THE PRELIMINARY STUDY ON THE FACTORS CAUSING OROFACIAL CLEFT ABNORMALITIES IN SWISS-WEBSTER MICE

• Main Author: Nurul Jihadah, Mutiah
• Format: Final Project
• Language: Indonesia
• Subjects: Ilmu hayati ; Biologi
• Online Access: https://digilib.itb.ac.id/gdl/view/47345
• Institution: Institut Teknologi Bandung

The etiology of congenital malformations such as the incidence of Orofacial Cleft (OC), involves a combination of endogenous factors and environmental factors. In the incidence of OC, one of the influential environmental factors is nicotine, the main teratogen compound in cigarettes. Nicotine can interfere with orofacial development by interacting with various endogenous factors, including the ARHGAP29 gene which regulates the development of the palate. However, the interaction between environmental factors and each endogenous factor is not fully known. This study aims to confirm the possibility of nicotine interactions with endogenous factors in the critical period of OC incidence. To determine the critical period of OC incidence, three groups of Swiss-Webster mice were exposed to a dose of 1.67 mg / gBB of nicotine by intraperitoneal injection in three periods. The treatment I represent the period of facial formation (E5-7); treatment II, orofacial preparation phase (E9-12); and treatment 3, the period of palate formation (E12-14). E-18 embryonic palate tissue was isolated and the significance of nicotine influence was tested by ANOVA and Post-HocTukey Test. To ascertain the possibility of nicotine interaction with the genes, multiple alignments of the exon 12 palate DNA ARHGAP29 sequences of the critical period of OC was carried out. As many as 1.93% of 21 treatment I embryos, 10.4% of 26 treatment II embryos, and 21.2% of 43 treatment III embryos experienced OC. Statistics show that nicotine causes OC significantly (p = 0.002) and the critical period of OC is the period of preparation of the palate. Multiple alignments show deletion, addition, and DNA base substitution. Nicotine causes placental vasoconstriction resulting in hypoxia and a decrease in folate levels which play a role in DNA synthesis and repair. The risk of damage to the ARHGAP29 gene increases and also increases the risk of OC due to the failure of elevation and unification of the palate plate. It was concluded that nicotine was confirmed to interact with genes in the critical period of OC incidence.