Histopathological Effect of Ketoconazole on Rat Placenta

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

doi:10.1292/jvms.70.1179

Cited by 22 publications

(21 citation statements)

References 23 publications

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“…The current study shows that CrVI induces toxic lesions in the LZ and BZ of the placenta. Several EDCs have been reported to cause lesions in the placenta such as ketoconazole (hypertrophy) [68], cadmium and lead (necrosis) [69], 6-mercaptopurine (cystic degeneration of glycogen cells) [70], and busulfan (apoptosis of trophoblasts and endothelial cells) [22] [71]. CrVI increased hypertrophy of the BZ and induced hem- orrhagic lesions in BZ above the decidual bed (Fig.…”

Section: Discussionmentioning

confidence: 99%

Chromium VI − Induced developmental toxicity of placenta is mediated through spatiotemporal dysregulation of cell survival and apoptotic proteins

Banu

Stanley

Sivakumar

et al. 2017

Reproductive Toxicology

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Environmental contamination with hexavalent chromium (CrVI) is a growing problem both in the U.S and developing countries. CrVI is a heavy-metal endocrine disruptor; women working in Cr industries exhibit an increased incidence of premature abortion and infertility. The current study was designed to understand the mechanism of CrVI toxicity on placental cell survival/death pathways. Pregnant mothers were treated with or without CrVI (50 ppm K2Cr2O7) through drinking water from gestational day (GD) 9.5–14.5, and placentas were analyzed on GD 18.5. Results indicated that CrVI increased apoptosis of trophoblasts, vascular endothelium of the metrial glands and yolk sac epithelium through caspase-3 and p53-dependent pathways. CrVI increased apoptosis in labyrinth and basal zones in a caspase-3-independent manner via AIF, and through an ATM-p53-NOXA-PUMA-p27 network. CrVI downregulated cell survival proteins Bcl-2, Bcl-XL and XIAP in the placenta. CrVI disrupts placental histoarchitecture and increases cell death by spatiotemporal modulation of apoptotic signaling.

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Section: Discussionmentioning

confidence: 99%

Chromium VI − Induced developmental toxicity of placenta is mediated through spatiotemporal dysregulation of cell survival and apoptotic proteins

Banu

Stanley

Sivakumar

et al. 2017

Reproductive Toxicology

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“…Especially, basal zone is the site of production of steroids and peptide hormones that play an important role for maintaining pregnancy (Davies and Glasser, ). In the normal placental development, the basal zone is composed of small cytotrophoblastic elements on GD 12 (Furukawa et al, ). The cytotrophoblastic elements differentiate into glycogen cells after GD 14, and the size of the basal zone consequently becomes smaller in accordance with development of placenta after GD 15, and then finally glycogen cells will disappear until GD 21 (Furukawa et al, ; Furukawa et al, ).…”

Section: Discussionmentioning

confidence: 99%

Effect of PPARβ/δ Agonist on the Placentation and Embryo‐Fetal Development in Rats

Nishimura¹,

Nakano²,

Chowdhury

et al. 2013

Birth Defects Research Pt B

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“…Thirdly, placental hypertrophy is induced as a hormone imbalance reaction, such as estrogen deficiency 43,44 and ovariectomy with estrogen and progesterone treatment 45 . Pathological sequential changes of ketoconazoleinduced placental hypertrophy were recently investigated in rats 46 , as described below.…”

Section: Histopathology Of the Placenta In The Ratmentioning

confidence: 99%

Toxicological Pathology in the Rat Placenta

et al. 2011

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The placenta grows rapidly for a short period with high blood flow during pregnancy and has multifaceted functions, such as its barrier function, nutritional transport, drug metabolizing activity and endocrine action. Consequently, the placenta is a highly susceptible target organ for drug- or chemical-induced adverse effects, and many placenta-toxic agents have been reported. However, histopathological examination of the placenta is not generally performed, and the placental toxicity index is only the placental weight change in rat reproductive toxicity studies. The placental cells originate from the trophectoderm of the embryo and the endometrium of the dam, proliferate and differentiate into a variety of tissues with interaction each other according to the development sequence, resulting in formation of a placenta. Therefore, drug- or chemical-induced placental lesions show various histopathological features depending on the toxicants and the exposure period, and the pathogenesis of placental toxicity is complicated. Placental weight assessment appears not to be enough to evaluate placental toxicity, and reproductive toxicity studies should pay more attention to histopathological evaluation of placental tissue. The detailed histopathological approaches to investigation of the pathogenesis of placental toxicity are considered to provide an important tool for understanding the mechanism of teratogenicity and developmental toxicity with embryo lethality, and could benefit reproductive toxicity studies.

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Histopathological Effect of Ketoconazole on Rat Placenta

Cited by 22 publications

References 23 publications

Chromium VI − Induced developmental toxicity of placenta is mediated through spatiotemporal dysregulation of cell survival and apoptotic proteins

Chromium VI − Induced developmental toxicity of placenta is mediated through spatiotemporal dysregulation of cell survival and apoptotic proteins

Effect of PPARβ/δ Agonist on the Placentation and Embryo‐Fetal Development in Rats

Toxicological Pathology in the Rat Placenta

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