2,3,7,8-Tetrachlorodibenzo-p-dioxin induces a proteomic pattern that defines cleft palate formation in mice

Objective ntify the differential protein pattern in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced cleft palates using a proteomic approach. s tation day (GD) 12, TCDD (64 g/kg; n = 30) or corn oil control (n = 30) was given to time-pregnant C57BL/6J mice by gavage. The anatomical, histological, proteomic changes in the palates of the fetal mice were studied on GD18. Total protein was extracted from the palate tissue and examined by 2-dimensional gel electrophoresis (2-DE). Spots differentially expressed between the two groups were selected for analysis by matrix assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS). The proteins were identified by data searching in the Mascot database. s D group, the incidence of cleft palate was 100%. Ten differential protein spots with the largest fold change were selected for further identification by mass spectrometry, 7 showed significantly higher volumes and 3 showed significantly lower volumes in TCDD palates than the control palates (all p < 0.05). Peroxiredoxin-1 were robustly up-regulated in the cleft palate group, as well proteins linked to energy metabolism, cell migration, and apoptosis. sions redoxin-1 protein may be associated with cleft palate in mice induced by TCDD. The embryo mouse palate tissues energy metabolism cells migration/apoptosis related proteins have the disorder.