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Results for “Triethyltin Compounds”

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PubMed1986

Trimethyltin exposure produces an unusual form of toxic auditory damage in rats.

A single injection of trimethyltin chloride (TMT; 2, 4, or 6 mg/kg) is shown to produce a frequency-specific, dose-dependent auditory impairment, as well as to decrease the amplitude of the acoustically elicited startle response, in exposed rats. This finding stands in contrast to data presented earlier on the effects of triethyltin bromide (TET), which produces changes in startle response without affecting auditory acuity. Animals intoxicated with TMT at moderate doses appear to recover their auditory acuity over the course of several weeks. This slow recovery of auditory function, which is uncharacteristic for chemical ototoxicity, suggests that TMT may be a useful model agent for studying ototoxic mechanisms.

Acoustic Stimulation↗

PubMed1987

Effects of triethyltin bromide on protein phosphorylation in subcellular fractions from rat and rabbit brain.

Phosphorylation of specific proteins in subcellular fractions of rat brain is affected by the presence of low concentrations (1-50 microM) of triethyltin bromide (Et3SnBr), in vitro. SDS-PAGE and autoradiography showed that Et3SnBr increased phosphorylation of an Mr = 42,000 phosphorylation of an Mr = 52,000 component. The Mr = 42,000 and 76,000-80,000 phosphoproteins have been identified as the alpha-subunit of pyruvate dehydrogenase (PDH) and synapsin, respectively. Et3SnBr-induced phosphorylation of rabbit brain PDH results in partial inactivation of the PDH complex.

Animals↗

PubMed1986

The reduction of dithiobis(2-nitrobenzoate) by rat liver mitochondria.

5,5'-Dithiobis(2-nitrobenzoate) (DTNB) is reduced in mitochondrial suspensions to 5-mercapto-2-nitrobenzoate (MNB) by 3-hydroxybutyrate and isocitrate. Although most of the MNB produced is found in the suspension medium, there is also some within the particles. The amount of MNB found in these fraction varies with the DTNB concentration used and is much lower if mitochondrial glutathione (GSH) is depleted with 1-chloro-2,4-dinitrobenzene. If hydroxybutyrate is present, the reduction of DTNB is increased by ATP and oligomycin. The pellet contains only a little MNB and GSH but these are considerably elevated by antimycin and rotenone as well as by ATP and oligomycin. If isocitrate is present, the reduction of DTNB is greatly stimulated by valinomycin, triethyltin and, to a lesser extent, oligomycin. MNB in the pellet falls and GSH concentrations are unchanged. The results suggest that with hydroxybutyrate (an NAD reducing substrate), the rate of reduction of DTNB is limited by the rate of regeneration of GSH while with isocitrate (an NADP reducing substrate) it is limited by the rate of export of MNB from the matrix.

3-Hydroxybutyric Acid↗

PubMed1987

Acute poisoning with triethyltin in the rat. Changes in cerebral blood flow, cerebral oxygen consumption, arterial and cerebral venous blood gases.

Experiments were conducted with rats in two groups. In group 1 (survival group) triethyltin was administered i.p. once in a dose of 2.5 mg/kg body weight and in group 2 (terminal group) the animals received triethyltin in a dose of 9 mg/kg of body weight. Twelve and twenty-four hours after triethyltin injection a decrease of 30 to 40% in cerebral blood flow was observed in both groups. A decrease of systemic arterial blood pressure and changes in hematocrit value were found at that time. Progressive bradycardia was noted in all animals at all times of observation. Additionally, 48 h after intoxication, cerebral blood flow was increased in both groups by 13 to 24% above control values. The described changes were accompanied by macroscopic features of brain edema and changes in the cerebral vascular network. Cerebral oxygen consumption was augmented by about 18% 12 h after triethyltin injection in group 1. After 24 h it decreased by about 60% compared with control values, and after 48 h it returned to normal. In group 2 cerebral oxygen consumption was decreased significantly throughout the observation period. This reflects the state of cerebral metabolism at these stages of cerebral edema. The results underscore the necessity of simultaneous monitoring of cerebral blood flow and blood gases in order to distinguish between the particular stages of brain edema revealed by biochemical tests.

Animals↗

PubMedDate not supplied

Pattern reversal and flash evoked potentials following acute triethyltin exposure.

Until recently, pattern reversal visual evoked potentials (PREPs) had not been used to examine effects of neurotoxic agents, despite their clinical utility. Acute exposure to triethyltin (TET), which produces cerebral edema and myelin splitting, increased flash evoked potential (FEP) latencies in previous reports [17,18]. We recorded PREPs and FEPs in adult Long-Evans hooded rats before, and 24 hr after, exposure to 0, 4.5 or 6.0 mg/kg IP of TET bromide. Significant increases in latency and changes in amplitude of PREP peaks were found in the 6 mg/kg rats. FEP peak latency increases did not meet the criterion for statistical significance. Thus, under the conditions recorded, PREPs were better than FEPs as a measure of TET-induced neurotoxicity.

Animals↗

PubMed1983

Discrimination of auditory from nonauditory toxicity by reflex modulation audiometry: effects of triethyltin.

The evaluation of toxicity in sensory systems presents particular problems because of the need to distinguish specific sensory loss from other toxic effects. It has recently been shown that modulation of reflex behavior by low-intensity test stimuli can be used to provide a rapid assessment of sensory acuity and of ototoxic hearing loss. In this report the ability of the method to distinguish the known neuromuscular consequences of triethyltin (TET) from hearing loss is demonstrated. Rats treated with TET bromide (30 mg/liter) in their drinking water for 3 weeks showed a profound decrease in acoustic startle reflex amplitudes which was apparent prior to overt neuromuscular weakness and subsequent hindlimb paralysis. Following cessation of treatment, startle levels recovered to preexposure values. Despite these large changes in startle reflex amplitudes, TET treatment did not alter the ability of pure tone stimuli to modulate reflex behavior. These results indicate that TET as administered in these studies disrupted neuromuscular function but did not affect hearing.

Analysis of Variance↗

PubMed1975

The neurotoxic effects of triethyltin (TET) sulfate on myelinating cultures of mouse spinal cord.

Well myelinated cultures of mouse spinal cord, exposed to varying concentrations of triethyltin sulfate, were examined at different time intervals by light and electron microscopy. At a high concentration of TET (10(-6)M) for 1-2 hours, the myelin sheaths and cells showed marked degenerative changes. At lower concentrations of TET (10(-7)-10(-9) M) intramyelinic and other types of vacuole formation were seen; however, these lesions were always accompanied by changes in the perikarya, dendrites and axons of neurons and in the astrocytes. Also, there was an apparent increased number of neurofilaments and neurotubules in many axons. The findings are discussed in relation to the lesions induced in the experimental animal by alkyl tin intoxication.

Culture Techniques↗

PubMedDate not supplied

[Anti-cerebral edema properties of PEG 300 in triethyltin poisoning].

The polyethylene glycols (PEG) frequently used as solvents of non hydrosoluble molecules present toxic and pharmacodynamic properties. The effect of PEG 300 (10 ml/kg) on the modifications of the central nervous system (CNS) previously induced by a subchronic intoxication with triethyltin salt (TEE) (2 mg/kg p.o. for 5 days) has been studied in rat. The following parameters are recorded: measure of brain edema, concentration of the aminergic neurotransmitters in four different brain areas, neurological status, behaviour, mortality. The PEG 300 antagonizes or reduces some of the effects of the TEE: edema, behavioral disturbances, mortality. On the opposite, no change in the amines and their metabolites induced modifications is observed. This selective antagonism towards some of the components of TEE brain toxicity brings more information on pharmacological properties of this solvent and opens a discussion on the role of neurotransmitters on brain edema.

Animals↗

PubMed1983

The pattern of myelin proteins in triethyltin (TET) intoxication.

Myelin proteins isolated from the brain of Wistar rats intoxicated chronically with triethyltin sulfate (TET) according to the technique of ETO et al. (1971) were investigated. Among the various protein fractions, the Agraval protein happened to be most evidently affected, demonstrating considerably reduced percentages. However the results did not prove that any of the individual myelin proteins was specifically affected by TET intake. The interesting point in chronic TET poisoning was that some clinical symptoms as well as disturbances in myelin proteins demonstrated a clear tendency to retrogression despite of the continued intoxication. These observations indicate obviously that during chronic TET intake, some kind of biochemical adaptation to the noxious action of the poison on the myelin sheath takes place.

Animals↗

PubMed1976

Triethyltin sulfate-induced neuropathy in rats. Electrophysiologic, morphologic, and biochemical studies.

Adult rats given high orally administered doses of triethyltin (TET) sulfate lost weight, developed hind limb wasting, and became paraplegic or quadriplegic within three weeks of intoxication. A 33% reduction in the motor nerve conduction velocity (MNCV) of the sciatic nerve in the absence of significant demyelination was observed. There was observed, however, intramyelinic edema formation and an increased number of axonal neurofilaments and neurotubules; changes that paralleled the decrease in MNCV during the period of intoxication. Although the animals became asymptomatic and the MNCV normalized within two to three weeks of discontinuing the TET intoxication, the intramyelinic vacuoles and the increased numbers of neurofilaments and neurotubules persisted.

Animals↗

PubMedDate not supplied

Effects of trimethyltin and triethyltin on lever pressing, water drinking and running in an activity wheel: associated neuropathology.

Rats were given single injections of saline solution, or doses of triethyltin, or trimethyltin, and their drinking behavior, lever pressing for food pellets and running in an activity wheel were measured continuously for 16 consecutive days. At doses of 3.0 and 4.5 mg/kg, triethyltin decreased lever pressing, drinking and running, usually for more than a week. Subsequently, drinking and running showed increases. Only the highest dose (4.5 mg/kg) produced decreases in body weight. Doses of 6.0 and 9.0 mg/kg trimethyltin generally decreased lever pressing, drinking and running for several days, but large increases were observed subsequently for all of these measures. Rats receiving 9.0 mg/kg died 6 to 8 days after trimethyltin administration, but rats receiving 6.0 mg/kg continued to show increases in behavior for 12 to 16 days after trimethyltin administration. Examination of the brains by light microscopy of the same animals used in the behavioral studies showed high correlations between behavioral changes and neuropathology in individual animals.

Animals↗

PubMed1984

Decreased adenosine cyclic 3',5'-monophosphate phosphodiesterase activity in rat brain following triethyltin intoxication.

The possible involvement of cerebral cAMP-phosphodiesterase (PDE) in the intoxication and brain edema formation after exposure to triethyltin (TET) has been studied in vitro and in vivo in the rat. In vitro studies showed an irreversible inhibition of the particulate and soluble phosphodiesterase activities. In vivo, both high i.v. single dose and repeated oral administration of low TET doses led to a significant decrease of the particulate activities. Phosphodiesterase inhibition preceded edema formation. The soluble activities were less influenced and their inhibition could be a consequence of the edema formed in the brain tissue rather than of a TET direct action upon the enzyme. Kinetic analysis of the brain particulate enzyme from the TET-treated rats showed a significant decrease in the Vmax of the substrate high affinity enzyme form when compared to controls.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMedDate not supplied

Chronic neonatal organotin exposure alters radial-arm maze performance in adult rats.

Long-Evans rats were intubated with 0.3 or 1.0 mg/kg of triethyltin sulfate (TET) or 0.3 mg/kg of trimethyltin hydroxide (TMT) from postnatal day 3-29. 1.0 mg/kg of TMT was given on alternate days beginning on postnatal day 3. Learning and memory were assessed in an automated radial-arm maze when the rats were 180-200 days old. With this maze accuracy and activity data can be collected simultaneously. TET or TMT treatment resulted in an increase in the number of days required to adequately perform and radial-arm maze task, and a transient deficit in accuracy. However, the most pronounced effect in both TET and TMT-treated animals was hyperactivity which became manifest on the second day of testing and persisted throughout the remainder of testing.

Analysis of Variance↗

PubMedDate not supplied

Acute triethyltin exposure: effects on the visual evoked potential and hippocampal afterdischarge.

Acute administration of triethyltin (TET) produces a well-described sequence of pathological events characterized by intramyelinic vacuolation, edema, and histotoxic hypoxia. Recent behavioral studies have attempted to characterize the functional consequences of TET exposures. In this study, the effects of exposure on the visual evoked response (VER) and hippocampal afterdischarge (AD) were determined. Rats were administered either 0, 0.188, 0.375, 0.75, or 1.50 mg/kg TET bromide IP each day for 6 consecutive days. TET increased latencies of P1, N1, P2, N2, and N3 peaks of the VER. The increased latencies are consistent with delayed conduction produced by alterations in the myelin of the optic nerve. TET increased the frequency of spikes within ADs, increased the severity of postictal EEG depressions, and prolonged recovery of excitability following ADs. These effects may be partially explained as reflecting a generalized CNS depression.

Animals↗

PubMedDate not supplied

Effects of triethyltin on schedule dependent and schedule induced behaviors under different schedules of reinforcement.

The subacute effects of triethyltin (TET) on operant responding and adjunctive behavior were assessed using either a fixed ratio (FR-30) or fixed interval (FI-1 min) schedule of reinforcement. Response rate decreased for rats on the FR-30 schedule given 1.5 mg/kg whereas animals on the FI-1 min schedule showed decreases in presses and pellets obtained at 1.5 mg/kg and in water intake at 1.0 and 1.5 mg/kg. When the animals on the FI-1 min schedule were allowed to recover body weight, decreases in presses, pellets obtained, licking, and water intake occurred at 0.5, 1.0 and 1.5 mg/kg. Schedule induced and schedule dependent behaviors were affected by low doses of TET. Rats at recovered body weight were most sensitive and affected by the lowest TET doses.

Analysis of Variance↗

PubMed1976

Triethyltin toxicity as a model for degenerative disorders.

Triethyltin (TET) toxicity in mice was examined as a model for certain degenerative disorders. Spontaneous and elicited behavioral tests, electrophysiological measures and nervous system protein characterizations were used to study anomalies resulting from TET treatments. TET animals exhibited lowered spontaneous locomotor activity levels, increased sciatic nerve excitation threshold and conduction velocities, and increased power levels in the slower frequency components of their electroencephalograms. Performance in an active avoidance task suggest that the gross ultrastructural changes commonly seen in TET intoxication are not primarily responsible for the observed neurophysiological changes. Possible sites of action of TET, in both the peripheral and central nervous systems, that would produce these neurophysiological changes and the relationship of these changes to the behavioral symptoms are discussed.

Animals↗

PubMed1976

Core formation in the muscles of rats intoxicated with triethyltin sulfate.

Young adult Osbourne-Mendel rats intoxicated for up to 23 days with triethyltin sulfate (TET) at a dose of 20 mg/liter of drinking water given ad libitum, developed core-like structures in type 1 extrafusal fibers of the soleus muscles. Frozen sections revealed an absence of oxidative enzyme activity (NADH-tetrazolium reductase) and diminished or absent myosin ATPase (pH 9.4) in the core regions. The main electron microscopic features within the cores were loss of mitochondria and streaming of the Z-disks. The histochemical and electron microscopic similarities and differences between the TET-induced cores, other core models, and those reported in some human neuromuscular disorders are discussed. The present experiments do not clarify whether the cores are produced from a direct effect of TET upon skeletal muscle or upon the neural component of the motor unit.

Animals↗

PubMed1981

Developmental and behavioral effects of early postnatal exposure to triethyltin in rats.

On Day 5 of postnatal life, rat pups received a single injection of triethyltin and were later tested for a variety of developmental and adult behaviors. A within-litter dosing design was used with one male and one female from each litter (N = 8 pups/litter) receiving either 0 (normal saline vehicle), 3, 6 or a high dose of either 9 or 12 mg/kg triethyltin bromide (TET). The high doses of TET produced 50% and 80% mortality, respectively. For the 3 and 6 mg/kg groups, TET-exposure resulted in a transient decrease in body weight, and a permanent decrease in brain weight. Preweaning TET-exposed pups were less successful in descending a rope, and were less active in both a homing orientation test and a figure-eight maze. When tested as adults, however, these animals were consistently more active than controls in the figure-eight maze. These results indicate that a single exposure to TET in ;the developing rat, unlike the adult, produces permanent alterations in both brain and behavior. Acute postnatal exposure to toxicants may have general applicability as a model for developmental neurotoxicity.

Aging↗