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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/108398

    Title: Molecular mechanisms of discrotophos-induced toxicity in HepG2 cells: The role of CSA in oxidative stress
    Authors: Chen, 許游章;Hseu You-Cheng;Tung-Wei Hsu;Tung-Wei Hsu;Heng-Dao Lin;Heng-Dao Lin;Chin Hui Che;Chin Hui Chen;Ssu Ching Ch;Ssu Ching
    Contributors: 保健營養生技學系
    Date: 2017-02
    Issue Date: 2017-12-08 14:10:34 (UTC+8)
    Abstract: Dicrotophos (Dic), an insecticide and acaricide, is used against a variety of sucking, boring and chewing pests. It was proven that Dic induced oxidative DNA damage in HepG2 cells. However, the molecular mechanisms of this compound were still unclear. First of all, the cytotoxicity and oxidative DNA damage were confirmed. Next, using RNA-seq for detecting differential expressed genes (DEGs) in cells treated with 50 μM Dic for 24 h, we showed that the dysregulation of these genes, irrespective of up (1298 genes) or down (2125 genes) regulation, could be attributed to some diverse pathways/metabolisms using KEGG analysis, particularly in DNA damage responses (DDRs) such as oxidative phosphorylation, nucleotide excision repair and cell cycle arrest. Validation of some randomly selected DDR genes confirmed RNA-seq results. We further demonstrated that Dic induced ROS overproduction, the loss of mitochondrial depolarization and cell cycle arrest in the G0/G1 phase. In addition, we also definitely clarified the role of CSA, a nucleotide excision repair enzymes in Dic-treated cells. Collectively, our results showed that various mechanisms of Dic-induced toxicity in HepG2 cells including downregulation of some genes related to nucleotide excision repair including CSA and increased oxidative stress.
    Appears in Collections:[食品營養與保健生技學系] 期刊論文

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