Effect of cisplatin on rat placenta development

Furukawa, Satoshi; Hayashi, Seigo; Usuda, Koji; Abe, Masayoshi; Hagio, Souichiro; Ogawa, Izumi

doi:10.1016/j.etp.2011.08.008

Cited by 23 publications

(22 citation statements)

References 30 publications

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“…The cell proliferative activity in the labyrinth zone is at its peak on GD 13 and then reduces toward late gestation (Furukawa et al, 2015). Therefore, the effect of these agents on the labyrinth zone is closely related to the proliferation period, and the developed lesions depend on the timing of treatment period, such as 6-mercaptopurine (Furukawa et al, 2011a) and cisplatin (Furukawa et al, 2013b). By contrast, chlorpromazine induces the nonspecific transient developmental retardation of placenta caused by apoptosis independently of the cell proliferation period (Furukawa et al, 2015).…”

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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“…18 Several pharmacokinetic studies on animals have confirmed these hypotheses. [19][20][21] Despite the fact that platinum-based chemotherapy is the most frequently used systemic therapy in pregnant women with cervical cancer, only 1 small study and 1 case report have analysed maternofetal passage of cisplatinum. 22,23 It was therefore the intention of the present prospective study to extend the current literature data about the safety of chemotherapy during gestation and to reinforce our own results on in vivo measurement of platinum concentrations.…”

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confidence: 99%

How much platinum passes the placental barrier? Analysis of platinum applications in 21 patients with cervical cancer during pregnancy

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Oppelt

Favero

et al. 2015

American Journal of Obstetrics and Gynecology

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“…After 6-mercaptopurine-treatment on GD 11, 13 or 15, the severity of labyrinth zone hypoplasia progressed in accord with the early time point of treatment, but the basal zone hypoplasia is induced by only the GD11-treatment (Furukawa et al, 2011a). With cisplatin, the metrial gland hypoplasia is induced by the treatment on GDs 11 and 12, but not on GDs 13 and 14 (Furukawa et al, 2013b). With GW501516, PPAR␤/␦ agonist, the cystic degeneration is induced by the treatment on GD 15 or 17, but not on GD 11 or 13 (Nishimura et al, 2013).…”

Section: Discussionmentioning

confidence: 71%

“…The peak period of cell proliferation is different among each constitutive cell of the placenta, and each part/zone of the placenta has a specific sensitive period for toxicants. To support this, we previously reported that anti-cancer drug induced placental lesions were different among the treatment timings in 6-mercaptopurine (Furukawa et al, 2011a) and cisplatin (Furukawa et al, 2013b).…”

Section: Introductionmentioning

confidence: 68%