Disease relevance of Trimethylstannane

• Pathogenesis of trimethyltin neuronal toxicity. Ultrastructural and cytochemical observations [1].
• Experiments where the slice has been used to study the neurotoxin trimethyltin are discussed, along with its use as a model for investigating the neurodegenerative problems associated with hypoxia, ischemia, and epilepsy [2].
• To study the role of cytokines in the early stages of brain injury, we examined alterations in the 17-day-old mouse hippocampus during trimethyltin-induced neurodegeneration characterized by neuronal necrosis, microglia activation in the dentate, and astrocyte reactivity throughout the hippocampus [3].
• Administration of trimethyltin (TMT) to the rat results in loss of hippocampal neurons and an ensuing gliosis without BBB compromise [4].
• The cerebellum shows limited if any damage after TMT; however, in combination with the i.c.v. injection, elevations were seen in GFAP and in EB-22, a murine acute-phase response gene homologous to the alpha (1)-antichymotrypsin gene [5].

Psychiatry related information on Trimethylstannane

• We describe detailed clinical observations, serial neuropsychological test results, electroencephalographic findings, and exposure data in this patient, confirming the limbic system effects of trimethyltin and relating them to the known histopathologic pattern of this condition [6].
• 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 [7].
• 6. These results show that, in contrast to the previously reported amnesia models, the impairments induced after exposure to CO or intoxication with trimethyltin could be alleviated not only by sigma1 receptor agonists but also by sigma2 agonists [8].
• Trimethyltin (TMT) impairs auditory thresholds within minutes of systemic administration [9].
• Two time intervals were investigated: 5 days after trimethyltin treatment, when CA3 damage becomes manifest and is associated with increased aggression, seizure susceptibility, and memory deficit, and 16 days after trimethyltin, when neuronal damage is almost maximal and seizure susceptibility is declining [10].

High impact information on Trimethylstannane

• The interactions of four chemicals (lead, ethanol, polychlorinated biphenyls, and trimethyltin) with different cell signaling systems, particularly the phospholipid hydrolysis/protein kinase C pathway, are discussed [11].
• Acute administration of TMT caused large dose- and time-dependent decreases in synapsin I and p38 in hippocampus; the same proteins were largely unaffected in a nonlimbic structure, the frontal cortex [12].
• Immunohistochemistry of GFAP revealed widespread astrocytic reactivity as a consequence of exposure to TMT, a response that resulted in part from the proliferation of astrocytes [12].
• TMT caused large dose- and time-dependent increases in GFAP that were not confined to hippocampus [12].
• Brain weights and histology were used to verify the cytopathological effects of TMT [12].

Chemical compound and disease context of Trimethylstannane

• Stannin (Snn) is a highly conserved vertebrate protein that has been closely linked to trimethyltin (TMT) toxicity [13].
• The molecular mechanisms underlying the selective toxicity of trimethyltin (TMT) remain unclear [14].
• Triethyltin intoxication has been associated with central intramyelin edema, while trimethyltin has been shown to produce neuronal necrosis in selected limbic and sensory regions of the brain [15].
• In this study, we investigated possible neuroprotective effects of FK506 in experimental temporal lobe epilepsy (TLE) induced by kainic acid (KA) or trimethyltin (TMT) [16].
• GM1 ganglioside (one week each at 10, 5, and 2.5 mg GM1/kg per day, ip) or gradual food restriction leading to a reduction in body weight to 75% of control were tested for their ability to block or reverse histopathologic and behavioral effects of trimethyltin (TMT) poisoning in rats [17].

Biological context of Trimethylstannane

• The ultrastructural cytopathologic and cytochemical effects of trimethyltin (TMT) neurotoxicity were delineated in hippocampal and pyriform neurons of acutely intoxicated adult rats [1].
• Trimethyltin, when given by gavage to rats, has an LD50 of 12.6 mg/kg [18].
• Structure, dynamics, and membrane topology of stannin: a mediator of neuronal cell apoptosis induced by trimethyltin chloride [19].
• Atlas 1.2K Clontech array detected 115 genes changed in the hippocampus with TMT and included genes associated with immediate-early responses, calcium homeostasis, cellular signaling, cell cycle, immunomodulation and DNA repair [20].
• Trimethyltin is a neurotoxicant which produces a distinct pattern of neuronal cell death following peripheral administration of a single dose (8 mg/kg, i.p.) in rats [21].

Anatomical context of Trimethylstannane

• The Mg-ATP-dependent generation of the delta psi was prevented by addition of dicyclohexylcarbodiimide and trimethyltin, inhibitors of proton-translocating ATPases in this and other subcellular organelles [22].
• The present study used trimethyltin (TMT)-intoxicated rats as a model for the behavioural syndrome seen after neuronal damage to the limbic system [23].
• Trimethyltin (TMT) selectively damages neurons in rodent and human central nervous system after a single exposure [24].
• Snn is localized in tissues with known sensitivity to trimethyltin (TMT), including the central nervous system, immune system, spleen, kidney and lung [25].
• Trimethyltin (TMT) is primarily a CNS neurotoxin affecting neurons within the hippocampal pyramidal band and the fascia dentata [26].

Associations of Trimethylstannane with other chemical compounds

• Here, we present the NMR binding studies of trimethyltin (TMT) and dimethyltin (DMT) chlorides with a linear peptide (ILGCWCYLR) derived from the membrane protein stannin (SNN) [27].
• TET and TMT caused similar morphological changes: large holes extending through the plasma membrane appeared initially in the flattened cell bodies, cytoplasmic extensions were retracted, and long cellular processes formed [28].
• (1) Morphologically, trimethyltin produced a progressive loss of hippocampal CA3 and CA4 pyramidal cells, starting from four days after peroral treatment with trimethyltin hydroxide (9 mg/kg), as described previously [29].
• According to our previous study, trimethyltin (TMT), a neurotoxicant, induces the loss of pyramidal neurons in the rat hippocampus, which is preceded by a transient increase in plasma corticosterone concentration [30].
• Ascorbate attenuates trimethyltin-induced oxidative burden and neuronal degeneration in the rat hippocampus by maintaining glutathione homeostasis [31].

Gene context of Trimethylstannane

• Reduction of TMT-induced neuronal death by erythropoietin was specifically prevented by a neutralizing anti-BDNF antibody (15 microg/mL), indicating the involvement of this neurotrophin in erythropoietin neuroprotective effect [32].
• Cellular localization and temporal elevation of tumor necrosis factor-alpha, interleukin-1 alpha, and transforming growth factor-beta 1 mRNA in hippocampal injury response induced by trimethyltin [3].
• In vivo activation of c-Jun N-terminal kinase signaling cascade prior to granule cell death induced by trimethyltin in the dentate gyrus of mice [33].
• Therefore, we studied the effects of S100B and trimethyltin (TMT) on human astrocytes and microglia with two glial models, primary cultures of human fetal astrocytes and a microglia cell line [34].
• In this study, the hippocampal neurotoxicant trimethyltin (TMT) was used to examine possible differential susceptibility associated with the apolipoprotein E genotype [35].

Analytical, diagnostic and therapeutic context of Trimethylstannane

• Retinal neurons from rats acutely intoxicated with trimethyltin (TMT) were examined by light and electron microscopy to determine if there is a relationship between the subcellular response of a neuron to TMT and its morphologic subspecialization [36].
• Transplantation of both types of tissue produced behavioral recovery on both tasks in rats with hippocampal lesions that had not been exposed to trimethyltin [37].
• Antagonism by d-amphetamine of trimethyltin-induced hyperactivity evidence toward an animal model of hyperkinetic behavior [7].
• An acute intraperitoneal injection of the organometal trimethyltin (TMT) results in neurodegeneration of the hippocampal CA3-4 pyramidal cell layer [38].
• Here we examined the effect of acute administration of the limbic system neurotoxin trimethyltin (TMT) (8 mg/kg i.p.) on APP-751 and APP-695 mRNA expression in the rat hippocampus (CA1, CA2, CA3 and CA4) using in situ hybridization techniques [39].

References