Objective: To explore the role of histone H3 acetylation in cleft palate induced by 2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD) in C57BL/6J mice, and its mechanism.
Methods: On gestation day 10 (GD10), 36 pregnant mice were randomly divided into two groups as the treated group(n = 18) and the control group( n = 18). The mice in the treated group received intragastric administration with TCDD 28 μg/kg, while the mice in the control group received equivalent corn oil. The pregnant mice were sacrificed on GD13. 5, GD14. 5 and GD15. 5, collecting fetal palates to determine the activities of histone acetyltransferases (HATs) by Colorimetric and the expression level of acetylated histone H3 (Acetylated histone H3, Ac-H3) by Western-blot.
Results: The activity of HATs was 0.409 7 ± 0.0147, 0.522 3 ± 0.017 1 and 0.643 5 ± 0.013 9 in control group on GD13.5, GD14.5 and GD15.5; 0.865 0 ± 0.0129, 0.719 1 ± 0.017 8 and 0.551 2 ± 0.016 8 in TCDD group. The activity of HATs in TCDD group was higher than that in control group on GD13. 5, GD14. 5, showing significantly difference between the two groups (t = - 56. 932, t = - 19. 516, P < 0.01); however, the activity of HATs in TCDD group was significantly lower than that in control group on GD15. 5 (t = 10. 382, P < 0.01). The expression level of Ac-H3 was 0.745 0 ± 0.113 5, 1.055 9 ± 0.249 4 and 1.795 5 ± 0.081 9 in control group on GD13. 5, GD14. 5 and GD15. 5; while 1.4490 ± 0. 1460, 1. 641 8 ± 0.099 7 and 1. 512 1 ± 0. 150 2 in TCDD group. The expression of Ac-H3 in TCDD group was higher than that in control group on GD13. 5, GD14. 5, showing significantly difference( t = -6. 593, -3. 779, P <0. 01, P <0.05) ; However, the expression of Ac-H3 in TCDD group was statistically lower than that in control group (t = 2. 870, P <0. 05).
Conclusion: The acetylation of histone H3 was involved in the cleft palate of C57BL/6J mice induced by TCDD, which may be one of the mechanisms in TCDD-induced cleft palate.