Abstract
4-Hexylresorcinol (4HR) has been used as a food additive, however, it has been recently demonstrated as a Class I histone deacetylase inhibitor (HDACi). Unlike other HDACi, 4HR can be taken through foods. Unfortunately, some HDACi have an influence on craniofacial growth, therefore, the purpose of this study was to evaluate the effects of 4HR on craniofacial growth. Saos-2 cells (osteoblast-like cells) were used for the evaluation of HDACi and its associated activities after 4HR administration. For the evaluation of craniofacial growth, 12.8 mg/kg of 4HR was administered weekly to 4 week old rats (male: 10, female: 10) for 12 weeks. Ten rats were used for untreated control (males: 5, females: 5). Body weight was recorded every week. Serum and head samples were collected at 12 weeks after initial administration. Craniofacial growth was evaluated by micro-computerized tomography. Serum was used for ELISA (testosterone and estrogen) and immunoprecipitation high-performance liquid chromatography (IP-HPLC). The administration of 4HR (1–100 μM) showed significant HDACi activity (p < 0.05). Body weight was significantly different in male rats (p < 0.05), and mandibular size was significantly smaller in 4HR-treated male rats with reduced testosterone levels. However, the mandibular size was significantly higher in 4HR treated female rats with increased growth hormone levels. In conclusion, 4HR had HDACi activity in Saos-2 cells. The administration of 4HR on growing rats showed different responses in body weight and mandibular size between sexes.
Highlights
Growth and development are largely controlled by genetic regulation
HDAC8 knockout mice resulted in impairment of skull development [10]. These results indicate that Histone deacetylases (HDACs) extensively and intimately affect skeletal development and bone maintenance
The activity of HDAC was decreased by the administration of 4HR (1–100 μM; Figure 1A)
Summary
Twins who share identical genomes develop remarkable differences in their genomic distribution over time [1]. This means that both genetic and environmental regulations affect gene expression and its activity, and epigenetics could be a major explanation for this phenomenon. Epigenetics means structural chromatin changes that do not involve alterations in the DNA sequence. This includes chromatin remodeling, DNA methylation, histone modification, and micro-RNAs. Of the mechanisms of epigenetic regulations, histone protein modification is the mechanism that induces gene expression and suppression by post-translational modification via acetylation, methylation, and phosphorylation in the histone N-terminal region of the nucleosome [2]
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