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PubMed2000

Trimethyltin and triethyltin differentially induce spontaneous noradrenaline release from rat hippocampal slices.

The environmental contaminants trimethyltin (TMT) and triethyltin (TET) stimulated the spontaneous release of [(3)H]noradrenaline ([(3)H]NA) from hippocampal slices in a time- and concentration-dependent manner. TMT was the most potent compound, exhibiting an EC50 value 10-fold lower (3.8 microM) than that of TET (39.5 microM). Metal-evoked [(3)H]NA release did not increase in the absence of desipramine and was completely blocked by reserpine preincubation, indicating a vesicular origin of [(3)H]NA release but not a mechanism involving reversal of the transmitter transporter. The voltage-gated Na(+) channel blocker tetrodotoxin (TTX) did not affect metal-evoked [(3)H]NA release. [(3)H]NA release elicited by TMT was partially extracellular Ca(2+)-dependent, since it was significantly decreased in a Ca(2+)-free EGTA-containing medium, whereas TET induced an extracellular Ca(2+)-independent release of [(3)H]NA. Neither inhibitors of Ca(2+)-entry through Na(+)/Ca(2+)exchanger and voltage-gated calcium channels, nor agents that interfere with Ca(2+)-mobilization from intracellular stores affected [(3)H]NA release induced by TMT. TET-evoked [(3)H]NA release was reduced by ruthenium red, which depletes mitochondrial Ca(2+)stores, but was not modified by caffeine and thapsigargin, which interfere with Ca(2+)mobilization from endoplasmic reticulum. The fact that TET effect was also attenuated by DIDS, an inhibitor of anion exchange, indicates that the effect of TET on spontaneous [(3)H]NA release may be mediated by intracellular mobilization of Ca(2+) from mitochondrial stores through a Cl(-) dependent mechanism.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMedDate not supplied

Neurotoxicological effects of trimethyltin on the stellate ganglion.

Hamsters treated with trimethyltin (TMT), 3 or 4 mg/kg IP, developed neurological symptoms, including tremor, within 24 hours. Postganglionic action potentials were recorded from isolated stellate ganglia of untreated hamsters (control ganglia) and TMT-treated hamsters (TMT ganglia). Compound action potentials (nicotinic transmission) of control and TMT ganglia were not significantly different. The afterdischarges induced by preganglionic stimulation at 30 Hz for 2 sec in the presence of 10(-3) M hexamethonium (muscarinic transmission) were significantly smaller in TMT ganglia than in control ganglia. The discharges induced by the muscarinic cholinoceptor agonist. McN-A-343, were also smaller in the TMT ganglia. Two other muscarinic processes, posttetanic potentiation and potentiation of the compound action potential by McN-A-343, were not significantly reduced in the TMT ganglia. Morphological studies of the ganglia revealed marked changes in the TMT ganglia with severe neuronal degeneration including vacuole formations and accumulations of lysosomes in the cytoplasm. These results demonstrate that TMT has marked anatomical effects on the stellate ganglion that may lead to the reduction in muscarinic cholinergic transmission.

Action Potentials↗
PubMed1983

Antagonism by d-amphetamine of trimethyltin-induced hyperactivity evidence toward an animal model of hyperkinetic behavior.

In male rats of the Long-Evans strain, either 7.0 mg/kg of trimethyltin (TMT) or 0.9% NaCl was administered by intragastric gavage. After a period of recovery from the typical signs of trimethyltin toxicity, each rat was tested at 72-hr intervals for its locomotor activity in an open field apparatus, the floor of which was divided into square grids. The baseline activity of each of the trimethyltin-treated rats was significantly greater than the saline-treated controls. d-Amphetamine, injected intraperitoneally in a dose of 0.5 or 2.0 mg/kg, augmented the hyperactivity of the trimethyltin-treated animals. However, a 4.0 mg/kg dose of d-amphetamine markedly attenuated the hyperactivity of trimethyltin-treated rats while elevating that of the controls. Since trimethyltin produced an autism-like behavioral disorder involving hyperactivity, preservation, aggressiveness and impairment in problem-solving and memory function, the placating effect of amphetamine supports the proposition that the pathology due to trimethyltin may represent an experimental analogue to the hyperkinetic syndrome in children.

Animals↗
PubMed1986

Effects of chemicals on delayed matching in pigeons IV: Effects of trimethyltin.

The effects of trimethyltin on delayed matching to sample performance of male White Carneaux pigeons were studied using the delayed matching-to-sample and the reversed delayed matching-to-sample procedures. In the delayed matching-to-sample procedure, pigeons were trained to peck a red or green center key 15 times to turn it off. After a 2- or 5-sec delay, one side key was illuminated by a red color and the other by a green color. One peck on the side key whose color was the same as the center key had been, produced food. After performance had stabilized, trimethyltin was administered intramuscularly at 3 different dosages (1.0, 1.3, and 1.75 mg/kg) to 3 different groups of birds. Birds received 3 injections of the same dose with injections at least 14 days apart. Trimethyltin produced dose-dependent decreases in matching accuracy, with smaller effects on response rate. Delay duration-dependent decreases in matching accuracy were also observed, whereas effects on response rate were independent of delay duration. These behavioral effects disappeared with time in all but one animal, who was unable to perform even 89 days after trimethyltin. There was no evidence of cumulative effects of trimethyltin in the other animals. After completion of the experiments with the delayed matching-to-sample procedure, pecking the key different in color from the sample key was required for reinforcement (reversed delayed matching-to-sample). There were no differences between trimethyltin-treated birds and non-treated controls in acquiring the reversal performance.

Animals↗
PubMedDate not supplied

Physiological methods for assessment of Trimethyltin exposure.

Trimethyltin has been reported to produce morphological alterations in the brain which are primarily restricted to the limbic system. A variety of physiological measures of limbic system integrity are discussed in terms of their ability to detect TMT-induced dysfunction. In addition, several measures of sensory dysfunction are discussed. It is concluded that limbic system dysfunction induced by this compound is detected more efficiently by intrahippocampal evoked potentials than by more gross measures of dysfunction. It is also concluded that relying upon preliminary descriptions of pathological alterations to direct physiological studies may provide an incomplete description of neurotoxicity.

Animals↗
PubMed1987

Effect of trimethyltin on ornithine decarboxylase in various regions of the mouse brain.

Male C57B1/6N mice, 8-10 weeks old were given a single oral dose of 0, 1.0 or 3.0 mg/kg body weight of trimethyltin hydroxide (TMT). Levels of ornithine decarboxylase (ODC) activity were measured in several brain areas, 1, 2 and 7 days later. The lower dose of TMT produced a decrease of ODC in the caudate nucleus and hippocampus at all time points studied. Hypothalamus, cerebellum and brain stem levels of this enzyme were unaltered. At the higher dose of TMT, ODC activity in hippocampus, cerebellum and brain stem were increased relative to controls at 1 and 2 days after treatment, while other regions were not significantly affected. These elevated ODC levels returned to control values within 7 days. Thus, trimethyltin treatment causes changes in ODC activity in a region and dose-specific manner.

Animals↗
PubMed1985

Nephrotoxic effect of trimethyltin in rats.

Male Wistar (Porton) rats were dosed by gavage with trimethyltin chloride in arachis oil at doses of 3, 6 and 10 mg/kg. Water consumption and urine production were monitored for 3 days after dosing and at the end of this period the rats were killed and the kidneys were examined histologically. Within 6 h of dosing there was an increase in urine production and in the pH of the urine in all treated groups. Within 24 h of dosing there was an increase in water consumption. Histopathological examination of the kidney at 3 days post-treatment showed nephrotoxic changes ranging from slight vacuolisation of the proximal tubular cells with loss of the brush borders in the 3 mg/kg group to extensive vacuolar degeneration with tubular dilation and evidence of cellular regeneration in the 10 mg/kg group. The results suggest that trimethyltin causes a rapid kidney dysfunction in rats by cytotoxic action on the cells of the proximal tubular epithelium and that this action is dose-related.

Animals↗
PubMed1984

The effects of trimethyltin chloride on the acquisition of long delay conditioned taste aversion learning in the rat.

Naive rats injected with LiCl at various times following consumption of a novel saccharin solution subsequently avoided the ingestion of saccharin with the degree of the aversion related to the interval between ingestion and LiCl administration. Although a similar relationship was also evident in animals which had received a single intragastric administration of trimethyltin chloride 21 days prior to the pairing of saccharin and LiCl, the trimethyltin-pretreated subjects receiving delayed injections of LiCl displayed weaker taste aversions than those not exposed to trimethyltin. This disruption in the acquisition of taste aversions over long delays is consistent with other work suggesting that trimethyltin disrupts tasks involving short-term memory. The utility of the conditioned taste aversion paradigm in detecting and characterizing drug toxicity was discussed.

Animals↗
PubMed1983

Distribution of trimethyltin in various tissues of the male mouse.

Trimethyltin (TMT) levels were determined in various tissues of male mice at 1, 2, 4, 6, 10 and 16 h after administration (4.26 mg/kg; i.p.). Peak TMT levels in kidneys, liver, blood, lungs and testes were observed at 1 h following administration. Penetration into the brain, skeletal muscle and adipose tissue was also observed where maximum TMT levels were achieved 6-16 h following administration. 16 h post-treatment, the order of mean tissue concentrations, of the compound was: liver greater than testes greater than kidneys greater than lungs greater than brain greater than skeletal muscle greater than adipose tissue greater than blood. TMT was retained at peak levels in most tissues until, by 16 h, the animals exhibited tremors and convulsions followed by death. The mean concentration of TMT in the brain associated with delayed (central nervous system) (CNS) excitability at 16 h was 1.53 micrograms/g of wet tissue. These results indicate that TMT rapidly distributes and, although water-soluble, persists in tissues following an i.p. administration.

Adipose Tissue↗
PubMed1985

Development of locomotor activity of rat pups exposed to heavy metals.

Cadmium (Cd), triethyltin (TET), and trimethyltin (TMT) are heavy metals which are neurotoxic to developing animals. In the present experiment, preweaning assessment of locomotor activity was used to detect and differentiate between the developmental toxicity of these metals. On postnatal day (PND) 5, rat pups received a single injection of either Cd, TET, or TMT. A within-litter design was used for dosing; 1 male and 1 female pup from each litter (N = 10 litters/compound) received either the vehicle, low, medium, or high dosage of the compound. Preweaning motor activity was assessed in 30-min sessions in figure-eight mazes from PND 13 to 21. Motor activity of control animals progressively increased in the initial days of testing, and then both within-session and between-session habituation developed. A single exposure to Cd, TET, and TMT produced hyperactivity by the end of the preweaning period but these metals differed in the day of peak activity, the onset of hyperactivity, and the development of habituation.

Animals↗