超氧化物歧化酶
转录组
丙二醛
氧化应激
生物化学
谷胱甘肽
碱性磷酸酶
过氧化氢酶
抗氧化剂
生物
谷胱甘肽过氧化物酶
分子生物学
化学
基因
基因表达
酶
作者
Xue Jiao,Zheng yao Guo,Jia Sun,Cheng Bi,Qian Ai-dong,Yuehong Li
标识
DOI:10.1016/j.aquatox.2023.106709
摘要
Perfluorocaproic acid (PFHxA) has received much attention as an emerging pollutant linked to neurological problems in humans and fish. However, the potential mechanism remains unknown. In this study, the pathological damage to tissue sections demonstrated that perfluorocaproic acid caused brain tissue damage, and the increased antioxidant index malondialdehyde (MDA) and decrease in superoxide Dismutase (SOD), acid phosphatase (ACP), alkaline phosphatase (AKP), glutathione peroxidase (GSH-Px), Catalase (CAT), and Lysozyme (LZM) that perfluorocaproic acid activated antioxidant stress and caused brain damage. Transcriptome sequencing discovered 1,532 divergent genes, 931 upregulated, and 601 down-regulated. Furthermore, according to GO enrichment analysis, the differently expressed genes were shown to be involved in biological processes, cellular components, and molecular functions. The MAPK, calcium, and Neuroactive ligand-receptor interaction were considerably enriched in the KEGG enrichment analysis. We then analyzed qRT-PCR and chose ten essential differentially expressed genes for validation. The qRT-PCR results followed the same pattern as the RNA-Seq results. In conclusion, our study shows that perfluorocaproic acid exposure causes oxidative stress in the brain. It establishes a theoretical foundation for future research into genes linked to perfluorocaproic acid toxicity.
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