de Conti Aline, Kobets Tetyana, Tryndyak Volodymyr, Burnett Sarah D, Han Tao, Fuscoe James C, Beland Frederick A, Doerge Daniel R, Pogribny Igor P
*Division of Biochemical Toxicology and Division of Systems Biology, National Center for Toxicological Research, Jefferson, Arkansas 72079.
*Division of Biochemical Toxicology and Division of Systems Biology, National Center for Toxicological Research, Jefferson, Arkansas 72079
Toxicol Sci. 2015 Apr;144(2):217-26. doi: 10.1093/toxsci/kfu313. Epub 2014 Dec 23.
Furan is a heterocyclic organic compound produced in the chemical manufacturing industry and also found in a broad range of food products, including infant formulas and baby foods. Previous reports have indicated that the adverse biological effects of furan, including its liver tumorigenicity, may be associated with epigenetic abnormalities. In the present study, we investigated the persistence of epigenetic alterations in rat liver. Male F344 rats were treated by gavage 5 days per week with 8 mg furan/kg body weight (bw)/day for 90 days. After the last treatment, rats were divided randomly into 4 groups; 1 group of rats was sacrificed 24 h after the last treatment, whereas other groups were maintained without further furan treatment for an additional 90, 180, or 360 days. Treatment with furan for 90 days resulted in alterations in histone lysine methylation and acetylation, induction of base-excision DNA repair genes, suggesting oxidative damage to DNA, and changes in the gene expression in the livers. A majority of these furan-induced molecular changes was transient and disappeared after the cessation of furan treatment. In contrast, histone H3 lysine 9 and H3 lysine 56 showed a sustained and time-depended decrease in acetylation, which was associated with formation of heterochromatin and altered gene expression. These results indicate that furan-induced adverse effects may be mechanistically related to sustained changes in histone lysine acetylation that compromise the ability of cells to maintain and control properly the expression of genetic information.
呋喃是一种在化学制造业中生产的杂环有机化合物,在包括婴儿配方奶粉和婴儿食品在内的多种食品中也有发现。先前的报告表明,呋喃的不良生物学效应,包括其肝脏致瘤性,可能与表观遗传异常有关。在本研究中,我们调查了大鼠肝脏中表观遗传改变的持续性。雄性F344大鼠每周5天经口灌胃给予8毫克呋喃/千克体重/天,持续90天。在最后一次治疗后,大鼠被随机分为4组;一组大鼠在最后一次治疗后24小时处死,而其他组在不进行进一步呋喃治疗的情况下再维持90、180或360天。用呋喃治疗90天导致组蛋白赖氨酸甲基化和乙酰化改变,碱基切除DNA修复基因的诱导,提示DNA氧化损伤,以及肝脏中基因表达的变化。这些呋喃诱导的分子变化大多是短暂的,在呋喃治疗停止后消失。相反,组蛋白H3赖氨酸9和H3赖氨酸56的乙酰化呈现持续且随时间依赖的下降,这与异染色质的形成和基因表达改变有关。这些结果表明,呋喃诱导的不良反应可能在机制上与组蛋白赖氨酸乙酰化的持续变化有关,这种变化损害了细胞维持和正确控制遗传信息表达的能力。