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PubMed1992

Subchronic toxicity and reproduction effects of tri-n-butyltin oxide in Japanese quail.

A subchronic toxicity/reproduction study was performed in Japanese quails that were fed a diet containing 0, 24, 60, and 150 mg tri-n-butyltin oxide (TBTO) per kg basal diet for 6 weeks. Eggs produced during the 6 weeks of treatment were incubated and hatched, and chicks hatched from eggs collected in weeks 5 and 6 of exposure were reared for 2 weeks. In parent quail, neither diminished food consumption nor any overt toxic or histopathologic signs were observed following exposure to TBTO. A statistically significant decrease in hatch-ability and increase in percent of chicks found dead in the shell were observed following TBTO exposure at concentrations of 60 and 150 mg/kg food. However, no significant, adverse effects were recorded on total egg production, eggshell thickness and cracked eggs. Blood chemistry parameters of birds measured at the last day of TBTO treatment revealed a statistically significant decrease in serum aspartate aminotransferase (ASAT) enzyme activity among both sexes in all treatment groups. In addition, a statistically significant dose-related decrease in serum calcium level was observed in females only, while serum follicle stimulating hormone (FSH) levels were statistically significantly reduced in male birds in all treatment groups (approximately 50% of the controls). Moreover, a significant decrease in hepatic microsomal 7-ethoxyresorufin (EROD) activity was recorded in females fed 24 and 60 mg TBTO/kg diet and males fed 60 and 150 mg TBTO/kg diet, whereas pentoxyresorufin-o-deetylase (PROD) activity was only significantly decreased in males fed 150 mg TBTO/kg diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Immunotoxicity in channel catfish, Ictalurus punctatus, following acute exposure to tributyltin.

Tributyltin (TBT) is a trialkylated organotin formulated for use primarily as a biocide for aquatic and agricultural industries. Although macrophages isolated from toadfish (Opsanus tau) are sensitive to exposure, very little is known about the effects of TBT on fish humoral immunity and non-specific cytotoxic cell (NCC) functions. To evaluate the effects of TBT on these parameters, channel catfish (Ictalurus punctatus) were given a single intraperitoneal injection of corn oil with 0 (vehicle control) or with 0.01, 0.1, and 1.0 mgTBT/kg as TBTCl. Three and seven days later, NCC activity and phagocyte oxidative burst were evaluated and related to allometric indices and hematology. The humoral immune response to Edwardsiella ictaluri was evaluated fourteen days after treatment. Peripheral blood neutrophilia and specific antibody secreting cell (SASC) numbers were the most sensitive parameters and were affected in all three TBT treatment groups. Allometric indices, peripheral blood lymphocyte and monocyte percentages, NCC activity, and phagocyte oxidative burst were less sensitive and were affected only at the highest dose of TBT.

Animals↗
PubMed1992

Comparative sensitivity of gametes and early developmental stages of a sea urchin species (Echinometra mathaei) and a bivalve species (Isognomon californicum) during metal exposures.

Bioassays were developed using sperm of a sea urchin (Echinometra mathaei), and sperm, embryos, and larvae of a bivalve species (Isognomon californicum). Sea urchin spawning was restricted to only a few months of the year and viability of sperm throughout the year varied from 5 to 75%. Sea urchin fertilization assays were affected by temporal variation in sperm viability. Spawning in this bivalve species occurs year-round and there is little temporal variation in sperm viability. Since stringent sperm:egg ratios are not required for the bivalve embryo and larval assays, these were less affected by variation in gamete quality. The relative sensitivity of the various assays were compared during exposure to three different metal pollutants: cadmium, copper, and tributyltin. Gametes and embryos were relatively resistant to cadmium toxicity, but larvae were very sensitive. With copper and tributyltin, sea urchin and bivalve fertilization assays were the least sensitive; and bivalve growth assays were the most sensitive, followed closely by the bivalve embryo assays. On the basis of sensitivity, ease and time required to conduct the assay, and salinity tolerance, the bivalve embryo assay was recommended as the overall single most reliable toxicity bioassay. However a multispecies, multidimensional approach using sperm fertilization assays as well as embryo assays should be employed, perhaps in a hierarchal manner. Larval growth assays were deemed too tedious and time consuming to be used routinely, but due to their high sensitivity, should still be considered as a valuable comparative tool.

Animals↗
PubMed1992

Tributyltin-induced effects on early life stages of minnows Phoxinus phoxinus.

Toxicity and histopathological effects of tributyltin chloride (TBT) were studied in early life stages of minnows Phoxinus phoxinus. Eggs and yolk sac fry (newly hatched larvae) were exposed in a static-renewal procedure to aqueous TBT concentrations ranging from 0.82 to 19.51 micrograms/L for 3 to 10 days at 16 degrees C and 21 degrees C, respectively. Aqueous TBT concentrations were determined by capillary GC-FPD and revealed a concentration decrease during the static phase. TBT exposure led to mortality, behavioral, gross morphological and histopathological effects. In larvae, increased mortality, deformation of body axis, paralysis and opaque eyes occurred at 4.26 micrograms/L TBT and higher both in the embryonic-larval and larval exposure. Histological changes were evident at initial TBT concentrations of 0.82 up to 19.51 micrograms/L, and were more pronounced after embryonic-larval exposure than after larval exposure. Degenerative alterations occurred in skin, skeletal muscle, kidney, corneal epithelium, lens, pigment layer of the retina and choroid, retina, and CNS including spinal cord. Hydropic vacuolation of the cytoplasm and, in more pronounced cases, irreversible nuclear alterations such as pycnosis, karyorrhexis and karyolysis were also evident. Exposure to 0.82 micrograms/L TBT resulted in alterations in skin, muscle and kidney, with greater effects occurring at 21 degrees C than at 16 degrees C. Toxicity was significantly reduced in the presence of sediment. The observed histopathological effects suggest that early life stages of fish may be negatively affected in environments that are considerably polluted by TBT.

Abnormalities, Drug-Induced↗
PubMed1994

Hematology and serum biochemistry of Japanese quail fed dietary tri-n-butyltin oxide during reproduction.

During a subchronic toxicity and reproduction study with tri-n-butyltin oxide (TBTO) concentrations of 0, 24, 60, and 150 mg/kg diet in Japanese quail, preliminary data on hematology and serum biochemistry were obtained. The absence of serious effects in blood parameters in both adult quail and developing chicks are discussed in view of the adverse effects of TBTO on reproduction.

Administration, Oral↗
PubMed1990

Isolation and genetic study of triethyltin-resistant mutants of Saccharomyces cerevisiae.

Three mutants of Saccharomyces cerevisiae resistant to triethyltin (an inhibitor of mitochondrial ATPase) on non-fermentative media, and non-resistant to this drug on fermentative media, were isolated and named TTR1, TTR2 and TTR3. Apart from triethyltin resistance, these mutants show the following common characteristics: (1) Increased intracellular cytochrome c concentration. (2) Increased respiration rate. (3) Decreased growth yield. (4) Increased growth sensitivity to several drugs inhibiting oxidative phosphorylation: namely, CCCP (permeabilizing inner mitochondrial membrane to protons), valinomycin (permeabilizing inner mitochondrial membrane to potassium) and oligomycin (inhibitor of mitochondrial ATPase). (5) Increased sensitivity to carbon source starvation. For each mutant, these characteristics appeared to be due to a single pleiotropic nuclear mutation. Mutation TTR1 causes additional phenotypic characteristics which do not appear in mutants TTR2 and TTR3: (1) Pinkish coloration of colonies which is more pronounced after a long growth period. (2) Inability of the cells to store glycogen. (3) Growth defect of the cells on a galactose-containing medium. (4) Inability of a diploid homozygote mutant strain to sporulate. All these phenotypic characteristics have already been described in yeast mutants deregulated in cAMP-dependent protein phosphorylation. Crossing of a strain bearing the TTR1 mutation with a strain mutated in the adenylate cyclase structural gene suggested that the TTR1 phenotype is due to a modification in regulation of cAPK by cAMP, making cell multiplication possible without intracellular cAMP.

Alleles↗
PubMed1990

Mitochondrial modifications in a single nuclear mutant of Saccharomyces cerevisiae affected in cAMP-dependent protein phosphorylation.

This paper reports studies of bioenergetic modifications in a TTR1 single-nuclear mutant, isolated as resistant to triethyltin, an inhibitor of mitochondrial ATPase, and effective in cAMP-dependent protein phosphorylation. This mutant appears to have lost the wild-type cell ability to respond to a decrease of oxygen concentration in the growth medium by a decrease of cytochrome concentration in the cell. ATP synthesis rate in mutant cells in both the prestationary and stationary phase of growth appeared increased in comparison to wild-type cells, as too was respiration rate. A comparative study of mitochondria extracted from wild-type and from TTR1 mutant cells showed an increase in respiration rate, an increase in ATP synthesis rate, and an increase in TPP+ uptake in mutant mitochondria. The specific ATPase activity, as well as its sensitivity to TET, appears to be similar for mitochondria extracted from both strains. It was proposed that the modification of mitochondrial biogenesis in the TTR1 mutant may be due to a response of the cell to an increase in ATP hydrolysis caused by the mutation. It is also possible that the modification in cAMP-dependent protein kinase regulation which appeared to occur in this mutant affects protein(s) involved in mitochondrial biogenesis.

Adenosine Triphosphatases↗
PubMed1986

In vitro studies on the embryotoxic potential of (bis[tri-n-butyltin])oxide in a limb bud organ culture system.

(Bis[tri-n-butyltin])oxide (TBTO) was studied for its toxic potential on prenatal development. The effect of this substance on limb differentiation (mouse embryos) in organ culture was evaluated. In the organ culture system using mouse limb buds, TBTO interfered with morphogenetic differentiation at doses as low as 0.03 microgram/ml (5 X 10(-8)M). This is one of the lowest concentrations of a substance ever found to be active in this in vitro system. The in vitro studies suggest a high embryotoxic potential of TBTO. The low embryotoxicity found in the in vivo studies may be due to limited exposure of the embryos by the original unmetabolized substance.

Abnormalities, Drug-Induced↗
PubMed1989

Time-dependent deficits in delay conditioning produced by trimethyltin.

Trimethyltin (TMT) produces behavioral and cognitive deficits resulting, in part, from limbic system toxicity. To determine whether these effects result from learning deficits or accelerated memory loss, the present experiment examined two delay conditioning paradigms in rats previously treated with either saline or TMT. Saline-treated Long-Evans rats receiving injections of lithium after consuming saccharin-flavored water later avoided saccharin ingestion: the degree of avoidance varied inversely with the time (0.5, 3 or 6 h) separating initial saccharin availability and lithium injection. Rats treated with TMT (8 mg/kg IV, 30 days prior) showed impaired conditioning at the long but not the short or intermediate delay conditions, suggesting that the deficits were mnemonic and not associative. Similar delay-dependent deficits in rats treated with TMT were observed in a passive avoidance task that arranged one of two delays between response emission and shock delivery during training. The effects of TMT on delay conditioning were accompanied by reduced bodyweight and hippocampal pathology. In summary, TMT appears to alter the temporally dependent association of events (entering darkened compartment versus saccharin consumption) and consequences (foot shock versus lithium administration) during acquisition. Furthermore, the observed deficits in delay conditioning produced by TMT did not appear to be task specific, with similar effects determined with tests of both somatosensory and gustatory avoidance learning designed to distinguish between functional alterations due to deficits in memorial processes from those due to altered sensory, motor, or associative processes.

Animals↗
PubMed1982

Acute treatment with trimethyltin alters alcohol self-selection.

Male rats of the Long-Evans strain were divided into two equal groups of nine each and given either 7.0 mg/kg trimethyltin (TMT) or 0.9% saline by intragastric gavage. The pattern of self-selection of alcohol in concentrations of 3%--30% was examined in both groups at 21 and 150 days following the gavage. The TMT-treated rat consistently drank less alcohol than did the controls at every concentration of alcohol. This difference in alcohol intake was equally significant when the rats were tested in a food-contingent, schedule-induced polydipsia situation. Further, although the TMT-lesioned animal consumed fewer calories per day in the form of alcohol, their overall daily caloric intakes were slightly higher than those of the controls. These results are interpreted as a consequence of damage to structures of the forebrain and as part of a syndrome of behavioral and neurological pathology.

Alcohol Drinking↗
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↗
PubMed1982

Some effects of dibutylchloromethyltin chloride and other reagents on mitochondrial K+ flux.

Respiration-dependent K+ fluxes across the limiting membranes of isolated rat liver mitochondria, measured by means of 42K, are stimulated by the oxidative phosphorylation inhibitor dibutylchloromethyltin chloride (DBCT). A lack of effect of Cl- concentration indicates that the stimulation of K+ flux by DBCT is not attributable to Cl-/OH- exchange activity. The mercurial mersalyl was previously shown to stimulate respiration-dependent K+ influx. The combined presence of mersalyl plus DBCT results in a greater stimulation of K4 influx than is caused by either DBCT or mersalyl alone. The oxidative phosphorylation inhibitor oligomycin, which alone has no effect on respiration-dependent K+ influx, enhances the stimulatory effect of mersalyl on K+ influx. The data are consistent with, although not proof of, a direct interaction of the K+ transport mechanism with the mitochondrial energy transduction apparatus.

Animals↗
PubMed1990

Acetazolamide inhibits the recovery from triethyl tin intoxication: putative role of carbonic anhydrase in dehydration of central myelin.

The vacuolar degeneration of central myelin was produced in Sprague-Dawley rats by oral administration of triethyl tin. The wet weight of brain stems which seems to reflect the degree of accumulation of water increased during the administration of the toxin, whereas the activity of 2', 3'-cyclic nucleotide 3'-phosphodiesterase altered less remarkably. When TET was withdrawn from the drinking water, the rats showed a dramatic clinical improvement along with reduction in wet weight of brain stems. Treatment with acetazolamide following TET inhibited the clinical improvement and reduction in wet weight of brain stems. The present results indicates that central myelin has plasticity in recovering from the vacuolar degeneration by removing the accumulated fluid and carbonic anhydrase is possibly involved in the dehydration of myelin in such a recovery phase.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗