilization). Approximate TBT concentrations in seawater estimated from bioaccumulation factor in the squid liver were 0.1-5.8 ng litre(-1) in waters around Japan, tr-0.8 ng litre(-1) in oceanic waters in the northern hemisphere, and tr-0.4 ng litre(-1) in the southern hemisphere oceans.
The accumulation, transformation, and depuration of tri-n-butyltin (TBT) were studied over periods of approximately 60-70 days using marine mussels, Mytilus graynus and Mytilus edulis, under natural conditions. M. graynus collected at a lightly polluted site were transplanted to a highly polluted site and M. edulis collected at a highly polluted site were transplanted to a lightly polluted site. TBT taken up in M. graynus showed a bioconcentration factor of 10 500 in the accumulation phase. Di-n-butyl(3-oxobutyl)tin, which is a main metabolite of TBT in M. edulis, showed a longer half-life (8.13 days) than that of the parent compound (4.82 days) in the depuration phase. On the other hand, another metabolite, di-n-butyl(3-hydroxybutyl)tin, showed a shorter half-life (3.98 days) than that of the parent compound. The different half-lives among TBT and its metabolites are responsible for the different metabolic patterns in blue mussels at each sampling time.
A novel method for palladium-catalyzed cyanation of aryl bromides promoted by low-level tri-n-butyltin chloride or cyanide is described. The method features low catalyst loading and mild reaction conditions. KCN is used as the cyanide source. Only trace levels of the tri-n-butyltin compound are required to achieve high conversion and yield in the cyanation of aryl bromides, iodides, and triflates.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Mammalian exposure to toxic levels of the trialkyltin compounds, triethyltin (TET) and trimethyltin, results in pathological manifestations largely restricted to the nervous system. The remarkable features of TET toxicity are cerebral edema and muscular weakness. Rats exposed orally to TET (10-30mg TET Br/l of drinking water) progress through an increasingly compromised state beginning with mild ataxia and hindlimb weakness after one week, spastic paresis of the hindlimbs by two weeks; and hindlimb paraplegia and sensory changes by 3 weeks. Histopathological studies of chronic TET-exposed rats report minimal ultrastructural damage to distal peripheral nerves, myelin, and muscle. Chromatolytic reactions are observed in some alpha motor neurons; intramyelinic vacuolization in the ventral roots and horn is substantial by 3 weeks. Myelin vacuolization and degeneration are observed to a lesser extent in the dorsal roots of the spinal cord. Wet weights and myofiber diameters of EDL and soleus muscles are reduced during chronic TET intoxication, but no histopathology is evident using light microscopy. Conduction of compound action potentials in vivo along distal sensory fibers, ventral roots and distal motor fibers (in sciatic n.) is normal in 3 week TET rats as compared to control; however, nerve conduction velocity is decreased in the segment of the H-reflex arc involving the dorsal roots. Earlier studies by Stoner and coworkers led to suggestions that the neuromuscular junction may be preferentially affected by TET and could contribute, in part, to the symptoms of muscular weakness. In support of this hypothesis preliminary studies from our laboratory and others indicate that neurotransmission is functionally depressed at the myoneural junction following chronic TET treatment in vivo or when applied in vitro to isolated muscle preparations. Stimulated, but not unstimulated, release of acetylcholine from the vascular perfused rat phrenic nerve-hemidiaphragm preparation is decreased by TET especially at higher stimulation rates (20 Hz). In vitro administration of TET Br (10(-6)M) results in an irreversible decrease in the amplitude of evoked endplate potentials; chronic in vivo exposure to TET causes a decrease in the resting membrane potential of soleus muscle (in situ recordings) and provokes a peculiar post-stimulus (200Hz bursts) elevation of spontaneous miniature endplate potentials in isolated cut diaphragm preparations.(ABSTRACT TRUNCATED AT 400 WORDS)
Explore the source record for details and available documents.
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.
A method is described for the simultaneous determination of butyl- and phenyltin compounds in oyster samples. The organotin compounds were extracted (as chlorides) from oyster homogenates with hydrochloric acid and benzene in the presence of 0.05% tropolone. These compounds were converted into pentyl derivatives with pentyl Grignard reagent and then analysed by capillary gas chromatography with a flame photometric detector equipped with a 393-nm filter. The recoveries of six organotin compounds added to oyster samples ranged from 71 to 74%. The detection limits of butyl- and phenyltin compounds were in the 5-9 pg range as tin. We detected significant amounts of three organotin compounds (di- and tributyltin and triphenyltin) in oyster samples.
The reactions with DNA of two antitumor active organotin(IV) compounds, the dimer of bis[(di-n-butyl 3,6-dioxaheptanoato)tin] (C(52)H(108)Sn(4)O(1) x 2H(2)O), compound 1, and tri-n-butyltin 3,6,9-trioxodecanoate (C(19)H(40)SnO(5) x 1/2H(2)O), compound 2, were analysed by circular dichroism, DNA melting experiments and gel mobility shift assays. It is found that both complexes modify only slightly the B-type circular dichroism spectroscopy (CD) spectrum of calf thymus DNA. On the other hand, both complexes were found to affect significantly the parameters of the thermally induced helix-to-coil transition. Addition of 1 or 2 to calf thymus DNA samples does not favor DNA renaturation after melting ruling out formation of interstrand crosslinks. Moreover, the effects of both compounds on plasmid DNA gel mobility were investigated. From the analysis of the present results it is inferred that both organotin(IV) compounds do interact with DNA, probably at the level of the phosphate groups.
A novel electrospray ionization (ESI) mass spectrometric approach for the structure elucidation of ionic organotin(IV) compounds or complexes with weakly bonded ligands as for example monodentate carboxylates or sulfonates is proposed using both positive-ion and negative-ion ESI tandem mass spectra. The ionization mechanism of organotin(IV) compounds involves the cleavage of the most labile bond with an ionic character yielding two complementary ions, [Cat]+ and [An]-. Positively charged species containing tin atom, [Cat]+, are analyzed in the positive-ion mode and negatively charged species without the tin atom, [An]-, in the negative-ion mode. Fragmentation patterns of [C24H29N2Sn]+, [C21H22NSn]+, and [C17H30NSn]+ ions are proposed based on the detailed interpretation of MSn spectra, which is simplified by an easy recognition of characteristic tin isotopic clusters in particular fragment ions. Proposed fragmentation mechanisms are supported by comparison with MSn spectra of deuterium-labeled analogues. The applicability of this method is illustrated on two sets of organotin(IV) compounds, including seven [2,6-bis(dimethylaminomethyl)phenyl]diphenyltin(IV) derivatives with small inorganic counteranions X (Br, NO3, SCN, BF4, SeCN, CN, PF6), six organotin(IV) complexes containing two C,N-chelating ligands with azo dyes, and the identification of unknown hydrolysis products.
Organotin compounds are used in a variety of applications including stabilizers, catalysts, antifouling agents, and biocides. Because of the widespread use of organotin compounds in industry and their wide range of toxic effects, it is important to measure worker exposure to specific organotin compounds. Three butyltin compounds were selected for this study--butyltin trichloride, dibutyltin dichloride, and tributyltin chloride. These three compounds are typically present in the same work environment; therefore, developing a sampling and analytical method that would allow all three butyltin compounds to be sampled and analyzed simultaneously was desired. A derivatization procedure using sodium tetraethylborate (STEB) was selected for study and validation. The validation study demonstrated that sampling using the Occupational Safety and Health Administration (OSHA) Versatile Sampler (OVS) with XAD-2 resin sorbent and analysis using gas chromatography/flame photometric detection (GC/FPD) can be used to evaluate worker exposures to specific butyltin chlorides over the range of 5 to 270 micrograms/m3 collected at a flowrate of 0.25 L/min over a 3-hour period for a 45-L air sample. Breakthrough studies at 1.5 times the occupational exposure guideline (OEG) of 0.05 mg/m3 showed that samples could be collected at flowrates up to 0.5 L/min for 12 hours without breakthrough. The 14-day storage stability study showed apparent degradation of tributyltin and monobutyltin within a 3-day storage period at both ambient and refrigerated temperatures. There was no further degradation from 3 to 14 days. The stability of dibutyltin was unaffected by storage condition over the 14-day storage study. Subsequent stability studies incorporating a spiking solution control sample were conducted extending the stability study out to 27 days. These data show that all three butyltins were stable at either ambient or refrigerated conditions.