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PubMed1991

Cytotoxic action of triphenyltin on mouse thymocytes: a flow-cytometric study using fluorescent dyes for membrane potential and intracellular Ca2+.

Effects of triphenyltin on mouse thymocytes were examined using fluorescent dyes to monitor membrane potential and intracellular Ca2+. Triphenyltin at 3 x 10(-7) M to 1 x 10(-6) M hyperpolarized thymocytes and depolarized them at 3 x 10(-6) M or more, associated with increasing intracellular Ca2+. Hyperpolarization was suppressed by quinine, but not by tetraethylammonium and 4-aminopyridine, suggesting the involvement of Ca(2+)-activated K+ current. Triphentyltin failed to hyperpolarize thymocytes in Ca(2+)-free solution. Results indicate that triphenyltin promotes Ca(2+)-influx to thymocytes. Such an action of triphenyltin may be related to the immunotoxicity of organotins.

4-Aminopyridine↗
PubMed1992

Triphenyltin-induced increase in the intracellular Ca2+ of dissociated mammalian CNS neuron: its independence from voltage-dependent Ca2+ channels.

To test the possibility that triphenyltin (TPT) increases the intracellular Ca2+ ([Ca2+]i) in neurons as found previously in thymocytes, the effect of TPT on [Ca2+]i was examined in rat cerebellar neurons by a flow-cytometer with fluorescent dyes. TPT at concentrations ranging from 3 x 10(-7) M to 1 x 10(-5) M dose-dependently increased the [Ca2+]i. The TPT-induced increase in [Ca2+]i was not attenuated by a Ca2+ channel blocker, suggesting that it was not dependent on voltage-dependent Ca2+ channels. As the concentration of external Ca2+ ([Ca2+]e) increased, TPT produced a more profound increase in the [Ca2+]i. However, the increase in the [Ca2+]i by TPT was observed even in nominally [Ca2+]e-free solution. These results suggest two possibilities. First, TPT may promote Ca(2+)-influx to the neuron. Secondly, TPT may affect the intracellular Ca-store sites. This study is relevant to the neurotoxicity of organotins because it has become progressively clear that sustained increases in the [Ca2+]i can activate various Ca(2+)-dependent degradative processes.

Animals↗
PubMed1992

Characterization of the triphenyltin-induced increase in intracellular Ca2+ of mouse thymocytes: comparison with the action of A23187.

The properties of triphenyltin (TPT) in increasing intracellular Ca2+ ([Ca2+]i) of thymocytes was studied, in comparison with those of A23187, by the use of fluorescent dyes to monitor membrane potential and [Ca2+]i. Both 1 microM TPT and 30 nM A23187 increased the [Ca2+]i associated with the hyperpolarization mediated by Ca(2+)-dependent K+ conductance. The time course for the TPT-induced increase in the [Ca2+]i was much slower than that of A23187. When the external Ca2+ ([Ca2+]o) was removed, TPT produced a slight, but persistent, increase in the [Ca2+]i while A23187 caused only a transient increase in the [Ca2+]i. Reintroduction of Ca2+ to the external solution produced an increase in [Ca2+]i in both cases. Therefore, these results suggested that the increase in the [Ca2+]i of thymocytes induced by TPT and A23187 was dependent on the presence of [Ca2+]o and an intracellular Ca store. The potency of TPT in increasing the [Ca2+]i was greater than those of diphenyltin and monophenyltin, suggesting an involvement of the lipophilic property of organotins in increasing [Ca2+]i. The TPT-induced increase in the [Ca2+]i may be partly responsible for the toxicity of TPT on organs and/or organ systems.

Animals↗
PubMed1991

[The effects of prenatal triphenyltin exposure on learning and development in the rat].

The toxicity of prenatal triphenyltin (TPT) exposure was studied in THA rats. Doses of 0 (control), 4 or 8 mg/kg/day of TPT were administered to pregnant rats from day 6 to day 20 of gestation by gastric intubation. In dams, the body weight of the 8 mg/kg group was significantly lower than that of control group, and 2 of 4 rats died on the expected day of delivery. In offspring, little effect of TPT on body weight, pinna detachment, incisor eruption, eye opening, surface righting, cliff avoidance, pivoting and negative geotaxis was found in either the 4 mg/kg or 8 mg/kg groups. In the Sidman avoidance test, the avoidance rate of the TPT groups was lower than that of the control group, and significant differences were found in the female groups. In a reversed test on the water E-maze test, the swimming time to the goal and the number of errors were increased in the TPT groups. These results suggest that prenatal TPT administration disrupts the learning acquisition of rats.

Animals↗
PubMed1994

[Comparative study on placental transfer and maternal distribution of organic and inorganic tin following oral administration in pregnant rats].

Placental transfer and body distribution of triphenyl tin chloride (TPTC) and tin chloride (SnCl2) were investigated in pregnant rats. Pregnant wistar rats were orally administered TPTC at 0, 1.0 and 2.0 mg/rat/day during 6-10 and 14-18 days of gestation, and with SnCl2 at 0 and 20 mg/rat/day on 7, 10 and 15 days of gestation (group treated 3 times) or 6-10 and 13-16 days of gestation at 0 and 20 mg/rat/day (group treated 9 times). On day 20 of gestation in rats treated with TPTC, and day 17 in rats with SnCl2, fetuses, placentas, maternal blood and organs were obtained for analyses. Mean fetal tin levels from rats treated with 1.0 and 2.0 mg TPTC were 0.05 and 0.11 microgram/g wet weight, respectively, these values being significantly (P < 0.01) higher than in the control group. The latter was higher than the former at a significance level of 5%. No significant difference between fetal tin levels from rats treated with SnCl2 and the control group could be detected. Following oral TPTC administration, tin was present in maternal liver, kidney and brain in high concentrations. Following the oral administration of SnCl2, the tin level was highest in bone and kidney, but none could be detected in the brain.

Administration, Oral↗
PubMed2005

Organotins disrupt the 11beta-hydroxysteroid dehydrogenase type 2-dependent local inactivation of glucocorticoids.

Organotins, important environmental pollutants widely used in agricultural and industrial applications, accumulate in the food chain and induce imposex in several marine species as well as neurotoxic and immunotoxic effects in higher animals. Reduced birth weight and thymus involution, observed upon exposure to organotins, can also be caused by excessive glucocorticoid levels. We now demonstrate that organotins efficiently inhibit 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), converting active 11beta-hydroxyglucocorticoids into inactive 11-ketoglucocorticoids, but not 11beta-HSD1, which catalyzes the reverse reaction. Di- and tributyltin as well as di- and triphenyltin inhibited recombinant and endogenous 11beta-HSD2 in lysates and intact cells with IC50 values between 500 nM and 3 microM. Dithiothreitol protected 11beta-HSD2 from organotin-dependent inhibition, indicating that organotins act by binding to one or more cysteines. Mutational analysis and 3-D structural modeling revealed several important interactions of cysteines in 11beta-HSD2. Cys90, Cys228, and Cys264 were essential for enzymatic stability and catalytic activity, suggesting that disruption of such interactions by organotins leads to inhibition of 11beta-HSD2. Enhanced glucocorticoid concentrations due to disruption of 11beta-HSD2 function may contribute to the observed organotin-dependent toxicity in some glucocorticoid-sensitive tissues such as thymus and placenta.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed1983

[The effect of triphenyltin fluoride on aggregation, ATP secretion and malondialdehyde formation of rabbit platelets in vitro].

Recent studies have demonstrated that triphenyltin fluoride (TPTF), widely used as an agricultural chemical and a marine antifoulant, inhibits collagen-induced platelet aggregation and ATP secretion in rabbits ex vivo. The aim of the present investigation was to elucidate the mechanism of the inhibitory action of TPTF by investigating platelet malondialdehyde (MDA) formation, aggregation and ATP secretion following the stimulation by various stimuli of rabbit platelets treated in vitro with TPTF, other triphenyl metals and aspirin. Although no inhibitory effect of TPTF was found on sodium arachidonate-induced platelet aggregation and ATP secretion, TPTF inhibited dose-dependently both platelet aggregation and ATP secretion induced by collagen. The antiaggregating (IC50) concentration of TPTF was 6.0 X 10(-6) M against collagen. In addition, TPTF prevented the collagen-, and thrombin-induced formation of MDA, but had little inhibitory effect on the conversion of exogenous arachidonic acid to MDA in platelets. In contrast, aspirin (10(-3) M) inhibited platelet aggregation, ATP secretion and MDA formation induced by all the stimuli tested. Other triphenyl metals did not any inhibitory effect on collagen-, and sodium arachidonate-induced platelet aggregation and ATP secretion even at a final concentration at 10(-3) M. These results suggest that TPTF has a specific inhibitory effect on platelet aggregation and ATP secretion by acting at some step(s) of platelet membrane between the binding site of collagen and thrombin and the release of arachidonic acid.

Adenosine Triphosphate↗
PubMed2004

Profiles of polychlorinated biphenyl congeners, organochlorine pesticides, and butyltins in southern sea otters and their prey.

Concentrations of organochlorine pesticides, polychlorinated biphenyl (PCB) congeners, and butyltins were measured in sea otters and selected prey species (invertebrates) collected from the California (USA) coast. Polychlorinated biphenyls, DDTs (sum of p,p'-dichlorodiphenyldichloroethylene [p,p'-DDE], p,p'-dichlorodiphenyldichloroethane [p,p'-DDD], and p,p'-DDT), and butyltins were the major contaminants found in sea otters and their prey. Lipid-normalized concentrations of PCBs and DDT in sea otter livers were 60- and 240-fold greater than those found in the prey. Great biomagnification of PCBs and DDT in sea otters is suggested to result from their high per-capita intake of diet compared with those of other marine mammals. Profiles of PCB congeners in sea otters and prey species suggest a great capacity of sea otters to biotransform lower-chlorinated congeners. Sea otters seem to possess a greater ability than cetaceans to metabolize PCBs. The 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents of non- and mono-ortho PCBs in sea otters and certain prey species were at or above the theoretical threshold for toxic effects.

Animals↗
PubMed2004

Highly persistent butyltins in northern marine sediments: a long-term threat for the Saguenay Fjord (Canada).

An exhaustive study of the distribution of butyltin species was conducted in the sediment of the Saguenay Fjord (Canada), a semi-enclosed marine system with sediment permanently submitted to sub-Arctic cold conditions. Concentrations of total butyltins (tributyltin [TBT], dibutyltin, and monobutyltin) ranged from 6 to 288 ng Sn/g dry weight and were typical of those reported for contaminated coastal areas despite limited seasonal traffic of commercial vessels in the fjord. The distribution profiles of butyltin species in four sediment cores clearly indicated the high persistence of TBT that was dominating other species. The particular oceanographic conditions of the Saguenay Fjord (low seawater temperature, anoxic sediments, and low exchange rate of deep waters) combined with a high sediment/pore-water partition coefficient (Kdobs = 1.0 x 10(4) to 1.2 x 10(4) L/kg) and a low sediment/ water diffusive flux of TBT (J1 = 13 x 10(-8) mol/m2/year) are responsible for the burial and preservation of TBT in this marine ecosystem. The half-life of TBT in deep sediment was estimated to be approximately 87+/-17 years (+/-SEM), which implies a much slower degradation rate than any previously reported. Finally, a flood event that occurred five years before the sampling enabled us to calculate a very slow diffusive flux from the preflood to the postflood layer (J2 = 2 x 10(-8) mol/m2/year), indicating an almost permanent sequestration of TBT in the buried layers.

Canada↗
PubMed2005

Influence of sediment quality on the responses of benthic invertebrates after treatment with the fungicide triphenyltin acetate.

After decades of pollution, benthic communities in floodplain lake ecosystems are likely to be exposed to a diverse assortment of sediment-bound historical toxicants and nutrients as well as pulses of newly discharged or deposited toxicants. The aim of this study was therefore to analyze the effects of background sediment pollution on the responses of benthic invertebrates to an experimental toxic shock in a laboratory setting. Sediment from a relatively clean and a historically polluted floodplain lake located along the River Waal, a branch of the River Rhine, The Netherlands, was selected, and the fungicide triphenyltin acetate (TPT) was used as the acute stressor. Juvenile stages of the mayfly Ephoron virgo and the midge Chironomus riparius were chosen as test organisms because of their different response to sediment-bound toxicants and food quantity and quality. Our results demonstrated that the type of sediment had no effect on survival and growth of C. riparius when exposed to sediment-associated TPT and that E. virgo was more affected by sediment-associated TPT on clean sediment than on polluted sediment. For the mayfly, no cumulative response of the historical pollution and the recent toxic shock was observed. This observation is discussed in view of the variable content of organic matter, acting both as food and as sorbent, and leads to the hypothesis that a very strong sequestering of TPT in historically polluted sediment prevents expression of toxic effects.

Animals↗
PubMed2005

Potentiometric membrane electrode for salicylate based on an organotin complex with a salicylal Schiff base of amino acid.

A novel salicylate-selective electrode based on an organotin complex with a salicylal Schiff base of amino acid salicylaldehydeaminoacid-di-n-butyl-Sn(IV) [Sn(IV)-SAADB] as ionophore is described, which exhibits high selectivity for salicylate over many other common anions with an anti-Hofmeister selectivity sequence: Sal- >> PhCOO- > SCN- > Cl04- > I- > NO3- > NO2- > Br- > Cl- > CH3COO-. The electrode, based on Sn(IV)-SAADB, with a 30.44 wt% PVC, a 65.45 wt% plasticizer (dioctyl phthalate, DOP), a 3.81 wt% ionophore and a 0.3 wt% anionic additive is linear in 6.0 x 10(-6) - 1.0 x 10(-1) mol l(-1) with a detection limit of 2.0 x 10(-6) mol l(-1) and a slope of 62.0 +/- 1.2 mV/decade of salicylate concentration in a phosphate buffer solution of pH 5.5 at 25 degrees C. The influence on the electrode performances by lipophilic charged additives was studied, and the possible response mechanism was investigated by UV spectra. The electrode was applied to medicine analysis and the result obtained has been satisfactory.

Amino Acids↗
PubMed1981

Triphenyltin fluoride (TPTF) as a diabetogenic agent. TPTF induces diabetic lipemia by inhibiting insulin secretion from morphologically intact rabbit B-cell.

Recent work in our laboratory has shown that oral administration of triphenyltin fluoride (TPTF) evokes hypertriglyceridemia in rabbits. The present experiments were conducted to elucidate the mechanism of TPTF-induced hypertriglyceridemia in rabbits by a combined biochemical and ultrastructural approach. After a single TPTF administration, fasting blood glucose and plasma triglyceride levels increased significantly (P less than 0.02) for about 20 days. On the other hand, both plasma and adipose tissue lipoprotein lipase (LPL) activity was markedly decreased (P less than 0.001) during this period, and triglyceride production rates on day 2 after TPTF administration was significantly decreased (P less than 0.01). Density-gradient ultracentrifugation showed a remarkable accumulation of chylomicron and VLDL in the composition of plasma lipoproteins. Insulin injection to the hypertriglyceridemic rabbits induced a significant recovery of the decreased plasma LPL activity with a concomitant decrease of plasma triglyceride levels, while abeyance of insulin injection resulted in a decrease of LPL activity again. A significant inhibition of insulin release in response to the loading of glucose, glucagon, or arginine was observed in the TPTF rabbits (P less than 0.02). Inhibition of glucagon release was also observed in the arginine-loading test (P less than 0.01). Electron microscopic studies showed small abnormalities in the pancreatic islets of TPTF-treated rabbits. These findings suggest that TPTF inhibits insulin release from rabbit islets, subsequently inducing diabetic lipemia due to the insulin deficiency. Furthermore, it is possible to provide a new animal model for diabetes and diabetic lipemia by administration of TPTF to rabbits.

Animals↗