Ding Xiaoqian, Jiang Shan, Li Xia, Wang Yu, Zheng Zhilong, Qin Yanjie
Key Laboratory of Marine Bio-resource Restoration and Habitat Reparation in Liaoning Province, Dalian Ocean University, Dalian 116023, China; Key Laboratory of Mariculture and Stock Enhancement in North China's Sea, Ministry of Agriculture and Rural Affairs, Dalian Ocean University, Dalian 116023, China.
Key Laboratory of Marine Bio-resource Restoration and Habitat Reparation in Liaoning Province, Dalian Ocean University, Dalian 116023, China; Key Laboratory of Mariculture and Stock Enhancement in North China's Sea, Ministry of Agriculture and Rural Affairs, Dalian Ocean University, Dalian 116023, China.
Comp Biochem Physiol C Toxicol Pharmacol. 2022 Sep;259:109398. doi: 10.1016/j.cbpc.2022.109398. Epub 2022 Jun 24.
The cytotoxic effect and cell death were studied in loach fin cells in vitro after enrofloxacin (ENR) exposure. The semi-lethal concentration of ENR for loach cells was calculated as 1296.2 ± 3.11 mol/L (about 512.5 mg/L). Loss of cell viability, increase in vacuoles, disappearance of microvilli, and apoptotic bodies were evident in cells exposed to 400, 800, and 1200 μmol/L ENR. Besides, dose-dependent inhibitory effects on SOD, CAT, Na-K-ATPase, and Ca-ATPase activities were also observed in loach cells exposed to ENR. Quantitative gene expression results showed that ENR induced caspase-3- and caspase-8-mediated apoptosis as well as caspase-activated DNase in loach cells. The findings also indicated a role of JNK pathway in ENR-induced apoptosis in loach cells. Transcriptome sequencing results showed 10,016 differentially expressed genes in ENR vs. control groups, which were all enriched in "Molecular Function" process in GO term. Furthermore, 6763 genes were enriched in 291 KEEG pathways, with most of them belonging to immune and material metabolic pathways. The large number of transcriptome data and pathways determined in this study provide a database foundation for the toxicity analysis of ENR in loach cells, which must be thoroughly examined to further investigate the cytotoxic mechanism of antibiotics in fish cells.
研究了恩诺沙星(ENR)暴露后对泥鳅鳍细胞的细胞毒性作用和细胞死亡情况。计算得出ENR对泥鳅细胞的半致死浓度为1296.2±3.11μmol/L(约512.5mg/L)。在暴露于400、800和1200μmol/L ENR的细胞中,细胞活力丧失、液泡增加、微绒毛消失以及凋亡小体明显可见。此外,在暴露于ENR的泥鳅细胞中还观察到对超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、钠钾ATP酶和钙ATP酶活性的剂量依赖性抑制作用。定量基因表达结果表明,ENR在泥鳅细胞中诱导了半胱天冬酶-3和半胱天冬酶-8介导的凋亡以及半胱天冬酶激活的脱氧核糖核酸酶。研究结果还表明JNK途径在ENR诱导的泥鳅细胞凋亡中起作用。转录组测序结果显示,ENR组与对照组之间有10016个差异表达基因,这些基因在基因本体(GO)术语的“分子功能”过程中均有富集。此外,6763个基因富集在291条京都基因与基因组百科全书(KEGG)途径中,其中大多数属于免疫和物质代谢途径。本研究确定的大量转录组数据和途径为ENR在泥鳅细胞中的毒性分析提供了数据库基础,必须对其进行深入研究,以进一步探究抗生素在鱼类细胞中的细胞毒性机制。