细胞凋亡
线粒体
基因敲除
PARP1
细胞生物学
致癌物
化学
丙烯酰胺
癌症研究
毒性
生物
基因
生物化学
聚ADP核糖聚合酶
聚合酶
共聚物
有机化学
聚合物
作者
Lujia Zhang,Dong Li,Liuqing Yang,Yinghua Luo,Fang Chen
出处
期刊:Food Chemistry
[Elsevier]
日期:2021-08-10
卷期号:368: 130816-130816
被引量:18
标识
DOI:10.1016/j.foodchem.2021.130816
摘要
Acrylamide (AA), a potential carcinogen, is commonly formed in foods rich in carbohydrates at high heat. It is known that AA-induced mitochondrial dysfunction is responsible for its toxicity. Previously we found AA exposure increased miR-27a-5p expression in livers of SD rats. Here, the regulation mechanism of miR-27a-5p in mitochondrial dysfunction was investigated in rat liver cell lines (IAR20) and SD rats. The results showed that the overexpressed miR-27a-5p contributes to modulating mitochondrial dysfunction and Btf3 is identified as its target gene. The knockdown of Btf3 increases the cleaved PARP1 level and the phosphorylation of ATM and p53, which results in mitochondria-dependent apoptosis. Therefore, the miR-27a-5p-Btf3-ATM-p53 axis might play a vital role in the promotion of AA-induced cell apoptosis through disrupting mitochondrial structure and function. This would provide a potential target for the assessment and intervention of AA toxicity.
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