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PubMed1981

Behavioral toxicity of acute and subacute exposure to triethyltin in the rat.

The behavioral effects of both acute and subacute triethyltin (TET) exposure were examined in the rat. Animals acutely exposed to TET at doses of 0, 1.5 and 3.0 mg/kg showed a dose-related decrease in motor activity when tested between 2 and 4 hr following exposure. Subacute (3 week) exposure to TET in the drinking water (5 or 10 ppm) resulted in performance decrements in the following: maze activity, open field behavior, acoustic startle response and landing foot-spread. Early signs of behavioral deficits were observed 2 weeks after 10 ppm TET. These effects were reversible within one month after termination of exposure.

Animals↗
PubMed1991

Myelin basic protein-messenger RNA (MBP-mRNA) expression during triethyltin-induced myelin edema.

Triethyltin (TET) is a neurotoxicant that produces severe but transient cerebral edema, characterized ultrastructurally by vacuolation of the intraperiod line of central nervous system (CNS) myelin. TET has been reported to depress levels of myelin basic protein (MBP), a protein thought to play a critical role in myelin compaction. In the present study, the genomic expression (i.e., mRNA) of MBP was monitored throughout the pathogenesis of TET-induced myelin edema and recovery in Sprague-Dawley rats given a single injection of a neuropathic (8.0 mg/kg) or non-neuropathic (0.8 mg/kg) dose of TET-bromide. Levels of MBP-mRNA from the anterior and posterior brain were collected 1 hr, 3 hr, 2d, and 7d, postexposure. The optic nerve and caudal brainstem, representing anterior and posterior brain sites, respectively, were examined at the same time-points for ultrastructural evidence of edema and recovery. Our data indicate that neuropathic doses (8.0 mg/kg) of TET significantly stimulated MBP transcript throughout the brain at all exposure time-points. The magnitude and time-course of this stimulation differed in the anterior and posterior brain, with the latter region showing higher levels of MBP-mRNA. In the posterior brain, the highest levels of mRNA correlated with the appearance of edema in the caudal brainstem. In the anterior brain, MBP-mRNA levels were only marginally increased over controls. Ultrastructural evidence of myelin edema was confined to the brainstem in rats treated with neuropathic dose of TET. Intralamellar vacuolation appeared at 3 hr and 2d postexposure and could be correlated with peak levels of MBP transcript, whereas, recompacted myelin, which appeared by 7d postexposure, was associated with declining levels of the mRNA. Ultrastructural changes in the oligodendroglia were suggestive of metabolic stimulation and correlated with high MBP-mRNA levels. In summary, these data indicate that an initial genomic event in TET-induced myelin edema is stimulation of MBP transcript.

Animals↗
PubMed1975

Histochemistry of neuronal degenerative changes.

Classical forms of degenerative changes of neurocytes, defined by Nissl and Spielmeyer as neuronal diseases were produced experimentally in rats. The individual neuronal changes were induced with the aid of X-ray irradiation, TET administration, ligation of the carotid artery followed by oxygen deficient breathing (anoxia), and by sectioning of the sciatic nerve. The so produced experimental models of neuronal diseases were the subject of morphological and cytochemical studies with special attention payed to enzymic and autoradiographic reactivity. Basing on the results of performed investigations, the author inferred that from a pathogenetic point of view, not all of the respective forms of neuronal diseases postulated by the classification of Nissl and Spielmeyer can be regarded as separate, distinct forms of degenerative changes. From the results obtained it would appear that pathogenetically distinct are only the following diseases: acute nerve cell swelling, shrinkage of perikaryons, homogenizing changes of Purkinje cells and axonal degeneration. The so called severe disease as well as the ischemic disease should be regarded as transitory forms of neuronal changes developing from shrunken neurocytes. It has also been suggested that the pathogenesis of homogenizing changes in Purkinje cells is distinct from that responsible for the development of ischemic changes in the course of cerebral anoxia and ischemia. This suggestion is substantiated by the observed differences in cytoenzymic reactivity between homogenized Purkinje cells and ischemically changed neurocytes.

Animals↗
PubMed1990

Control of brain fatty acids.

Saturated and monounsaturated fatty acids are mainly synthetized in the brain, but some of them could originate from the diet; in contrast polyunsaturated fatty acids are derived from dietary linoleic and linolenic acid. Saturated fatty acid biosynthesis occurs via three main pathways in mammalian cells. One is de novo synthesis of fatty acids from acetyl-CoA via malonyl-CoA; this system has been isolated in soluble form (the soluble system) from various animal tissues including brain. The second and third pathways involve elongation: in the mitochondrial system, acetyl CoA is the principal substrate in extracts from all organs, even brain; in the microsomal system, however, malonyl-CoA acts as donor of the 2 carbon fragments. In vivo studies in brain have shown that very long chain fatty acids are synthesized by elongation rather than by a than by a de novo mechanism. Feeding animals with oils that have a low n-3 acid content (linolenic series) results in all brain cells and organelles reduced amounts of 22:6 n-3 which is compensated for by an increase in 22:5 n-6. The speed of recuperation from these anomalies is extremely slow for brain cells, organelles and microvessels, in contrast with other organs. Essential fatty acids for the brain could be those with very long chains as shown with cell culture. They are probably synthesized in the liver from linolenic acid. They can also be supplied directly by food. During the period of cerebral development there is a linear relation between the n-3 acid content of the brain and that of food until linolenic acid represents approx. 200 mg per 100 g of food (for 1200 mg linoleic acid). A decrease in acids of the linolenic series in the membranes results in a 40% reduction of Na-K-ATPase in nerve terminals and a 20% reduction in 5'-nucleotidase in whole brain homogenate. A diet low in linolenic acid leads to anomalies in the electroretinogram which disappear partially with age, it seriously affects learning tasks. The presence of linolenic acid in the diet confers a greater resistance to certain neurotoxic agents.

Animals↗
PubMed1985

The use of sensory evoked potentials in toxicology.

The rationale for studying sensory systems as an integral part of neurotoxicological examinations is presented. The role of evoked potentials in assessing brain dysfunction in general and sensory systems in particular is also presented. Four types of sensory evoked potentials (brainstem auditory evoked response, somatosensory evoked potentials, flash evoked potentials, and pattern reversal evoked potentials) are discussed in terms of their demonstrated contributions to neurotoxicology and clinical neurology. Research needed to allow these methods to achieve their full value for neurotoxicology is identified and briefly discussed.

Acoustic Stimulation↗
PubMed1985

[Plasmids for naphthalene biodegradation incompatible with IncP-2 and IncP-7 group plasmids].

Fourteen conjugative naphthalene degradative plasmids have been classified by incompatibility. It is shown that the plasmids of IncP-9 group are characterized by the minor entry exclusion, with respect to the R plasmids belonging to IncP-2 or IncP-7 groups. On the other hand, the naphthalene degradative plasmids of incompatibility group P-7 exhibit a markedly pronounced entry exclusion, with respect to the R plasmids of the same incompatibility groups. Two naphthalene degradative plasmids reveal incompatibility with the reference plasmids of two Inc groups (P-2 and P-7). These plasmids control also resistance of bacterial cells to potassium tellurite, which is characteristic of the IncP-2 plasmids. Two other naphthalene degradative plasmids are capable of stable coexistence with the IncP-2, P-7 or P-9 reference plasmids.

Biodegradation, Environmental↗
PubMed1986

Simple inhibition studies for distinction between homodimeric and heterodimeric isoenzymes of glutathione transferase.

Simple inhibition studies in which fractional velocity is measured as a function of inhibitor concentration were used to distinguish heterodimeric from homodimeric isoenzymes of glutathione transferase. Homodimeric isoenzymes from rat, mouse, and human tissues were shown to give graphs of fractional velocity versus the logarithm of inhibitor concentration that were characterized by a sigmoid curve shape and a maximal slope of -0.58 at 50% inhibition, characteristic for linear inhibition of monomeric or non-cooperative oligomeric enzymes. In contrast, inhibition curves for heterodimeric isoenzymes from rat liver displayed significant deviations from these characteristics. The basis for the identification of heterodimers was the finding that the kinetic properties of subunits were additive such that the inhibition curve of a heterodimeric isoenzyme could be predicted from those of the corresponding homodimers. The method should be valuable in the differentiation between the multiple forms of glutathione transferase in tissues not previously characterized. It is suggested that the method should be applicable for discrimination also in other isoenzyme families consisting of oligomeric structures of identical and nonidentical subunits.

Animals↗
PubMed1980

Metabolic basis of brain edema.

A large number of metabolic factors have been incriminated in the pathogenesis of the various forms of brain edema. Ultimately we must learn more about the factors responsible for the integrity of the membranes of the capillary endothelium, neurons, and glia. What determines normal membrane fluidity, and how is it modified in disease? What is the mechanism of action of glucocorticosteroids in the treatment of vasogenic edema? The role of free radicals, polyunsaturated fatty acids, and excitatory neurotransmitters on cellular membranes and the distribution of sodium and water in the various compartments of the brain require further study.

Animals↗
PubMed1983

Use of environmental challenges in behavioral toxicology.

The term environmental challenges encompasses variables that are either known or suspected to affect a baseline of behavior. Environmental challenges can be used to provide information that is important for characterizing the behavioral effects of prior exposure to a toxicant, as well as for revealing effects of the toxicant that may not otherwise be apparent in the baseline under investigation. The use of environmental challenges can be applied in studies of all known classes of behavior, and in each case is limited only to the extent that appropriate variables can be identified and manipulated. Use of environmental challenges may be particularly relevant for studies of schedule-controlled operant behavior because many of the controlling variables have already been well specified. The rationale for using environmental challenges to characterize the behavioral effects of toxicants is very similar to that for using pharmacological challenges; both represent promising new research strategies in behavioral toxicology.

Animals↗
PubMedDate not supplied

[Proton nuclear magnetic resonance in the pharmacologic study of cerebral edema].

Wistar male rats have been orally administered 2 mg X kg-1j-1 of triethyltin (TET) chloride for 5 consecutive days. The result was a cerebral edema which constituted a reproducible and useful experimental model for pharmacological screening of drugs used in ageing. Water content modifications and clinical behaviour for 11 days from the beginning of experiment have been linked to T1 and T2 proton relaxation times measured by nuclear magnetic resonance (1H-NMR). The observation of 3 central nervous system structures, which differ in white matter content, has lead to the conclusion that NMR is a more sensitive technique to follow up the edema evolution than the water content measurement alone; it has also allowed to discriminate intra from extra-cellular edema (osmotic and TET edema), and has proved the action of two drugs which are used in aging process treatment on the TET edema (dihydroergotoxine 2 X 10 mg X kg-1j-1 and (--) eburnamonine 2 X 50 mg X kg-1j-1). In the future the mastery of this technology will be used to study other nuclei (Na, K, P) which will bring more physiopathological informations and to pharmacological investigations of the brain by NMR tomography or focalised NMR.

Animals↗
PubMed1981

[Pathology of cerebral edema. II. Experimental models and modifying agents].

Current experimental models of brain edema are described and evaluated for their contribution to the knowledge of basic processes involved in its production as well their contribution to the understanding of different clinical forms. The participation of each main pathogenic mechanism in a given experimental model is analyzed and proves to vary with each particular model and site studied. The importance of various experimental models in the evaluation of different therapeutic procedures directed to control the genesis and evolution of brain edema is stressed.

Animals↗
PubMed1983

Effects of postnatal trimethyltin or triethyltin treatment on CNS catecholamine, GABA, and acetylcholine systems in the rat.

The effects on brain neurochemistry of two neurotoxic tin compounds, trimethyltin (TMT) hydroxide and triethyltin (TET) sulfate, were examined. Long-Evans rats were treated with TMT hydroxide (1 mg/kg, i.p.) on alternate days from day 2 to 29 of life. These treatments caused a weight deficit of 10-20% by the time the animals were killed on day 55 by head-focused microwave irradiation. These TMT treatments are known to cause severe neuronal loss in the hippocampus and lesser damage in other brain regions. Accordingly, the concentration of gamma-aminobutyric acid (GABA) was decreased in the hippocampus; however, acetylcholine and choline concentrations were unaffected. These data suggest that TMT-induced effects on GABA systems are greater than that due simply to generalized neuronal loss. The TMT treatments also caused a significant decrease in dopamine concentrations in the striatum, but did not alter the concentrations of dihydroxyphenylacetic acid or homovanillic acid, the acidic metabolites of dopamine. Conversely, concentrations of dopamine and norepinephrine in the brain stem and norepinephrine in the cerebellum were not altered. Despite reports in the literature of TMT-induced neuronal damage in areas of the cortex, no effects on GABA, acetylcholine, or choline levels were found in the cortical areas examined, or in the hypothalamus. TET sulfate (0.3 mg/kg/day) was administered for 6 consecutive days of every week during days 2-29 of life. This dose is lower than that needed to cause intramyelin edema, yet it does result in long-term behavioral changes. Despite this, no changes in the concentration of any of the measured neurotransmitters or their metabolites were detected. In concert, these data demonstrate that neurochemical methods should not be used as neurological "screens," but rather to define specific mechanisms suggested by detailed behavior, pharmacological, and/or physiological studies.

Acetylcholine↗
PubMedDate not supplied

Neonatal exposure to triethyltin disrupts olfactory discrimination learning in preweanling rats.

Triethyltin is an organotin compound that is known to produce neurotoxicity in both adult and developing organisms. Although this neurotoxicity has been documented with a variety of behavioral and biological measures, the effects of this compound on learning during early development have been less extensively studied. The present study reports four experiments that examined this question with an odor aversion learning paradigm in which pups received presentations of one odor paired with footshock and an alternate odor without shock. In Experiment 1, Long-Evans rat pups were injected IP on postnatal day 5 (PND 5) with either 0, 3 or 5 mg/kg TET and then tested for olfactory discrimination learning on PND 18. Only the 5-mg/kg dose impaired discrimination learning. In Experiment 2, PND 5 exposure to TET (5 mg/kg) disrupted olfactory learning on PND 18 but not on PND 12, whereas exposure on PND 10 disrupted learning at both ages of testing. In Experiment 3, PND 16 exposure to TET (5 mg/kg) also disrupted acquisition of olfactory learning on PND 18 but had no effect on retention of an olfactory discrimination that was acquired prior to TET exposure (i.e., on PND 14 and PND 15). Unconditioned responses to footshock were also unaffected by TET (Experiment 4). These findings indicate that neonatal exposure to TET impairs associative learning in developing rats and are discussed in relation to other studies of the developmental neurotoxicity of this compound.

Aging↗