Role of glutathione homeostasis on 2,3,7,8-tetrachlorodibenzo-p-dioxin induced cleft palates in mice

doi:10.19438/j.cjoms.2018.03.005

Abstract

Abstract: PURPOSE: To elucidate the impact of glutathione homeostasis in organogenesis stage embryos on 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD) -induced cleft palate in fetal mice. METHODS: Pregnant C57BL/6J mice were randomly allocated to blank control group, TCDD exposed group, L-buthionine-sulfoximine (BSO)exposed group and BSO+TCDD exposed group. Each GD10 animal was weighted and treated with 0.1mL normal saline (for blank control group and TCDD exposed group) or 600 mg/kg BSO (for BSO group and TCDD+BSO group). After 4 hours, TCDD was orally administrated to subjects in both TCDD group and TCDD+BSO group, but corn oil was used as vehicle control for control group and BSO group. Fetal mice palates were imaged using light microscopy on GD13.5, GD14, GD14.25, GD14.5, GD14.75 and GD15; scanning electronmicroscopy was used on GD13.5, GD14.5, and GD15.5, and cleft palate were recorded on GD17.5. Three GD14.5 palate sections from each group were examined by immunohistochemistry.SPSS13.0 software package was used for statistical analysis. RESULTS: TCDD successfully induced cleft palate. BSO can increase 5% of cleft palate. In the TCDD treated group, palatal shelves elevated 1 day later than in the control group. In the TCDD and BSO group, 0.25 day later than the TCDD group, all palates had elevated by GD 15.0. After elevation, the shelves contacted each other and fused. Under a high magnification (×2500), compared to the control group (GD14.5), TCDD group (GD 15), no filaments were observed and cell shapes were flat with unclear boundaries. The group treated with TCDD and BSO had no significant difference from the TCDD group in the end, but had temporal variations. The TCDD exposed group had a higher expression of CYP1A1 on the frontal epithelia than the control group. CONCLUSIONS: Breaking the balance of glutathione may decline the formation of filopodia and MEE motility due to reducing the consumption of reactive oxygen species, filopodia and MEE movement. This may result in accelerating the ultrastructure change of the palatal surface to a normal state, leading to a higher rate of cleft palate in TCDD-treated fetal mice.

Key words: TCDD, Cleft palate, GSH, BSO, CYP1A1

CLC Number:

R782.2.2

ZHAO Tong-chao, BIAN Yuan-yuan, ZHANG Tian-qi, ZHANG Dong-sheng, MA Li.. Role of glutathione homeostasis on 2,3,7,8-tetrachlorodibenzo-p-dioxin induced cleft palates in mice[J]. China Journal of Oral and Maxillofacial Surgery, 2018, 16(3): 215-221.

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