Abstract：Herein, we explored in detail the effects of TCS acute exposure at sublethal dosage on zebrafish embryonic development and lipid metabolism. TCS at 200µg/L significantly delayed the 72-hpf embryonic hatching with a decreased hatching percentage of 13.24% and an increased deformity rate of >80%. In the TCS-exposure group (4-120hpf), the main larval malformations were reflected in energy stasis、yolk cyst、dyssorption and swim sac closure, pericardial cyst, spinal curvature and so on. Using metascape online database, the target molecules of TCS, and the underlying GO (gene ontology) function clustering and KEGG (kyoto encyclopedia of genes and genomes) metabolic pathways were analyzed systemically. Most of the target genes were involved in various biological functions, such as carboxylate metabolism, steroid hormone receptor activity, lipid binding, lipid catabolic process, lipid homeostasis and regulation of lipid localization based on the roles in molecular function, biological process and cellular component. Three KEGG signaling pathways were found to be directly or indirectly concerned with lipid metabolism. The changes in biochemical indicators of 120-hpf larvae demonstrated that TCS exposure resulted in the significant increases of the total cholesterol (T-CHO) and triglycerides (TG) levels. By oil red O staining, we observed the prominent accumulation of lipid droplets in larval liver, egg yolk and blood vessels after exposure to TCS, especially in the liver and yolk. Lipid metabolism and energy supply are closely related to motor behavior. Using Noldus behavior analyzer, after TCS exposure, zebrafish voluntary motor activity was obviously inhibited, and the sensitivity to acoustic-optic stimulation was significantly decreased. The aforementioned toxic effects could be alleviated upon addition of 100µg/L sodium deoxycholate. These findings provide compelling evidence that low-dose TCS exposure induced zebrafish lipid-metabolism disorders by affecting hepatobiliary circulation and causing energy-supply obstacle.
王杨, 吴国辉, 钱秋慧, 赵晨曦, 闫瑾, 王学东, 王慧利. 三氯生对斑马鱼发育和脂质代谢的影响[J]. 中国环境科学, 2022, 42(3): 1394-1400.
WANG Yang, WU Guo-hui, QIAN Qiu-hui, ZHAO Chen-xi, YAN Jin, WANG Xue-dong, WANG Hui-li. Effects of triclosan environmental exposure on zebrafish development and lipid metabolism. CHINA ENVIRONMENTAL SCIENCECE, 2022, 42(3): 1394-1400.
Sifakis S, Androutsopoulos V P, Tsatsakis A M, et al. Human exposure to endocrine disrupting chemicals:effects on the male and female reproductive systems[J]. Environmental Toxicology& Pharmacology, 2017,51(4):56-70.
[2]
陈敏.三氯生与三氯卡班的生态毒性研究进展[J].广东化工, 2021,48(1):62-63. Chen M. Research progress on the ecotoxicity of triclosan and triclocarban[J]. Guangdong Chemical Industry, 2021,48(1):62-63.
[3]
唐宁,欧阳凤秀.生命早期环境内分泌干扰物暴露与儿童过敏性疾病关系的研究进展[J].上海交通大学学报:医学版, 2019,39(9):7. Tang N, Ouyang F X. Research progress on the relationship between exposure to environmental endocrine disruptors and childhood allergic diseases in early life[J]. Journal of Shanghai Jiaotong University (Medical Edition), 2019,39(9):7.
[4]
魏玉琴,沈春花.三氯生在水环境中的残留风险与去除研究进展[J].环境科学与技术, 2017,40(8):96-101. Wei Y Q, Shen C H. Research progress on residual risk and removal of triclosan in aquatic environment[J]. Environmental Science and Technology, 2017,40(8):96-101.
[5]
Nishi I, Kawakami T, Onodera S. Monitoring of triclosan in the surface water of the tone canal, Japan[J]. Bulletin of Environmental Contamination& Toxicology, 2008, 80(2):163-166.
[6]
Kai B. Fate of triclosan and triclosan-methyl in sewage treatment plants and surface waters[J]. Archives of Environmental Contamination& Toxicology, 2005,49(1):9-17.
[7]
Young T A, Heidler J, Matos-Perez C R, et al. Ab initio and in situ comparison of caffeine, triclosan, and triclocarban as indicators of sewage-derived microbes in surface waters[J]. Environmental Science& Technology, 2008,42(9):3335.
[8]
高海萍,周雪飞,张亚雷,等.三氯生对水生生物的毒性效应研究进展[J].环境化学, 2012,(8):1145-1150. Gao H P, Zhou X F, Zhang Y L, et al. Research progress on the toxic effects of triclosan on aquatic organisms[J]. Environmental Chemistry, 2012,(8):1145-1150.
[9]
孙冰,许慧慧,黄超,等.环境毒理学研究的重要模式生物——斑马鱼[J].环境与职业医学, 2016,33(6):610-614. Sun B, Xu H Hi, Huang C, et al. An important model organism for environmental toxicology research-zebrafish[J]. Environmental and Occupational Medicine, 2016, 33(006):610-614.
[10]
Xia M, Wang X, Xu J, et al. Tris (1-chloro-2-propyl) phosphate exposure to zebrafish causes neurodevelopmental toxicity and abnormal locomotor behavior[J]. Sci. Total Environ., 2021,758:143694.
[11]
Zhang Y, Mi L, Liu J, et al. Combined toxicity of triclosan, 2,4-dichlorophenol and 2,4,6-trichlorophenol to zebrafish (Danio rerio)[J]. Environmental Toxicology& Pharmacology, 2018,57(1):9-18.
[12]
王菲儿.典型重金属和阻燃剂类环境污染物对斑马鱼胚胎的发育毒性研究[D].武汉:华中农业大学, 2018. Wang F E. Developmental toxicity of typical heavy metals and flame retardant environmental pollutants to zebrafish embryos[D]. Wuhan:Huazhong Agricultural University, 2018.
[13]
施文海,陈化龙,贾中慧,等.脂质代谢与动脉粥样硬化[J].陕西新医药, 1974,7(1):47-55. Shi W H, Chen H L, Jia Z H, et al. Lipid metabolism and atherosclerosis[J]. Shaanxi New Medicine, 1974,7(1):47-55.
[14]
Carrillo-González D F, Hernández-Herrera D Y, Maldonado-Estrada J G. The role of L-carnitine in bovine embryo metabolism. A review of the effect of supplementation with a metabolic modulator on in vitro embryo production[J]. Anim. Biotechnol., 2021,21(6):1-11.
[15]
Zheng W, Wang Z, Collins J E, et al. Comparative transcriptome analyses indicate molecular homology of zebrafish swimbladder and mammalian lung[J]. PLoS One, 2011,6(8):e24019.
[16]
王亚梅.斑马鱼卵黄蛋白原受体基因的鉴定、表达和功能分析[D].兰州:西北师范大学, 2020. Wang Y M. Identification, expression and function analysis of zebrafish vitellogen receptor gene[D]. Lanzhou:Northwest Normal University, 2020.
[17]
Fraher D, Sanigorski A, Mellett N, et al. Zebrafish embryonic lipidomic analysis reveals that the yolk cell is metabolically active in processing lipid-science direct[J]. Cell Reports, 2016,14(6):1317-1329.
[18]
贺茜,沙金燕,崔英,等.过氧化物酶体研究进展[J].临床与病理杂志, 2001,21(5):416-418. He Q, Sha J Y, Cui Y, et al. Research progress of peroxisomes[J]. Journal of Clinical and Pathology, 2001,21(5):416-418.
[19]
Sant K E, Venezia O L, Sinno P P, et al. Perfluorobutanesulfonic acid disrupts pancreatic organogenesis and regulation of lipid metabolism in the zebrafish, danio rerio[J]. Toxicol. Sci., 2019,167(1):258-268.
[20]
任秀花,闫爱华,任知春.显示肝,肾上腺脂类油红O方法探讨[J].四川解剖学杂志, 2001,2:42-42. Ren X H, Yan A H, Ren Z H. Discussion on the method of displaying liver and adrenal lipid oil red O[J]. Sichuan Journal of Anatomy, 2001, 2:42-42.
[21]
邓军,杨丽华,周炳升.六溴环十二烷(HBCD)对斑马鱼发育早期能量代谢及软骨、肌肉和鱼鳍发育的影响[J].生态毒理学报, 2013,8(5):9. Deng J, Yang L H, Zhou B S. The effects of hexabromocyclododecane (HBCD) on energy metabolism and development of cartilage, muscle and fins during early development of zebrafish[J]. Journal of Ecotoxicology, 2013,8(5):9.
[22]
张肖霄.脱氧胆酸钠(SD)在脂肪细胞溶脂和微血管内皮细胞(MECs)凋亡方面的研究[D].上海:第二军医大学, 2017. Zhang X X. Research on the effects of sodium deoxycholate (SD) on lipolysis of adipocytes and apoptosis of microvascular endothelial cells (MECs)[D]. Shanghai:Second Military Medical University, 2017.
[23]
Kolodney M S, Rotunda A M. Methods and related compositions for reduction of fat and skin tightening[Z]. US, 2014/0004206A1.
[24]
Santiago-Vázquez M, Michelen-Gómez E A, Carrasquillo-Bonilla D, et al. Intralesional deoxycholic acid:A potential therapeutic alternative for the treatment of lipomas arising in the face[Z]. JAAD Case Rep., 2021,13(5):112-114.
