Trimethyltin poisoning � report of two cases

Fortemps, E; Amand, G.; Bomboir, A; Lauwerys, Robert; Laterre, Emile-Christian

doi:10.1007/bf00377794

Cited by 150 publications

(50 citation statements)

References 11 publications

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“…In monkeys intoxicated with trimethyltin, similar behavioral and neuropathologic alterations were noticed as in rodents (Brown et al, 1984;Reuhl et al, 1985). Also for humans accidentally exposed to trimethyltin a variety of psychomotor changes were reported, including irritability, depression, aggressiveness, headaches, tremors, convulsions, and changes in libido (Fortemps et al, 1978;Ross et al, 1981).…”

Section: Neurotoxicitymentioning

confidence: 81%

Biological activity of organotin compounds—An overview

Snoeij

Penninks

Seinen

1987

Environmental Research

348

131

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As a consequence of the rapid expansion of the uses and applications of the organotin compounds, the concern about their environmental and health effects is increasing. The main subject of this overview is the current understanding of the mammalian toxicity of the organotin compounds. Four different types of target organ toxicity, namely neurotoxicity, hepatotoxicity, immunotoxicity, and cutaneous toxicity, are discussed in more detail. The effects of the organotin compounds on the mitochondfial and cellular level are summarized and discussed in relation to the mode of action of these compounds on the central nervous system, the liver and bile duct, the immune system, and the skin. © 1987 Academic Press, Inc. ORGANOTIN COMPOUNDS: APPLICATIONS AND TOXICITY Organotin CompoundsTin can be present as an element in a wide variety of both inorganic and organometallic compounds. Organometallic tin compounds or organotins are characterized by the presence of at least one covalent carbon-tin bond. Although tin may exist either in the Sn 2+ or in the Sn 4+ oxidation state, almost all organotins have a tetravalent structure. Depending on the number of organic moieties, the organotin compounds are classified as mono-, di-, tri-, and tetraorganotins. In compounds of industrial importance, methyl, butyl, octyl, and phenyl groups form the organic substituents, while the anion is usually chloride, fluoride, oxide, hydroxide, carboxylate, or thiolate. All alkyltin compounds refered to in this article contain unbranched saturated hydrocarbon side chains (n-alkyltins).

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Section: Neurotoxicitymentioning

confidence: 81%

Biological activity of organotin compounds—An overview

Snoeij

Penninks

Seinen

1987

Environmental Research

348

131

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“…An increasing worldwide production of organotin products is expected in the future [3]. One of the most toxic alkyltin compounds, trimethyltin (TMT), is an intermediate in the production of other tin compounds, and a number of cases of human poisoning after exposure to this compound have been reported [4,5).…”

Section: Introductionmentioning

confidence: 99%

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

et al. 1987

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SUMMARYMale C57B 1 /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, l, 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.

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“…the hippocampus and the entorhinal and transentorhinal cortices. For these reasons TMT intoxication is regarded as a suitable model of chronic neurodegeneration with cognitive impairment, while the neuropathological, neurochemical and neurobehavioural alterations that occur in vivo have been widely analyzed in rodents, as well as in human cases of accidental poisoning with TMT (Fortemps et al 1978;Brown et al 1979;Chang et al 1982;Noland et al 1982;Stanton et al 1991;Feldman et al 1993;Geloso et al 1997Geloso et al , 2002Gui-bin et al 2000;Harry and Lefebvre d'Hellencourt 2003;Lattanzi et al 2007;Yoo et al 2007). The molecular and cellular pathogenesis of TMT-induced neurodegeneration is believed to be a composite picture involving several steps.…”

mentioning

confidence: 99%

Dysregulation of intracellular calcium homeostasis is responsible for neuronal death in an experimental model of selective hippocampal degeneration induced by trimethyltin

Piacentini

Gangitano

Ceccariglia

et al. 2008

Journal of Neurochemistry

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Trimethyltin (TMT) intoxication is considered a suitable experimental model to study the molecular basis of selective hippocampal neurodegeneration as that occurring in several neurodegenerative diseases. We have previously shown that rat hippocampal neurons expressing the Ca2+‐binding protein calretinin (CR) are spared by the neurotoxic action of TMT hypothetically owing to their ability to buffer intracellular Ca2+ overload. The present study was aimed at determining whether intracellular Ca2+ homeostasis dysregulation is involved in the TMT‐induced neurodegeneration and if intracellular Ca2+‐buffering mechanisms may exert a protective action in this experimental model of neurodegeneration. In cultured rat hippocampal neurons, TMT produced time‐ and concentration‐dependent [Ca2+]i increases that were primarily due to Ca2+ release from intracellular stores although Ca2+ entry through Cav1 channels also contributed to [Ca2+]i increases in the early phase of TMT action. Cell pre‐treatment with the Ca2+ chelator, 1,2‐bis(2‐aminophenoxy)ethane‐N,N,N′,N′‐tetraacetic acid tetrakis(acetoxymethyl ester) (2 μM) significantly reduced the TMT‐induced neuronal death. Moreover, CR+ neurons responded to TMT with smaller [Ca2+]i increases. Collectively, these data suggest that the neurotoxic action of TMT is mediated by Ca2+ homeostasis dysregulation, and the resistance of hippocampal neurons to TMT (including CR+ neurons) is not homogeneous among different neuron populations and is related to their ability to buffer intracellular Ca2+ overload.

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Trimethyltin poisoning � report of two cases

Cited by 150 publications

References 11 publications

Biological activity of organotin compounds—An overview

Biological activity of organotin compounds—An overview

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

Dysregulation of intracellular calcium homeostasis is responsible for neuronal death in an experimental model of selective hippocampal degeneration induced by trimethyltin

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