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PubMed2004

The ion channel of F-ATP synthase is the target of toxic organotin compounds.

ATP is the universal energy currency of living cells, and the majority of it is synthesized by the F1F0 ATP synthase. Inhibitors of this enzyme are therefore potentially detrimental for all life forms. Tributyltin chloride (TBT-Cl) inhibits ATP hydrolysis by the Na(+)-translocating ATP synthase of Ilyobacter tartaricus or the H(+)-translocating counterpart of Escherichia coli with apparent Ki of 200 nM. To target the site of this inhibition, we synthesized a tritium-labeled derivative of TBT-Cl in which one of the butyl groups was replaced by a photoactivatable aryldiazirine residue. Upon illumination, subunit a of the ATP synthase becomes specifically modified, and this labeling is suppressed in the presence of the original inhibitor. In case of the Na+ ATP synthase, labeling is also suppressed in the presence of Na+ ions, suggesting an interference in Na+ or TBT-Cl binding to subunit a. This interference is corroborated by the protection of ATP hydrolysis from TBT-Cl inhibition by 105 mM Na+. TBT-Cl strongly inhibits Na+ exchange by the reconstituted I. tartaricus ATP synthase. Taken together these results indicate that the subunit a ion channel is the target site for ATPase inhibition by toxic organotin compounds. An inhibitor interacting specifically with this site has not been reported previously.

Adenosine Triphosphatases↗
PubMed2000

Reduced sperm counts in guppies (Poecilia reticulata) following exposure to low levels of tributyltin and bisphenol A.

There is increasing evidence that normal male reproductive function can be disrupted by exposure to pollutants in the environment that can exogenously mimic, antagonize or block sex-hormone function. One possible consequence of exposure to these xenobiotics is disruption to spermatogenesis, but results thus far provide only indirect and inconsistent evidence. In this study we exposed adult male guppies (Poeciliidae: Teleostei) to environmentally relevant levels of the common xenobiotics tributyltin (11.2-22.3 ngl-1) and bisphenol A (274-549 micrograms l-1) in experimental aquaria. After 21 days of exposure, we found significant declines (by 40-75%) in total sperm counts for male fishes exposed to tributyltin and bisphenol A compared with controls. This short-term decline in sperm count is unlikely to be the result of endocrine-mediated alteration of the germ line, and we found no change in testis size or sperm lengths between treatments. However, Sertoli cells, which facilitate the transport of maturing sperm into the testicular deferent duct (where they are stored prior to ejaculation), are directly sensitive to xenobiotic action and it is therefore possible that spermatogenesis was inhibited through in vivo interference with normal Sertoli-cell function.

Animals↗
PubMed2004

Liquid-phase microextraction of tributyltin and triphenyltin coupled with gas chromatography-tandem mass spectrometry. Comparison between 4-fluorophenyl and ethyl derivatizations.

This paper describes the liquid-phase microextraction (LPME) of tributyltin (TBT) and triphenyltin coupled with gas chromatography-tandem mass spectrometry. The 4-fluorophenylation and ethylation reactions were used for the derivatization of the organotins. For the two derivatizations, the LPME parameters such as organic solvent, stirring rate, temperature, extraction time and the other additional conditions were examined. Using pure water, the calibration curves, method detection limits (MDLs) and reproducibilities (RSDs) of the two derivatizations were compared under the respective optimized procedures. The 4-fluorophenyl derivatization, which showed a lower MDL (0.36 ng/l) and better reproducibility (RSD = 11% at 10 ng/l) for TBT, was applied to the analysis of seawater. The TBT was detected in the range from 1.1 to 2.0 ng/l in the seawater samples collected in Osaka Bay.

Buffers↗
PubMedDate not supplied

Monomethyl-and trimethyltin compounds induce learning deficiencies in young rats.

Male rat pups were exposed to monomethyltin trichloride (MMTC) and trimethyltin chloride (TMTC) via their dams' drinking water throughout gestation and post partum until 21 days of age. At 11 days of age, the pups were tested for acquisition and extinction learning ability in an appetitive learning paradigm, and at 21 days for learning ability in a one trial swim escape learning test. At 11 days, pups from dams exposed to 120 mg/l Sn as MMTC and to 1.0 mg/l Sn as TMTC displayed statistically significant increases in acquisition time, while all dose groups (12, 40, 120 mg/l MMTC and 0.15, 0.5, 1.0 mg/l TMTC) displayed significant decreases in extinction learning ability as compared to controls. At 21 days of age, animals exposed to 12 mg/l and 120 mg/l MMTC displayed higher escape times than controls, as did animals exposed to 0.5 mg/l TMTC.

Animals↗
PubMed2003

Comparison of hepatotoxicity and metabolism of butyltin compounds in the liver of mice, rats and guinea pigs.

The hepatotoxicity of tributyltin chloride (TBTC) and dibutyltin dichloride (DBTC) was compared among mice, rats and guinea pigs in vivo. Further, the metabolism of these butyltin compounds in the liver was also investigated in these species. The oral administration of TBTC and DBTC to mice induced obvious liver injury, as demonstrated by both serodiagnosis and histopathological diagnosis. The concentrations of TBTC and DBTC that induced hepatotoxicity in mice at 24 h after oral administration were 180 and 60 micro mol/kg, respectively. In the case of rats, the liver injury induced by TBTC and DBTC was detected at 24 h by the serodiagnosis, but not by histopathological diagnosis. On the other hand, in guinea pigs, TBTC and DBTC administration did not produce any clear liver injury at 24 h, as evaluated by these two diagnostic methods. Thus, the following ranking was obtained with regard to increasing order of sensitivity to liver injury caused by TBTC and DBTC: mice, rats and guinea pigs. The total butyltin contents in the liver of mice were equivalent at 3 h and 24 h after the administration of TBTC or DBTC; however, the contents in the liver of rats and guinea pigs were relatively lower at 3 h and higher at 24 h than those of mice, although there were no differences between rats and guinea pigs in the total liver butyltin content. Concerning the liver metabolism of these butyltin compounds, the main form of butyltin compounds in these animals treated with TBTC was DBTC within 3 h after oral administration, while the main metabolites at 24 h were different in each species, indicating that the liver metabolism of TBTC might vary by animal type. When the animals were treated with DBTC orally, DBTC was hardly metabolized in the livers of these animals even at 24 h, and the liver levels of DBTC were two times greater in mice and guinea pigs than in rats at 3 h and were lower in mice at 24 h than in rats and guinea pigs. The analysis of cellular distributions of DBTC in the liver at 3 h after the administration showed that the levels of DBTC in the nuclear, microsomal and mitochondrial fractions of mice hepatocytes were relatively higher than in those of rats, which were greater than in those of guinea pigs. These results suggest differences in the sensitivity of mice, rats and guinea pigs to hepatotoxicity caused by butyltin compounds and demonstrate that the difference in the sensitivity of these animals to the hepatotoxicity induced by TBTC and DBTC may be partly due to differences in hepatic metabolism of TBTC and in the distribution of DBTC within cell organelles, respectively.

Administration, Oral↗
PubMed2004

In-situ partitioning of butyltin compounds in estuarine sediments.

The in-situ solid/pore-water partitioning of tributyltin (TBT), dibutyltin (DBT) and monobutyltin (MBT) was determined for an estuarine sediment profile collected from a commercial marina. Total butyltin levels exceeded sediment quality guideline values, and were 220-8750 microg/kg for TBT, 150-5450 microg/kg for DBT and 130-4250 microg/kg for MBT. Pore-water butyltin concentrations ranged from 0.05 to 2.35 microg/l for TBT, 0.07-3.25 microg/l for DBT, and 0.05-0.53 microg/l for MBT. The partitioning of butyltin compounds between the sediment solid-phase and pore-water was described by an organic carbon normalised distribution ratio (D(OC)). The observed D(OC) values were similar for TBT, DBT and MBT, and were 10(5)-10(6) l/kg. Values for the Butyltin Degradation Index (BDI) were larger than 1 at depths greater than 10 cm below the sediment/water-column interface. This indicates that substantial TBT degradation has occurred in the sediments, and suggests that natural attenuation may be a viable sediment remediation strategy.

Carbon↗
PubMed2006

Response to alkyltins of two Na+-dependent ATPase activities in Tapes philippinarum and Mytilus galloprovincialis.

Organotin effects on the Na-dependent ATPases involved in ionic regulation of aquatic animals are poorly known, in spite of the largely documented contamination of seafood, especially bivalve molluscs. This study deals with the in vitro effect of TBT on the Na,K-ATPase and the ouabain-insensitive Na-ATPase in gill and mantle microsomes from the cultured bivalve molluscs Tapes philippinarum and Mytilus galloprovincialis. In the mussel also MBT, DBT and TeET were tested. While in both species the Na-ATPase showed an overall refractoriness to organotins, the Na,K-ATPase was progressively inhibited by increasing TBT concentrations (0-34 microM). In both species the Na,K-ATPase activity was more strongly inhibited in the gills than in the mantle. At the maximal TBT concentration tested (34.4 microM), while gill Na,K-ATPase activity was abolished, mantle enzyme activity was, respectively, reduced to 20% in T. philippinarum and to 50% in M. galloprovincialis. Mussel Na,K-ATPase was differently susceptive to the organotins tested and in both tissues showed an inhibition efficiency order TBT>DBT>>MBT=TeET (no effect), tentatively related to the different organotin polarity and to a possible interaction with membrane-bound enzyme complexes. The different response of the two ATPases to organotins is consistent with the known different susceptivity of the two enzyme activities to environmental contaminants, assay conditions and endogenous factors.

Animals↗
PubMed1998

Trace analysis of tributyltin and triphenyltin compounds in sea water by gas chromatography-negative ion chemical ionization mass spectrometry.

An analytical gas chromatography-mass spectrometry (GC-MS) method using negative ion chemical ionization (NICI) has been investigated for the determination of trace tributyltin (TBT) and triphenyltin (TPhT) compounds in sea water. TBT and TPhT were extracted from samples as chloride under the acidic condition of HCl. Doping of the GC system with a dilute HBr-methanolic solution resulted in direct detection of the chlorides of TBT, TPhT and tripentyltin (TPenT, internal standard). As the result of HBr doping, a sharp peak of the respective organotin bromides appeared: during GC analysis, halogen exchange from the chloride to the bromide occurred. NICI-MS was highly selective and sensitive for the detection of TBT. TPhT and TPenT bromides. In the selected ion monitoring mode of NICI-MS, the minimum detectable amounts defined as the signal equal to three times the standard deviation (3 sigma) of the baseline noise were 20 and 25 pg ml-1 for TBT and TPhT, respectively. These amounts are approximately 250-400 times better than those in electron impact mode. The combination of GC using an apolar capillary column doped with a dilute HBr-methanolic solution and NICI-MS made it possible to determine TBT and TPhT at less than the ng l-1 level in sea water.

Gas Chromatography-Mass Spectrometry↗
PubMed2002

Inhibitory effects of organotin compounds on voltage-dependent, tetrodotoxin-resistant Na+ channel current in guinea pig dorsal root ganglion cells.

The effects of organotin compounds on voltage-dependent, tetrodotoxin (TTX)-resistant Na+ channel current (I(Na)) in single cells isolated from guinea pig dorsal root ganglion were investigated using a whole cell patch clamp technique. Extracellular application of tributyltin (TBT) inhibited I(Na) in a concentration-dependent manner with an IC50 of 7.2 microM. TBT (100 microM), when applied intracellularly, was without effect. Triphenyltin (TPT, 100 microM) and dibutyltin (DBT, 100 microM), applied extracellularly, inhibited I(Na) with an efficacy ranking of TBT>TPT>DBT. Monobutyltin (100 microM), whether applied externally or internally, had little effect on I(Na). TBT (30 microM) significantly prolonged both time to peak and half-decay time of I(Na) and shifted the activation curve of I(Na) in the positive direction without changing the slope. No such effect was produced by TPT (100 microM). The results indicate that organotin compounds inhibit voltage-dependent, TTX-resistant Na+ channel activity and suggest that the inhibitory action may account, at least in part, for their neurotoxic effects.

Animals↗
PubMed2004

Construction of azacycles based on endo-mode cyclization of allenes.

A new procedure for constructing monocyclic five- and six-membered azacycles by the endo-mode ring-closing reaction of allenylazido derivatives under neutral conditions has been developed. The azabicyclo[m.n.0] compounds were prepared by applying this newly developed procedure. The seven-membered azacycle was prepared when the allene possessing an unsubstituted carboxyl amido functionality was submitted to the basic conditions. In addition, indole and quinoline skeletons were synthesized using this procedure.

Alkadienes↗
PubMed2002

Mixture toxicity of priority pollutants at no observed effect concentrations (NOECs).

Environmental exposure situations are often characterised by a multitude of heterogeneous chemicals with ambiguous or unknown modes of action present at low concentrations. While multiple exposure is widely acknowledged, arguments are raised that adverse combined effects might not be evoked by mixtures of substances with dissimilar modes of action and being present at only low concentrations. In this study the combined effect of a multiple mixture composed of structurally dissimilar priority pollutants with mostly unknown modes of action has been investigated using an algal biotest. The concentrations of the components in the mixture equalled statistically estimated, individual no observed effect concentrations (NOECs). The observed mixture toxicity was not only clearly higher than expected for any single substance alone, but also well predictable using the concept of independent action.

Atrazine↗
PubMed2003

Effects of butyltin compounds on mitochondrial respiration and its relation to hepatotoxicity in mice and Guinea pigs.

Because the mechanisms responsible for the difference in toxicity between different experimental animal species remain unclear, the effects of tributyltin chloride (TBTC) and dibutyltin dichloride (DBTC) on mitochondrial respiration were compared among the livers of mice and guinea pigs in vitro and in vivo. Further, the levels of these butyltin compounds and their derivatives in the mitochondrial fractions of the hepatocytes were investigated in these animal species. Administration of TBTC and DBTC to mice resulted in the obvious elevation of serum enzymatic activities, as well as the inhibition of succinate-linked State 3 respiration in hepatic mitochondria at 24 h after administration. On the other hand, these metal compounds failed to induce such hepatotoxicity or to inhibit mitochondrial respiration in guinea pigs. There was no significant difference between mice and guinea pigs in the IC50 (metal concentration observed in 50% inhibition of mitochondrial respiration) of TBTC and DBTC against the succinate-linked State 3 respiration of hepatic mitochondria in vitro, although the mitochondrial respiration of succinate-linked State 3 was inhibited in the liver of mice treated with the metals in vivo. The levels of total butyltin compounds in the mitochondrial fractions of hepatocytes were higher in the mice than in the guinea pigs, and the main butyltin compound in the mitochondrial fractions was DBTC in both species at 24 h after TBTC or DBTC administration. The amount of sulfhydryl groups, which were capable of binding with DBTC, in mice hepatic mitochondria was twice as large as that in guinea pigs, and the affinity of DBTC for the isolated hepatic mitochondria was higher in mice than in guinea pigs in vitro. These results suggested that the induction of hepatotoxicity by TBTC and DBTC in vivo was closely associated with the depression of mitochondrial respiration and that the difference in susceptibility to the metal-induced mitochondrial damages between mice and guinea pigs might result from the high affinity of butyltin compounds, in particular DBTC, for hepatic mitochondria in mice containing higher levels of sulfhydryl groups, compared with guinea pigs.

Administration, Oral↗
PubMedDate not supplied

Comparative developmental toxicity of di-, tri- and tetrabutyltin compounds after administration during late organogenesis in rats.

Dibutyltin dichloride (DBT), tributyltin chloride (TrBT) and tetrabutyltin (TeBT) were compared for their developmental toxicity and teratogenic potential following administration during the susceptible period for teratogenesis of TrBT. Pregnant rats were given either DBT or TrBT at a dose of 165 or 330 mumol kg-1 or TrBT at a dose of 330, 660, 1320, 2640 or 5280 mumol kg-1 on days 13-15 of pregnancy. Treatment with DBT at 165 and 330 mumol kg-1 caused a significant decrease in the maternal body weight gain. A significant decrease in the fetal weight occurred at 165 and 330 mumol kg-1. No significantly increased incidences of postimplantation loss or of fetuses with malformations were found following treatment with DBT. Treatment with TrBT at 165 and 330 mumol kg-1 resulted in a significant decrease in the maternal weight gain. A significant decrease in the fetal weight was found at 330 mumol kg-1. A significantly and markedly increased incidence of fetuses with cleft palate was noted in both groups treated with TrBT. Treatment with TeBT caused a significantly decreased maternal body weight gain at doses of 660 mumol kg-1 and above. A significantly increased incidence of fetuses with cleft palate was observed at a dose of 5280 mumol kg-1. It could be concluded that there is a difference in the manifestation and degree of developmental toxicity between DBT, TrBT and TeBT.

Abnormalities, Drug-Induced↗
PubMed1994

Rapid cytoskeleton modification in thymocytes induced by the immunotoxicant tributyltin.

Treatment of rat thymocytes with the immunotoxic environmental pollutant tributyltin (TBT) caused a rapid decrease in the F-actin content resulting in the depolymerization of 80% of the total thymocyte F-actin in 10 min. Removal of extracellular Ca2+ and pretreatment of the thymocytes with the intracellular Ca2+ chelator, 1,2-bis(2-aminophenoxy)ethane-N',N',N',N',-tetraacetic acid, abolished the TBT-induced increase in cytosolic free Ca2+ concentration but reduced the depolymerization of F-actin by only 25%. Thus, the data suggest that 75% of the decrease in F-actin content in the thymocytes was due to other effects of TBT. Pretreatment of rat thymocytes with the alkylating agent N-ethylmaleimide completely inhibited TBT-induced F-actin disruption, suggesting that thiol group modification is involved. The TBT-induced decrease in thymocyte F-actin was not specific for any particular subpopulation of thymocytes. Furthermore, triphenyltin and the metabolite of TBT, dibutyltin, were also found to induce depolymerization of thymocyte F-actin, whereas nonimmunotoxic organotin compounds like trimethyltin and triethyltin had no effect. In conclusion, TBT was found to induce rapid depolymerization of F-actin in thymocytes through both Ca(2+)-dependent and Ca(2+)-independent mechanisms, suggesting that the potent immunotoxic effect of TBT may involve cytoskeletal modifications in addition to the perturbation of thymocyte Ca2+ homeostasis reported previously.

Actin Cytoskeleton↗
PubMed2002

Application of a heated electrospray interface for on-line connection of the AAS detector with HPLC for detection of organotin and organolead compounds.

A heated electrospray interface that affords high sensitivity and long-term signal stability for AAS detection of metal-containing analytes in organic or organic-water solvents after HPLC separation is described. The vitreous body of the electrospray interface is externally heated above the boiling point of the solvent and quartz furnace AAS is used for detection. Interface working conditions were optimized with a full experimental design for the detection of tin- (tetramethyl-, tetraethyl-, tetrabutyl-, and tetrapentyltin, tributyltin chloride, dibutyltin dichloride, and butyltin trichloride) and lead- (tetraethyl- and tetraphenyllead) containing compounds in the column eluate. The heated electrospray interface enables use of a wide range of flow rates - from 50 to 1000 micro L min(-1). The measurement sensitivity and detection limit achieved were compared with those obtained by use of the thermospray interface and post-column conversion of the organotin compounds to gaseous hydrides. The detection limits for the low-molecular weight species of the homologous series (2.8+/-0.1 ng (140+/-5 ng mL(-1)) for tetramethyltin and 3.1+/-0.2 ng (155+/-10 ng mL(-1)) for tetraethyltin) were obtained approximately one order of magnitude lower than those obtained by use of the thermospray interface. With this HPLC-ES-QFAAS system the tributyltin content of BCR reference material 477, mussel tissue, was analyzed. This system was also applied to analysis of tetraethyllead in gasoline samples.

Animals↗
PubMed1987

Increased free intrasynaptosomal Ca2+ by neurotoxic organometals: distinctive mechanisms.

Effects of several alkylmetals on free intrasynaptosomal Ca2+ concentration, [Ca2+]i, were studied in vitro using the fluorescent Ca2+ indicator fura-2. Neurotoxic alkylmetals methylmercury (Met-Hg), triethyllead (TEL), triethyltin (TET), and trimethyltin (TMT) (at 2.5-30 microM) increased [Ca2+]i to different degrees. Met-Hg was the most potent, elevating [Ca2+]i 100-800 nM, dose dependently and significantly more than high K+ (150 nM) or veratridine (350 nM). The effect of Met-Hg could not be inhibited with a Ca2+ channel blocker, verapamil, nor with a Na+ channel blocker, tetrodotoxin. Inhibition of the mitochondrial Ca2+ uptake in situ with rotenone + oligomycin decreased the potency of Met-Hg to elevate [Ca2+]i but did not change the resting [Ca2+]i. Met-Hg also slightly decreased synaptosomal ATP. TEL and TET elevated [Ca2+]i by 100-200 nM. The effect of TEL, but not that of TET, could be blocked with verapamil (36%) and veratridine (67%). TEL was less efficient in the presence of ouabain. Neither TEL nor TET had significant mitochondrial effects in situ contributing to [Ca2+]i. TMT increased [Ca2+]i less than TET while dimethyltin and methyltin were inactive. These results indicate that neurotoxic derivatives of alkylmetals studied increase [Ca2+]i. This occurs mainly either by nonspecific increase (Met-Hg, TET) of Ca2+ leakage through the plasma membrane and/or specific interference with the mechanisms regulating Ca2+ fluxes through the plasma membrane (TEL).

Adenosine Triphosphate↗