Change of embryotoxic susceptibility to di- n -butyltin dichloride in cultured rat embryos

Ema, Makoto; Iwase, Takayuki; Iwase, Yumiko; Ohyama, Naoki; Ogawa, Yoshiyuki

doi:10.1007/s002040050335

Cited by 20 publications

(7 citation statements)

References 31 publications

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“…In the rat embryo culture, DBTCl induces the craniofacial defects in the embryo from GDs 8.5 and 9.5, but not from GD 11.5 (Ema et al, 1996). In the normal rat development, the craniofacial primordium is already formed in a 15-20 somite embryo on GD 9.5-10 (Butcher, 1929;Kaufman, 1990).…”

Section: Discussionmentioning

confidence: 99%

Effect of dibutyltin on placental and fetal toxicity in rat

et al. 2017

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-In order to elucidate the effect of chorioallantoic and yolk sac placenta on the embryonic/fetal toxicity in dibutyltin dichloride (DBTCl)-exposed rats, we examined the histopathological changes and the tissue distribution of dibutyltin in the placentas and embryos. DBTCl was orally administered to the groups at doses of 0 mg/kg during gestation days (GD)s 7-9 (control group) and 20 mg/kg during GDs 7-9 (GD7-9 treated group), and GDs 10-12 (GD10-12 treated group). The total fetal mortality was increased, and malformations characterized by craniofacial dysmorphism were detected in the GD7-9 treated group. The embryonic/fetal weight and placental weight showed a decrease in both DBTCl-treated groups. Histologically, some embryos on GD 9.5 in the GD7-9 treated group underwent apoptosis without any changes of yolk sac. In the laser ablation-inductively coupled plasma-mass spectrometry analysis (LA-ICP-MS), tin was detected in the embryo, allantois, yolk sac, ectoplacental cone and decidual mass surrounding the conceptus on GD 9.5 in the GD7-9 treated group. Thus, it is considered that the embryo in this period is specifically sensitive to DBTCl-induced apoptosis, compared with other parts. The chorioallantoic placentas in both DBTCl-treated groups showed the developmental delay and hypoplasia in the fetal parts of placenta, resulting from apoptosis and mitotic inhibition. Thus, it was speculated that the DBTCl-induced malformations and fetal resorption resulted from the apoptosis in the embryo caused by the direct effect of DBTCl. The DBTCl-induced lesions in the chorioallantoic placenta were a non-specific transient developmental retardation in the fetal parts of placenta, leading to intrauterine growth retardation.

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Section: Discussionmentioning

confidence: 99%

Effect of dibutyltin on placental and fetal toxicity in rat

et al. 2017

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“…DBT appears to cause a variety of birth defects in rats and to disrupt normal embryonic development (Ema et al, 1996; Noda et al, 1993). Thymus atrophy and pancreatitis are consequences of DBT exposure in rats (Merkord et al, 1997; Pieters et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Dibutyltin activates MAP kinases in human natural killer cells, in vitro

et al. 2010

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Previous studies have shown that dibutyltin (DBT) interferes with the function of human natural killer (NK) cells, diminishing their capacity to destroy tumor cells, in vitro. DBT is a widespread environmental contaminant and has been found in human blood. As NK cells are our primary immune defense against tumor cells, it is important to understand the mechanism by which DBT interferes with their function. The current study examines the effects of DBT exposures on key enzymes in the signaling pathway that regulates NK responsiveness to tumor cells. These include several protein tyrosine kinases (PTKs), mitogen activated protein kinases (MAPKs) and mitogen activated protein kinase kinases (MAP2Ks). The results showed that in vitro exposures of NK cells to DBT had no effect on PTKs. However, exposures to DBT for as little as 10 min were able to increase the phosphorylation (activation) of the MAPKs. The DBT-induced activations of these MAPKs, appears to be due to DBT-induced activations of the immediate upstream activators of the MAPKs, MAP2Ks. The results suggest that DBT-interference with the MAPK signaling pathway is a consequence of DBT exposures, which could account for DBT-induced decreases in NK function.

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“…Ema et al [35,36] showed a direct correlation between the length of exposure to DBT and the onset of defects in developing rat embryos. Another study described toxic effects that cause anomalies in the development of testicles in mice [37].…”

Section: Evidence Of the Toxic Effects Of Tbtmentioning

confidence: 99%

The management of the effects of navigation on the marine environment: the case of tributyltin (TBT)

Sarti¹,

Mezzani²,

Ceccarelli³

et al. 2011

Chemistry and Ecology

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The aim of this study is to review the fact-finding and decision-making process of the international community which, via the International Maritime Organization, has led to a ban on the use of antifouling paints containing organotin compounds. This review focuses on the importance of scientific knowledge supporting the sustainable management of the environment and on the centrality of ecotoxicological studies on the effects of human activities on the enviroment. The Italian Coast Guard Corps guarantees compliance with the regulations, through the action of Port State Control carried out in ports and onboard vessels.

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Change of embryotoxic susceptibility to di- n -butyltin dichloride in cultured rat embryos

Cited by 20 publications

References 31 publications

Effect of dibutyltin on placental and fetal toxicity in rat

Effect of dibutyltin on placental and fetal toxicity in rat

Dibutyltin activates MAP kinases in human natural killer cells, in vitro

The management of the effects of navigation on the marine environment: the case of tributyltin (TBT)

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