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PubMed1987

Effects of trimethyltin on the mouse hippocampus and adrenal cortex.

The effects of trimethyltin (TMT) on the mouse adrenal histology and its relationship with neuropathology occurrence was studied. Young, male CD-1 mice were divided into three groups: group I, injected on 3 consecutive days with 1.0 mg TMT/kg body weight (b.w.); group II, injected on 2 consecutive days with 1.5 mg TMT/kg b.w.; and group III, injected with a single acute dose of 3.0 mg TMT/kg b.w. Control animals were injected with saline solution. The brain and adrenal glands were sampled for light-microscopic examination. Although all animals received the same total amount of TMT, pathological changes in the granule cells of the fascia dentate appeared to be group III greater than group II greater than group I, suggesting that acute exposures produced a more severe damage to the fascia dentate neurons. Likewise, the adrenal weights of the animals were group III greater than group II greater than group I greater than or equal to control. Significant proliferation and enlargement of the eosinophilic or the "X zone" were observed in the TMT-treated, particularly groups II and III, animals. The expansion of the eosinophilic cell layer (X zone) was accomplished at the expense of the cortical fasciculata cells. Transformation of fasciculata cells into eosinophilic cells could also be demonstrated. As the eosinophilic cells are known to be active in corticosterone production as seen in stress situations, the proliferation of these cells may reflect a feedback response to the hippocampal hyperexcitation.

Adrenal Cortex↗
PubMed1991

Immunotoxicity of bis(tri-n-butyltin) oxide in the rat.

Previous studies in the rat have shown that bis(tri-n-butyltin) oxide (TBTO), used as a biocide, was immunotoxic at dose levels that did not affect other organs. In order to determine a no-effect level, weanling rats were treated for at least 28 consecutive days with TBTO at 0, 0.5, 2, 5, or 50 mg/kg of diet. Studies on clinical chemistry, hematology, pathology, and immune function, that is, plaque-forming cell (PFC) assay, delayed-type hypersensitivity (DTH) response, and the splenic clearance of Listeria monocytogenes, were performed at the end of treatment. No treatment-related effects were noted on clinical chemistry and hematology parameters and on PFC and DTH response, whereas thymic atrophy and impaired clearance of L. monocytogenes were noted only at a dietary concentration of 50 mg/kg. These results confirm the thymus as a target organ of TBTO immunotoxicity. Under the conditions of these experiments the dietary concentration of 5 mg/kg, equivalent to a dose of 0.5 mg/kg body weight, represents a no observed effect level (NOEL) for immunotoxicity in the Sprague-Dawley rat.

Administration, Oral↗
PubMed1991

In vivo unwinding fluorimetric assay as evidence of the damage induced by fenarimol and DNOC in rat liver DNA.

Five pesticides [amitraz, cyanazine, cyhexatin, dinitro-o-cresol (DNOC), and fenarimol] were tested as pure active ingredients for in vivo induction of DNA strand breaks on rat hepatocytes after intraperitoneal (ip) treatment. Two pesticides, fenarimol and DNOC, were capable of inducing DNA damage because they significantly increased the DNA unwinding rate. On the contrary, amitraz, cyanazine, and cyhexatin were not DNA-damaging agents.

Animals↗
PubMed1995

Oral bis(tri-n-butyltin) oxide in pregnant mice. I. Potential influence of maternal behavior on postnatal mortality.

Pregnant Swiss mice were treated with 0, 5, 10, 20, and 30 mg/kg body weight of bis(tri-n-butyltin) oxide (TBTO) on d 6-15 of gestation. At birth litters were normalized to eight pups, and postnatal evaluation of pup growth rate and behavioral observations of dams were carried out. Litters were sacrificed on postnatal days (pnd) 7, 14, and 21, to perform hematological analysis, in connection with another study. Dam weight gain was impaired in all the treated groups (except at the lowest dose level) in the late phase of gestation. A high incidence of anticipated or delayed parturitions, without any correlation with fetal mass, was observed in the treated groups. All the treated dams showed a significant increase in resorptions, and a decrease in body weight gain between gestational day (gd) 6 and pnd 1. At birth, only the 20 and 30 mg/kg dose groups showed reduced litter size and reduced pup weight. Body weight gain reduction of pups persisted in wk 1 of life only in the 10 and 20 mg/kg dose groups. In addition, the maternal weight trend was affected during the lactation period in the higher dose groups. Postnatal death rate and growth rate of treated pups were affected by an altered maternal behavior; pups, apparently viable and with normal weight, were found often scattered throughout the cage with signs of wounds, and the percentage of dams that had not built a nest increased in the 10, 20, and 30 mg/kg dose groups. Total absence of parental care was noted in many litters, and many infanticidal events were reported. Our results seem to confirm low TBTO embryofetotoxicity, and strongly support the assumption that TBTO's toxicity to the mother is much stronger than its embryo-fetotoxic potential. Most of the reproductive parameters examined in this study were unaffected in the low-dose group, while some indices, such as gestation length and maternal weight gain between gd 6 and pnd 1, were markedly altered also at the 5 mg/kg dose level and appear to be sensitive parameters in assessing maternal toxicity.

Administration, Oral↗
PubMed1995

Oral bis(tri-n-butyltin) oxide in pregnant mice. II. Alterations in hematological parameters.

The effect of in utero TBTO exposure on blood composition in neonates, pups during weaning, and dams in the same period were investigated in mice. The dams were gavaged at dose levels 0, 5, 10, and 20 mg TBTO/kg body weight on gestational days 6-15. At birth, litters were culled to eight pups, and blood analysis was performed on excess pups. On d 7, 14, and 21 the entire litters were sacrificed and blood (WBC, RBC, HGB, HCT, MCV, MCH, MCHC, and differential leukocyte count) of dams and pups was analyzed. Blood analysis of neonates revealed enhanced WBC count and altered red-cell parameters. Increase in WBC persisted until postnatal day (pnd) 21, while red-cell parameters regained normal values on pnd 7. No significant differences were found in thymus and spleen weights in the treated groups. Dams presented no alteration in blood composition or of spleen or thymus weights. The results of this investigation revealed that in utero exposure to TBTO induces a nonspecific alteration of hematological parameters in mice, but further studies are necessary to understand whether our results are either dependent on maternal status or a direct effect of TBTO on embryonic tissue.

Animals↗
PubMed2003

Effects of simultaneous administration of tributyltin (TBT) and p,p(')-DDE on female offspring of Wistar rats.

p,p(')-DDE (DDE) and tributyltin (TBT) occur globally and in Japan were shown to bioaccumulate in marine products, thus serving as a source of contamination in the mammalian food chain. Consequently, fetuses and neonates, through maternal ingestion, may be exposed to DDE and TBT. Therefore, the effects of combined DDE and TBT were investigated in female Wistar rat offspring of dams ingesting these two contaminants. In this study, TBT suppressed the growth of female offspring and delayed eye opening. However, both growth retardation and delayed eye opening produced by TBT failed to occur in the presence of DDE. These results indicated that TBT or DDE affected the development of female rat offspring following maternal exposure and simultaneous administration of DDE prevented some of the observed effects of TBT through a mechanism that remains to be elucidated.

Animals↗
PubMed2002

Butyltins in sediments and three-spined stickleback (Gasterosteus aculleatus) from the marinas of the Gulf of Gdansk, Baltic Sea.

Fifty four sediment samples and three pooled samples of whole three-spined stickleback (Gasterosteus aculleatus) collected from four marinas located along the south-western coast of the Gulf of Gdańsk, Baltic Sea, Poland, were examined for butyltins (BTs) i.e., tributyltin (TBT), dibutyltin (DBT) and monobutyltin (MBT), to understand the degree of pollution and distribution pattern. Total butyltin concentrations in sediments from the marina of the city of Gdynia ranged between 130 and 20,000 ng Sn/g dry wt. with a mean value of 2,900 ng Sn/g. In sediments collected from the marinas located in the area of the Brave Vistula River Channel BT concentrations ranged between 10 to 15,000 ng Sn/g drywt. with a mean values between 500 and 5,500 ng Sn/g, and the innermost sites of each of four marinas were the most polluted. The mean BT concentrations in three-spined stickleback were between 1,500 and 3,100 ng Sn/g wetwt. and the values followed mean concentrations noted in sediments from the corresponding marina. The pleasure yachts are identified as the main source of BT pollution of sediment and fish. Tributyltin was a major form of BTs present in sediments (between 24 and 43%) and in three-spined stickleback (between 54 and 70%), suggesting a very recent use of marine paints containing TBT in pleasure yachts. Evidently at the Polish coast of the Baltic Sea TBT was continuously used in 1997 in marine paints for boats less then 25 m long.

Animals↗
PubMed1986

Catecholamine-induced transport systems in trout erythrocyte. Na+/H+ countertransport or NaCl cotransport?

It has previously been shown (Baroin, A., F. Garcia-Romeu, T. Lamarre, and R. Motais. 1984a, b. Journal of Physiology. 350:137, 356:21; Mahé, Y., F. Garcia-Romeu, and R. Motais. 1985. European Journal of Pharmacology. 116:199) that the addition of catecholamines to an isotonic suspension of nucleated red blood cells of the rainbow trout first stimulates a cAMP-dependent, amiloride-sensitive Na+/H+ exchange. This stimulation seems to be transient. It is followed by a more permanent activation of a coupled entry of Na+ and Cl-, which is inhibited by amiloride but also by inhibitors of band 3 protein (DIDS, furosemide, niflumic acid). The coupled entry of Na+ and Cl- could therefore result from the parallel and simultaneous exchange of Na+out for H+in (via the cAMP-dependent Na+/H+ antiporter) and Cl- out for HCO3- in (via the anion exchange system located in band 3 protein). However, in view of the following arguments, it had been proposed that NaCl uptake does not proceed by the double-exchanger system but via an NaCl cotransport: (a) Na+ entry requires Cl- as anion (in NO3- medium, the Na uptake is strongly inhibited, whereas NO3- is an extremely effective substitute for Cl- in the anion exchange system); (b) Na uptake is not significantly affected by the presence of HCO3- in the suspension medium despite the fact that in red cells, Cl-/HCO3- exchange occurs more readily than the exchanges of Cl- for basic equivalents in a theoretically CO2-free medium (the so-called Cl-/OH- exchanges). The purpose of the present paper was a reassessment of the two models by using monensin, an ionophore allowing Na+/H+ exchange. From this study, it appears that NaCl entry results from the simultaneous functioning of the Na+/H+ antiporter and the anion exchange system. The apparent Cl dependence is explained by the fact that, in these erythrocytes, NO3- clearly inhibits the turnover rate of the Na+/H+ antiporter. As Na+/H+ exchange is the driving component in the salt uptake process, this inhibition explains the Cl requirement for Na entry. The lack of stimulation of cell swelling by bicarbonate is explained by the fact that the rate of anion exchange in a CO2-free medium (Cl-/OH- exchange) is roughly equivalent to that of Na+/H+ exchange and thus in practice is not limiting to the net influx of NaCl through the two exchangers.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Optimization of radioiodination and biotinylation of monoclonal antibody chimeric BR96: an indirect labeling using N-succinimidyl-3-(tri-n-butylstannyl)benzoate conjugate.

Chimeric BR96 (chiBR96) is an oxidant sensitive, highly tumor-reactive and internalizing monoclonal antibody. Radioiodination of chiBR96 with direct labeling methods has a high risk of damaging the antibody's immunoreactivity. Combination of iodination and biotinylation of chiBR96 has been particularly difficult. In present studies, indirect radioiodine labeling by use of a conjugate of N-succinimidyl 3-(tri-n-butylstannyl)benzoate (ATE) was introduced for chiBR96 radioiodination and for combination of iodination and biotinylation of chiBR96. ATE was synthesised, radioiodinated with a modified and simplified method by omitting one step of separation. A same or slightly higher labeling efficiency was obtained comparing to earlier reports. Simultaneous biotinylation of the chiBR96 was performed by use of biotin reagent of N-hydroxysuccinimido-biotin. In a comparative study of biotinylated and unbiotinylated 125I-chiBR96 iodinated with ATE conjugate, it was found that 125I-chiBR96 with or without biotinylation had the same stability, immunoreactivity and biodistribution with a high tumor targeting capacity. Hence, the ATE conjugate radioiodination method enables the combination of iodination and simultaneous biotinylation of chiBR96.

Animals↗
PubMed2001

Two-generation reproductive toxicity study of tributyltin chloride in male rats.

A 2-generation reproductive toxicity study of tributyltin chloride (TBTCl) was conducted in male rats using dietary concentrations of 5, 25, and 125 ppm TBTCl to evaluate its effect on sexual development and the reproductive system. F1 males were killed on postnatal day 119 and F2 males were killed on postnatal day 91. TBTCl affected the male reproductive system of rats. The weights of the testis and epididymis were decreased and homogenization-resistant spermatid and sperm count were reduced mainly in the 125 ppm TBTCl group. Histopathologic changes were also observed in the testis of this group and included vacuolization of the seminiferous epithelium, spermatid retention, and delayed spermiation. However, the changes were minimal in nature. The weight of the ventral prostate was decreased to 84% of the control value in the 125 ppm group in the F1 generation and decreased to 84 and 69% of the control value in the 25 ppm and 125 ppm TBTCl groups, respectively, in the F2 generation. The serum 17beta-estradiol concentration was also decreased to 55% of the control value in the 125 ppm group in the F1 generation and decreased to 78 and 57% of the control value in the 25 ppm and 125 ppm TBTCl groups, respectively, in the F2 generation. However, the serum concentrations of luteinizing hormone (LH) and testosterone were not decreased in these groups. These changes corresponded with those caused by aromatase inhibition and therefore TBTCl might be a weak aromatase inhibitor in male rats.

Animals↗
PubMed2005

Glutamate excitotoxicity is involved in cell death caused by tributyltin in cultured rat cortical neurons.

Tributyltin, an endocrine-disrupting chemical, has been used as a heat stabilizer, agricultural pesticide, and component of antifouling paints. In this study, the neurotoxicity of tributyltin was investigated in cultured rat cortical neurons. Tributyltin caused marked time- and dose-dependent increases in the number of trypan blue-stained cells. Measurement of extracellular glutamate concentration showed that glutamate release was induced by tributyltin. Application of the glutamate receptor antagonists MK-801 and CNQX decreased the neurotoxicity. These results suggest that released glutamate and glutamate receptors are involved in tributyltin toxicity. Next, we examined whether various factors, believed to be involved in glutamate excitotoxicity also influence tributyltin toxicity. Cell death induced by tributyltin was found to be reduced by alpha-tocopherol (a membrane-permeable antioxidant), SB202190 (a p38 mitogen-activated protein kinase inhibitor), and U-0126 (an extracellular signal-regulated protein kinase kinase inhibitor). MK-801 and CNQX decreased the phosphorylation of ERK, but not that of p38. A caspase-3 inhibitor had no effect on tributyltin toxicity, and tributyltin did not change the nuclear morphology. These results suggest that the glutamate excitotoxicity caused by tributyltin is unrelated to apoptosis. In conclusion, we demonstrated that tributyltin induced glutamate release and subsequent activation of glutamate receptors, leading to neuronal death. We propose two independent neuronal death pathways by tributyltin; one is glutamate receptor-dependent cell death via ERK phosphorylation, and the other may be glutamate receptor-independent cell death via p38 activation.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1975

The neurotoxic effects of triethyltin (TET) sulfate on myelinating cultures of mouse spinal cord.

Well myelinated cultures of mouse spinal cord, exposed to varying concentrations of triethyltin sulfate, were examined at different time intervals by light and electron microscopy. At a high concentration of TET (10(-6)M) for 1-2 hours, the myelin sheaths and cells showed marked degenerative changes. At lower concentrations of TET (10(-7)-10(-9) M) intramyelinic and other types of vacuole formation were seen; however, these lesions were always accompanied by changes in the perikarya, dendrites and axons of neurons and in the astrocytes. Also, there was an apparent increased number of neurofilaments and neurotubules in many axons. The findings are discussed in relation to the lesions induced in the experimental animal by alkyl tin intoxication.

Culture Techniques↗
PubMed1976

Core formation in the muscles of rats intoxicated with triethyltin sulfate.

Young adult Osbourne-Mendel rats intoxicated for up to 23 days with triethyltin sulfate (TET) at a dose of 20 mg/liter of drinking water given ad libitum, developed core-like structures in type 1 extrafusal fibers of the soleus muscles. Frozen sections revealed an absence of oxidative enzyme activity (NADH-tetrazolium reductase) and diminished or absent myosin ATPase (pH 9.4) in the core regions. The main electron microscopic features within the cores were loss of mitochondria and streaming of the Z-disks. The histochemical and electron microscopic similarities and differences between the TET-induced cores, other core models, and those reported in some human neuromuscular disorders are discussed. The present experiments do not clarify whether the cores are produced from a direct effect of TET upon skeletal muscle or upon the neural component of the motor unit.

Animals↗
PubMed1997

Induction of tumor necrosis factor-alpha in vivo by a skin irritant, tributyltin, through activation of transcription factors: its pharmacological modulation by anti-inflammatory drugs.

Skin irritant reactions are under the control of a network of cytokines and lipid mediators. This study characterized the production of tumor necrosis factor-alpha (TNF) induced by a skin irritant treatment, tributyltin (TBT), in mice through transcription factor activation and its pharmacologic modulation by anti-inflammatory agents. The ears of BALB/c mice were painted with different amounts of TBT (67-536 nmol in acetone) or with acetone alone. At different times thereafter, TNF production was analyzed both at the mRNA and protein level, by semiquantitative RT-PCR and L929 cytotoxicity assay, respectively. TBT induced rapid (1 h) TNF gene expression and protein synthesis. Maximal TNF production was observed 2 h after treatment. The production of TNF was paralleled by accumulation of skin water; this was partially prevented by intraperitoneal injection of antibody against murine TNF. These data indicate that skin irritation induced by TBT is attributable, in addition to the actions of other inflammatory mediators, to the action of keratinocyte-derived TNF. TNF production was preceded by a rapid (5 min) activation of nuclear factor-kappaB (NF-kappaB), which was also maximal 30 min after treatment. TBT-induced accumulation of skin water and TNF production were significantly reduced by topical treatment with dexamethasone and pentamidine, two anti-inflammatory agents. Interestingly, dexamethasone, but not pentamidine, decreased TBT-induced NF-kappaB activation, confirming in vivo that the glucocorticoid receptor interacts functionally within the nucleus with other transcription factors opposing one another's activity.

Animals↗
PubMed1996

Role of mitochondria in tributyltin-induced interleukin-1alpha production in murine keratinocytes.

Tributyltin (TBT) salts are well known skin irritants in rodents and humans. TBT induced both the intracellular production of interleukin-1alpha (IL-1alpha) and its release into culture medium in a murine keratinocyte cell line (HEL30). Here, we report that mitochondria are important for TBT-induced IL-1alpha production. Confluent cells were treated with increasing concentrations of TBT (0--2.5 microM) or dimethylsulfoxide as vehicle control. At different times thereafter (0--24 h), nuclear extracts were analyzed for nuclear factor-(kappa)B (NF-(kappa)B) binding activity by electrophoretic mobility shift assay, and the released and cell-associated IL-1alpha was measured by enzyme-linked immunosorbent assay. TBT induced a direct and concentration-related activation of NF-(kappa)B, which peaked at 2 h and was blocked by pyrrolidinedithiocarbamate, a potent NF-(kappa)B inhibitor, and rotenone, an inhibitor of the electron entry from complex I to ubiquinone. Rotenone also induced a concentration-related inhibition of IL-1alpha synthesis induced by TBT, but rotenone did not completely abrogate TBT-induced IL-1alpha production, which suggests that other transcription factors may be involved in IL-1alpha production. Prolonged treatment with ethidium bromide, an inhibitor of mitochondrial DNA and RNA synthesis, was used to partially deplete cells of functional mitochondria. After 5 d of treatment, mitochondrial conversion of tetrazolium bromide to formazan was reduced by 50%, and IL-1alpha release was decreased by 65%, whereas no induction of intracellular IL-1alpha was observed. This effect was not due to inhibition of protein synthesis, because identical incorporation of [3H]leucine into protein in control and ethidium bromide-treated cells was identical. This impairment of mitochondrial metabolism inhibited NF-(kappa)B activation by TBT. These findings indicate that mitochondria may be the source of second messenger molecules important for TBT-induced IL-1alpha production.

Animals↗