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PubMed1976

The influence of adenine nucleotides and oxidizable substrates on triethyltin-mediated chloride uptake by rat liver mitochondria in potassium chloride media.

In a 100 mM-KCl medium, pH 6.8, containing ATP increasing concentrations of triethyltin cause an uptake of Cl- into mitochondria with a maximum at 1 muM. This can be inhibited by atractylate or oligomycin, but is virtually unaffected by the presence of rotenone. When the medium contains substrate (pyruvate, beta-hydroxybutyrate or succinate), both in the presence and absence of adenine nucleotides, Cl- uptake is greater with a maximum at 1-10 muM-triethyltin. If substrate oxidation is blocked by respiratory-chain inhibitors the Cl- uptake mediated by triethyltin is inhibited except in the media containing ATP, when the characteristics of Cl- uptake similar to that found in the medium containing ATP alone are observed. Under all conditions tested Cl- uptake is decreased by the presence of 2,4-dinitrophenol. It is concluded that energy from either the oxidation of substrate or the hydrolysis of ATP is associated with the generation of sufficient OH- to enable the triethyltin-mediated Cl-/OH- exchange to occur under the metabolic conditions relevant to this action of triethyltin.

Adenosine Triphosphate↗
PubMed1977

Binding of triethyltin to cat haemoglobin and modification of the binding sites by diethyl pyrocarbonate.

Cat haemoglobin binds 2 mol of triethyltin/mol of haemoglobin. Pretreatment of the haemoglobin with diethyl pyrocarbonate at pH6.0 prevents binding to one site only, whereas photo-oxidation with Methylene Blue removes both sites. Pretreatment of rat haemoglobin with diethyl pyrocarbonate also leads to the loss of one binding site. The possibility is discussed that the two binding sites for triethyltin on both cat and rat haemoglobin have a different chemical nature.

Animals↗
PubMed1979

A sequential study of changes in the brain and cerebrospinal fluid of the rat following triethyltin poisoning.

Following a single intravenous (i.v.) injection of triethyltin (10 mg/kg) in rats, vacuoles appeared in the myelin sheath within 3 h and they progressively increased in size between 6 and 24 h. Their development was closely correlated with a progressive increase in water, sodium, and chloride content of the brain, and of cerebrospinal fluid (CSF) pressure. Oedema was more extensive in tissues consisting predominantly of white matter rather than grey matter. The sustained increase in CSF pressure did not precede the development of lesions and was the result of, rather than the cause of, brain oedema and swelling. These findings indicate that triethyltin has a direct effect on the myelin sheath.

Animals↗
PubMed1986

Triethyltin-induced neuronal damage in neonatally exposed rats.

Neuropathological and biochemical effects of neonatal exposure to the alkyl metal triethyltin were examined in juvenile male Long Evans rats. Rats were injected intraperitoneally on postnatal day 5 with 6 mg/kg of triethyltin bromide and sampled on day 20. The brains of tin-treated animals weighed significantly less than either saline or starved controls and exhibited a marked caviation of the ventrolateral surfaces. Histologically, neuronal necrosis was noted in the entorhinal and transitional cortex, an observation confirmed by immunocytochemical staining of astrocytes. Hippocampal involvement was further evidenced by a protrusion of the molecular layer of the dentate gyrus, and an abnormal histochemical staining pattern of acetylcholinesterase in this layer. Sections stained by the Timm's method for the deposition of heavy metals showed a marked reduction in the staining of the hippocampal CA4,3,2 sectors and an absence of stained laminae in the outer molecular layer of the dentate gyrus. Receptor binding assays indicated a selective depression of the benzodiazepine receptor in the hippocampus of tin-treated pups compared to starved controls. Taken in concert, these data indicate that neonatal exposure to triethyltin produces severe neuronal damage in the posterior cortex and a derangement of hippocampal afferent circuitry.

Acetylcholinesterase↗
PubMed1984

Central neurotransmitter effects of organotin compounds: trials, tribulations and observations.

Administration of trimethyltin (TMT) or triethyltin (TET) compounds to rats during postnatal development has known behavioral and neuropathological consequences. By measuring the concentrations of dopamine, norepinephrine, homovanillic acid, dihydroxyphenylacetic acid, gamma-aminobutyric acid, acetylcholine, and choline in different brain areas of TMT and TET-treated animals, an attempt was made to correlate these functional deficits with changes in CNS neurotransmitter alterations in vivo. TET had no effect on any of the substances measured whereas TMT significantly decreased gamma-aminobutyric acid and dopamine levels, but only in hippocampus and striatum, respectively. All other neurotransmitter substances measured were not affected. These findings illustrate the complexity inherent in attempting to use neurochemical techniques alone as an index of toxicity in the absence of specific defined hypotheses.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Inactivation of yeast hexokinase B by triethyltin bromide and reactivation by dithiothreitol and glucose.

Binding of triethyltin bromide to yeast hexokinase B results in a rapid change in the reactivity of the sulfhydryl groups of the molecule. The change was characterized by an increased rate as well as extent of reaction of the -SH groups, and it preceded the onset of inhibition of the enzyme. Rapid gel filtration of the enzyme-triethyltin complex reversed this change in sulfhydryl reactivity, and when the eluted enzyme was subjected to short incubation periods, the slow inhibition that occurs with the unfiltered enzyme-triethyltin complex was no longer manifested. With prolonged incubation, however, the gel-filtered sample demonstrated increased rate of loss of enzyme activity, indicating that the gel filtration step did not completely reverse the effects of triethyltin on the enzyme. Active enzyme was recovered, following the inactivation of yeast hexokinase with triethyltin, by incubation of the inactivated enzyme with a large excess of glucose and dithiothreitol. Near total recovery of enzyme activity with reversion to native enzyme conformation was achieved following incubation at 35 degrees C of the enzyme with glucose and dithiothreitol each at 0.1 M. The possible involvement of either cysteine or histidine in the binding of triethyltin to the enzyme was probed, and it was concluded that neither of these amino acids are donor ligands for tin.

Dithiothreitol↗
PubMed1986

Organotin-protein interactions. Binding of triethyltin bromide to cat haemoglobin.

Triethyltin binds to native cat and rat haemoglobin but not to their denatured forms or to other animal haemoglobins. Two molecules of the organotin bind to one molecule of R-state cat haemoglobin with affinity constants of about 1 X 10(5) M-1. Little or no triethyltin is bound to the deoxygenated (T-state) protein. Binding appears to be dependent upon the existence of a specific three-dimensional configuration of cysteine and histidine residues. The properties of the triethyltin-cat haemoglobin complex are consistent with those of a haemoglobin conformer whose allosteric equilibrium is displaced toward the R-state. Its oxygen affinity and rate of oxidation by nitrite is increased, and the rate of reduction of the methaemoglobin derivative by ascorbate is decreased. These effects of triethyltin are opposite and antagonistic to the effects of inositol hexaphosphate. They are exerted on the alpha- as well as beta-haem groups, even though triethyltin is bound at sites on alpha-globin far removed from the haem groups.

Animals↗
PubMed1977

[Experimental triethyltin ocular hypertension. Pharmacological and histopathological studies (author's transl)].

The experiments were prompted by the need felt in pharmacology of eyes with hypertension of easy availability, rather long duration and fairly constant levels, to allow observation of the effects of hypotensive agents and to study their mechanism of action. Single doses of 1 mg Triethyltin, a substance producing a hydrodynamic compromission of the brain, were injected into the anterior chamber of rabbit eyes. A rise in ocular tension, beginning within 24 hours and lasting seven to ten days is obtained in about 70% of eyes. The pressure increase ranged from 12 to 30 mm Hg. Biomicroscopic and histologic examinations evidenced an uveitis-like reaction in the first week after treatment. Neoprene casts evidenced an impaired vascularization in the ciliary processes and choroid. Topical and parenteral administration of the most commonly used antiglaucomatous drugs showed how well this hypertension responded to hypotonizing agents. The occurrence of producing an ocular hypertension in the untreated fellow eye following repeated intra-cameral injections of small dosage (1 microgram) of Triethyltin, every two days for more than one month, in the other eye is described. Hypertension resulted in 40% of eyes.

Animals↗
PubMed1989

Increased methylation of chloroform extractable products and CTP: cholinephosphate cytidylyltransferase in brain membrane preparations from triethyltin-intoxicated rats.

Rats were chronically intoxicated with triethyltin in the drinking water (0.002%) for a period of 15 days. Starting with day 5 of the intoxication period a decrease in the body weight was observed and, in parallel, the development of a cerebral oedema could be followed by measuring white matter density. At the same time, an increase of phosphatidylethanolamine-N-methyltransferase and cholinephosphate cytidylyltransferase activities was noted. This increase might be a compensatory mechanism for counteracting the membrane damages induced by triethyltin.

Animals↗
PubMed1989

[Hyperbaric oxygenation in experimental toxic brain edema].

Hyperbaric oxygenation (HO) was used to treat the brain toxic edema excited by triethyltin++ chloride. Microscopic examination of the brains of two groups of animals (with and without HO) revealed the decay of pathologic signs of brain edema and reparative responses in the nervous tissue induced by HO.

Animals↗
PubMed1987

Effects of triethyltin on brain octopamines and their metabolism in the rat.

The effects of triethyltin given acutely on the cerebral level of p- and m-octopamines were studied in rats. These octopamines were reduced drastically in hypothalamus and brainstem, while noradrenaline and dopamine were only slightly decreased. No important changes were observed in the activities of tyrosine hydroxylase, dopamine beta-hydroxylase or monoamine oxidase. However, the activity of aromatic L-amino acid decarboxylase was significantly reduced. The addition of the inhibitor of dopa decarboxylase, Ro 44602, caused a total inhibition of this enzyme activity. These results are discussed in terms of the possible use of the triethyltin-induced cerebral oedema as a model for the study of some aspects of the phenolamine changes related to cerebral oedema processes.

Animals↗
PubMed1990

Differential effects of triorganotins on calmodulin activity.

In vitro effects of three triorganotins--tributyltin (TBT), triethyltin (TET), and trimethyltin (TMT)--on calmodulin (CaM) activity were studied. Stimulation of Ca2(+)-ATPase of rat brain synaptic membranes and phosphodiesterase (PDE) of bovine brain were assayed as indicators of CaM activity. The rat synaptic membranes were prepared and CaM was depleted by washing with 1 mM EGTA. All the three organotins inhibited the basal as well as CaM-stimulated Ca2(+)-ATPase in a concentration-dependent manner, suggesting their interaction with calcium pump. However, CaM-stimulated Ca2(+)-ATPase was more sensitive than the basal enzyme. The order of potency of the three organotin compounds was TBT greater than TET greater than TMT. The IC50 values of Ca2(+)-ATPase (basal) were 0.63, 35, and approximately 800 microM, respectively, whereas the values for CaM-stimulated Ca2(+)-ATPase were 0.05, 0.8, and 18 microM for TBT, TET, and TMT, respectively. CaM-deficient PDE did not show any sensitivity to these three organotin compounds, while TBT and TET significantly decreased the CaM-stimulated PDE activity. TMT, which was the least effective inhibitor of Ca2+ pump, did not alter PDE activity. Further, the inhibition of CaM-stimulated Ca2(+)-ATPase activity by these organotins could be reversed by excess addition of CaM. These results suggest that the organotins interact with CaM activity, as evidenced by their potent effect on CaM-dependent Ca2(+)-ATPase and PDE activities.

Animals↗
PubMed1992

Cellular and molecular effects of trimethyltin and triethyltin: relevance to organotin neurotoxicity.

Many of the neurotoxic aspects of organotin exposure have been described. Organotin exposure culminates in its accumulation in the CNS and PNS. The clinical picture is dominated by neurological disturbances; yet, the primary basis for their neurotoxicity is unknown. Trimethyltin (TMT) is primarily a CNS neurotoxin affecting neurons within the hippocampal pyramidal band and the fascia dentata. Triethyltin (TET) is a neurotoxin that produces a pathological picture dominated by brain and spinal cord edema. The first part of this review summarizes the current understanding of the interaction of TMT and TET with biologically active sites in the induction of neurotoxicity. In the second part, several hypotheses for the differential neurotoxic effects of these organotins and their shortcomings are discussed.

Animals↗