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PubMed2004

Rapid recovery of genetic diversity of dogwhelk (Nucella lapillus L.) populations after local extinction and recolonization contradicts predictions from life-history characteristics.

The dogwhelk Nucella lapillus is a predatory marine gastropod populating North Atlantic rocky shores. As with many other gastropod species, N. lapillus was affected by tributyltin (TBT) pollution during the 1970s and 1980s, when local populations became extinct. After a partial ban on TBT in the United Kingdom in 1987, vacant sites have been recolonized. N. lapillus lacks a planktonic larval stage and is therefore expected to have limited dispersal ability. Relatively fast recolonization of some sites, however, contradicts this assumption. We compared levels of genetic diversity and genetic structuring between recolonized sites and sites that showed continuous population at three localities across the British Isles. No significant genetic effects of extinction/recolonization events were observed in SW Scotland and NE England. In SW England we observed a decrease in genetic diversity and an increase in genetic structure in recolonized populations. This last result could be an artefact, however, due to the superposition of other local factors influencing the genetic structuring of dogwhelk populations. We conclude that recolonization of vacant sites was accomplished by a relatively high number of individuals originating from several source populations (the 'migrant-pool' model of recolonization), implying that movements are more widespread than expected on the basis of development mode alone. Comparison with published data on genetic structure of marine organisms with contrasted larval dispersal supports this hypothesis. Our results also stress the importance of local factors (geographical or ecological) in determining genetic structure of dogwhelk populations.

Animals↗
PubMedDate not supplied

Evolution of the intracellular changes in neurons caused by trimethyltin.

Rats have been given a single dose of trimethyltin (10 mg/kg) and the intracellular events have been followed particularly in hippocampus, cerebral cortex, cerebellum and spinal ganglion cells. The earliest change visible occurs 12 h after this dose and is found to be dense membrane-bound bodies, probably derived from branching tubulo-vesicular smooth endoplasmic reticulum formations. These occur in close connection with rought endoplasmic reticulum and polyribosomes and appear also to have some association with the Golgi complex. At 24 h there is a general vacuolation of Golgi cisterns and SER membranes, and the membrane-bound dense body formation is greatly increased. SER abnormalities are particularly conspicuous in Purkinje cells. In spinal ganglion cells, while vacuolation of Golgi cisterns is intense, dense bodies are inconspicuous and are replaced by increased autophagosomes, often of great complexity. By 48 h vacuolation of Golgi cisterns has waned, but accumulation of dense bodies and secondary lysosomes has steadily increased. In spinal ganglion cells autophagosomes only are increased as the Golgi vacuolation declines. At later times steady increases of lysosomal dense bodies is seen generally accompanied in hippocampal pyramidal cells and dentate fascia cells by abundant cell death. The suggestion is put forward that the Golgi complex may be the seat of the critical metabolic lesion and disturbances to protein transfer and protein synthesis follow. No explanation for the selective loss of hippocampal h1-5 (CA1-CA4 except Sommer's sector) pyramidal cells and of small dentate fascia neurons can be derived from these conclusions.

Amygdala↗
PubMed1975

Studies on energy-linked reactions: isolation, characterisation and genetic analysis of trialkyl-tin-resistant mutants of Saccharomyces cerevisiae.

Mutants of Saccharomyces cerevisiae resistant to triethyl tin sulphate have been isolated and are cross-resistant to other trialkyl tin salts. Triethyl-tin-resistant mutants fall into two general phenotypic classes: class 1 and class 2. Class 1 mutants are cross-resistant to a variety of inhibitors and uncoupling agents which affect mitochondrial membranes (oligomycin, ossamycin, valinomycin, antimycin, erythromycin, chloramphenicol, '1799', tetrachlorotrifluoromethyl benzimidazole carbonylcyanide-m-chlorophenylhydrazone and cycloheximide). Class 2 mutants are specifically resistant to trithyl tin and the uncoupling agent "1799' [bis-(hexafluoroacetonyl)-acetone]. Triethyl tin at neutral pH values is a specific inhibitor of mitochondrial energy conservation reactions and prevents growth on oxidisable substrates such as glycerol and ethanol. Triethyl-tin-resistant mutants grow normally on glucose and ethanol in the presence of triethyl tin (10 muM). Biochemical studies indicate that the mutation involves a modification of the triethyl tin binding site on the mitochondrial inner membrane, probably the ATP-synthetase complex. Triethyl tin resistance/sensitivity in yeast is determined by cytoplasmic (mitochondrial) and nuclear genes. The mutants fall into a nuclear and a cytoplasmic (mitochondrial) class corresponding to the phenotypic cross-resistance classes 1 and 2. In the cytoplasmic mutants the triethyl tin resistance segregates mitotically and the resistance determinat is deleted by the action of ethidium bromide during petite induction. Recombination studies indicate that the triethyl tin mutations are not allelic with the other mitochondrial mutations at the loci RI, RIII and OLI. This indicates that the binding or inhibitory sites of oligomycin and triethyl tin are not identical and that the triethyl tin binding site is located on a different mitochondrial gene product to those which are involved in oligomycin binding. Interaction and cooperative effects between different binding sites on the mitochondrial inner membrane have been demonstrated in studies of the effect of the insertion of the TETr phenotype into mitochondrial oligomycin-resistant mutants and provide an experimental basis for complementation studies at the ATP-synthetase level.

Adenosine Triphosphatases↗
PubMed1992

Presence of a sodium-translocating ATPase in membrane vesicles of the homoacetogenic bacterium Acetobacterium woodii.

Inverted membrane vesicles of the homoacetogenic bacterium Acetobacterium woodii catalyzed the hydrolysis of ATP with a rate of 100-150 nmol.min-1.mg protein-1. The ATPase was stimulated 1.4-1.6-fold by NaCl and inhibited by N,N'-dicyclohexylcarbodiimide tributyltin or azide. The degree of inhibition caused by F0-directed but not F1-directed inhibitors was affected by the Na+ concentration in the medium. These experiments indicated the presence of a sodium-translocating ATPase. This was verified by transport studies. Upon addition of ATP to inverted vesicles, 22Na+ was actively transported into the intravesicular space up to a 24-fold accumulation. Na+ transport was inhibited by the sodium ionophore N,N,N',N',-tetracyclohexyl-1,2-phenyl-enedioxydiacetamide but stimulated by valinomycin with potassium whereas the protonophore 3,5,-di-tert-butyl-4-hydroxybenzylidenemalonitrile was without effect. N,N'-dicyclohexylcarbodiimide and tributyltin inhibited 22Na+ transport. These experiments are in accordance with a primary electrogenic Na+ transport as catalyzed by a F1F0-ATPase.

Adenosine Triphosphatases↗
PubMed1994

Deactivation of F0F1 ATPase in intact plant mitochondria. Effect of pH and inhibitors.

By using a method especially adapted to intact (pea leaf) mitochondria, we studied the regulation of the F0F1 ATPase by the electrochemical proton gradient (delta mu H+) and by the matricial pH. The kinetics of decay of the ATP hydrolase activity was studied immediately after the collapse of the electrochemical proton gradient by an uncoupler. At pH 7.5, three inhibitors of the ATPase (venturicidin, tri-n-butyl tin and aurovertin), used at non-saturating concentrations, inhibited ATP hydrolysis to the same extent throughout the decay. This showed that the activity was totally controlled by the ATPase during all the decay and rules out any involvement of the phosphate or nucleotide carriers. This interpretation was confirmed by the fact that carboxyatractyloside, an inhibitor of the ATP/ADP antiporter, had a strong effect only on the initial rate of ATP hydrolysis, but not on the rate measured after some tens of seconds of decay. Oligomycin, at variance with the other ATPase inhibitors, interfered with the deactivation process, suggesting that its effect depends on the conformational state of the enzyme. Between pH 6.5 and 7.5, the hydrolase activity rose continuously and was still kinetically controlled by the ATPase. At higher pH value, the activity slightly decreased and appeared limited by at least one of the carriers. The activity of the ATPase itself, free of any transport process, seemed to increase monotonously with pH from 6.5 to 8. The electrochemical proton gradient is required to maintain the ATPase active, whereas no effect can be observed on transport processes. Matricial pH, while modulating the apparent catalytic turnover, has no marked effect on the rate of deactivation. These results, obtained with intact mitochondria, extend previous observations on the isolated enzyme and question the binding of IF1 as a rate-limiting step for ATPase deactivation.

Adenosine Triphosphate↗
PubMed1980

Effects of bis (tri-n-butyltin) oxide on endocrine and lymphoid organs of male rats.

A total of 160 Sprague-Dawley rats averaging in body weight, were used for histopathological and biochemical studies of toxicity of bis (tri-n-butyltin) oxide (TBTO). Short-term effects and long-term effects were examined. LD50 of TBTO by gastric tubing was 197 mg/kg. The effects of a single dose of TBTO were transient, and rapid recovery followed. TBTO at a a single dose of 100 mg/kg, or a total dose of 390 to 780 mg/kg in 13 weeks, or 780 to 1,560 mg/kg in 26 weeks, caused adrenal hypertrophy, flattening of the thyroid epithelium and atrophy of the thymus and lymph nodes. A single or repeated administration induced swelling and vacuolation of aldehyde-fuchsin-positive cells in the adenohypophysis. The immunohistochemical stainability of the cytoplasm of ACTH-cells was markedly depressed 24 hours after TBTO treatment, and that of the cytoplasm of TSH-cells was enhanced. Analogous an inverse relationship was also manifested in the hormonal levels of serum: levels of cortisol were elevated, while those of T-4 and TSH were depressed.

Adrenal Glands↗
PubMed1981

Effect of triethyl tin on myelination in the developing rat.

Myelinogenesis in developing rats was studied following chronic dosing with triethyl tin (TET), at a level of 1.0 mg TET/kg body wt/day. Experiments included starved controls with body weights depressed by 17 to 40% to equal those of the TET-treated groups. Rats at ages of 16, 21, and 30 days showed decreases relative to well-nourished controls in body weight, forebrain weight, myelin yield, cerebroside level, and specific activity of brain 2',3'-cyclic nucleotide-3'-phosphohydrolase when dosed with TET. At 30 days, myelin and cerebroside yields were reduced by approximately 55%, while CNP activity was reduced by less than 20%. No differences in the forebrain myelin protein composition between control, starved, and TET animals were noted. The rate of myelin protein synthesis relative to brain total protein (assayed by incorporation of intracranially injected [3H]glycine into brain homogenate and myelin proteins) was decreased in the TET rats in proportion to the decreased yield of myelin, but no particular myelin protein was preferentially affected. Matching starved controls exhibited similar body weight decreases, less pronounced forebrain weight decreases, and little or no decrease in myelin concentration. There was a relative increase in the myelin protein synthesis rate in the starved rats, indicating preferential utilization of limited protein precursors for myelin protein synthesis. Spinal cord myelin was also decreased in the TET rats, but less severely than in the forebrain. At all ages optic, but not sciatic, nerves showed decreases in myelin concentration with TET treatment. We conclude that TET inhibits forebrain growth and CNS myelination more severely than can be accounted for by a general metabolic insult.

Animals↗
PubMed1987

Effects of an extract of Ginkgo biloba on the 3',5'-cyclic AMP phosphodiesterase activity of the brain of normal and triethyltin-intoxicated rats.

For clarification of the beneficial effects of the extract of Ginkgo biloba (EGB) on triethyltin (TET) toxicity in rats, the phosphodiesterase (PDE) activities of the cerebral tissue were measured under in vitro and ex vivo conditions. Under in vitro conditions, low concentrations of EGB (0.25-4.0 mg/L) activated the enzyme, whereas after higher concentrations (5-250 mg/L), dose-dependent inhibition of the enzyme activity was observed. In the lower concentration range, the extract also partially restored the high-affinity PDE activity (measured with 0.25 microM cyclic AMP) of the particulate fraction of the brain inhibited by TET in vitro. In contrast, the inhibitory influence of TET on the low-affinity PDE activity (measured with 50 microM cyclic AMP) of the particulate fraction was enhanced by the extract. Although treatment with a single large dose of EGB lowered the particulate PDE activities of the brain of normal rats, no effects of the extract could be detected in animals after repeated daily administrations of EGB during a 4-day period. Curative treatment of the TET-intoxicated rats with EGB during a 7-day period accelerated the recovery of the edematous state of the white matter caused by the intoxication and also normalized the lowered PDE activity of the particulate fraction of the edematous brain tissue. Furthermore, when preventively administered, EGB counteracted both the edema formation and the fall in PDE activity observed with treatment by TET alone. These observations strongly suggest that some beneficial effects of EGB might be due to its modulating influences on cellular cyclic AMP levels via activation of membrane-bound PDE.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1991

Effect of ethanol on gamma-aminobutyric acid and glycine receptor-coupled Cl- fluxes in rat brain synaptoneurosomes.

Chloride fluxes in synaptoneurosomes in response to additions of gamma-aminobutyric acid, glycine, and ethanol were measured using a chloride-sensitive fluorescent probe 6-methoxy-N-(3-sulfopropyl)quinolinium (SPQ). The Cl- gradient was directed outward by bathing cells in a medium low in Cl- concentration. The synaptoneurosomes responded to both gamma-aminobutyric acid and glycine by outflow of Cl- ions, as judged from an increase in SPQ fluorescence. These effects were inhibited by picrotoxin and strychnine, respectively. Ethanol also produced an outflow of Cl- ions from the synaptoneurosomes. Both picrotoxin and strychnine inhibited this effect. When the antagonists were used together, the inhibiting effect was additive. These results indicate that ethanol affects both gamma-aminobutyric acid and glycine receptor-linked chloride fluxes in the rat brain.

Animals↗
PubMed1998

Enrichment with a polyunsaturated fatty acid enhances the survival of Saccharomyces cerevisiae in the presence of tributyltin.

The toxicity of inorganic metal species towards Saccharomyces cerevisiae has been shown to be markedly dependent on cellular fatty acid composition. In this investigation, the influence of fatty acid supplementation on the toxicity of the lipophilic organometal, tributyltin was investigated. Growth of S. cerevisiae was increasingly inhibited when the tributyltin concentration was increased from 0 to 10 microM. However, the inhibitory effect was partly alleviated by supplementation of the medium with 1 mM linoleate (18:2), a treatment that leads to large-scale incorporation of this polyunsaturated fatty acid (to > 60% of total fatty acids) in yeast membrane lipids. Cells that were previously enriched with 18:2 also showed reduced loss of vitality compared to cells grown in the absence of a fatty acid supplement, when exposed to tributyltin. For example, addition of tributyltin to a concentration of 0.1 microM was associated with an approximate 10% reduction in the H+ efflux activity of 18:2-enriched cells, but a 70% reduction in that of fatty acid-unsupplemented cells. Despite the increased tributyltin resistance of 18:2-enriched S. cerevisiae, the level of cell-associated tributyltin was found to be approximately two-fold higher in these organisms than in fatty acid-unsupplemented cells. These results demonstrate an increased resistance of 18:2-enriched membranes to the direct toxic action(s) of tributyltin. This is in contrast to the previously reported effect of 18:2 enrichment on sensitivity of S. cerevisiae to inorganic metal cations.

Culture Media↗
PubMed1984

Vascular permeability in acute triethyltin-induced brain edema studied with FITC-dextrans, sodium fluorescein and horseradish peroxidase as tracers.

In golden hamsters, a study was made on the vascular permeability changes which might take place during the formation of triethyltin (TET)-induced brain edema. For this purpose, the animals received a single intravenous (i.v.) injection of TET sulphate (5-10 mg/kg b.wt) and groups of animals were studied 4 to 24 h thereafter. By the use of a new density gradient technique based on polyvinylcoated silica particles (1), it was shown that white matter edema was present already at 4 h after the TET injection. The edema then progressed during the following 20 h. Electron microscopy revealed that fluid accumulated in myelin vacuoles of the hamsters in the same way as has been described in other animal species. The macromolecular tracer, horseradish peroxidase mol.wt 40,000 injected i.v., did not leak out of the cerebral vessels during the period when edema developed. In order to find out if the formation of edema is associated with a vascular permeability increase to other and smaller markers, we used several fractions of FITC-dextrans varying from mol.wt 3,000 to 70,000 and determined their intracerebral localization with a histotechnical procedure. FITC-dextrans, mol.wt 70,000, did not leak out of the cerebral vessels in any of the TET intoxicated hamsters during the observation period of 24 h. The same was true for most animals given the other dextran fractions. However, FITC-dextrans, mol.wt 3,000-20,000 were present outside the vessels in the edematous optic nerves and corpus callosum in a few TET treated animals taken 16-24 h after the TET injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Irritant dermatitis from tri-butyl tin oxide and contact allergy from chlorocresol.

A shipwright developed a delayed bullous irritant dermatitis from contact with a bis-tri-butyl tin oxide (TBTO) containing antifouling paint. He subsequently developed sensitization to 4-chloro-m-cresol, a constituent of a steroid cream. No cross sensitivity to 4-chloro-3,5 xylenol was seen. Low concentrations of 4-chloro-m-cresol in pet. may elicit a true positive reaction. TBTO is a strong irritant which will produce delayed bullous reactions in industrial use and on patch testing at 0.1% aqueous.

Adult↗
PubMed1991

Contact sensitivity (allergic contact dermatitis) to bis(tri-n-butyltin) oxide in mice.

Contact sensitivity (allergic contact dermatitis) to bis(tri-n-butyltin) oxide (TBTO) was demonstrated in the mouse. TBTO (in an acetone:olive olive oil vehicle) or acetone:olive oil alone (as a control) were applied to the shaved flank under an occlusive patch and animals were challenged on the dorsum of the ear 6 days later. Ear swelling was then measured using an engineer's micrometer, 2, 24, 48 or 72 h thereafter. Significant differences in ear swelling between control and TBTO-sensitized animals were found 24 h after challenge: thereafter the elicitation reaction declined rapidly whilst irritant swelling in control animals increased. Maximal elicitation of TBTO sensitivity could only be elicited by concentrations of TBTO that caused irritation. In a separate experiment, a single application of TBTO to the ears of naive animals provoked increase in auricular lymph node weight, cell yield and proliferation of lymph node cells during overnight culture. These data support the conclusion that TBTO is a contact sensitizer and illustrate the potential usefulness of the quantitative methods of contact sensitivity assessment which have been developed in the mouse.

Animals↗