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氯化镉(CdCl2)是一种常见的重金属化合物，其高毒性和高生物累积性对水生生物和生态系统构成了严重的威胁.为系统探讨CdCl2对鱼类的生态毒理效应，将受精后2 h(2 hours post fertilization, 2 hpf)的斑马鱼胚胎暴露于0、0.1、1.0 mg/L CdCl2中，培养至120 hpf,结合形态学、分子生物学及脂质组学等多种方法，评估了CdCl2对斑马鱼胚胎/仔鱼发育和脂代谢的影响.结果表明，0.1 mg/L CdCl2暴露轻度干扰斑马鱼胚胎生长发育和脂代谢，而1 mg/L CdCl2暴露显著抑制了斑马鱼胚胎的生长发育，同时严重干扰了脂代谢平衡，造成仔鱼体内脂质异常累积，溶血磷脂酰胆碱(lysophosphatidylcholine, LPC)、磷脂酰肌醇(phosphatidylinositol, PI)和磷脂酰甘油(phosphatidylglycerol, PG)等脂质的合成显著增加.qPCR结果进一步证实，CdCl2暴露显著上调了参与LPC、PI和PG合成与代谢相关基因的表达.综上所述，CdCl2通过干扰斑马鱼早期发育阶段磷脂类脂质合成和代谢相关基因的表达，引起仔鱼脂代谢异常.
Abstract：Cadmium chloride(CdCl2) is a common heavy metal compound, and its high toxicity and strong bioaccumulation potential pose serious threats to aquatic organisms and ecosystems. To systematically investigate the ecotoxicological effects of CdCl2 in fish, zebrafish embryos at 2 hours post-fertilization(hpf) were exposed to 0,0.1, and 1.0 mg/L CdCl2 until 120 hpf. Using multiple approaches including morphological observation, molecular biology, and lipidomics, the impacts of CdCl2 on zebrafish embryonic/larval development and lipid metabolism were examined. The results showed that exposure to 0.1 mg/L CdCl2 mildly interfered with embryonic growth and lipid metabolism, while 1 mg/L CdCl2 significantly inhibited embryonic development and severely disrupted lipid homeostasis, leading to abnormal lipid accumulation in larvae. The synthesis of lipids such as lysophosphatidylcholine(LPC), phosphatidylinositol(PI), and phosphatidylglycerol(PG) was significantly increased. qPCR results indicated that CdCl2 exposure markedly up-regulated the expression of genes involved in the synthesis and metabolism of phospholipids including LPC, PI, and PG. In summary, CdCl2 induces abnormal lipid metabolism in zebrafish larvae by interfering with the expression of genes related to phospholipid synthesis and metabolism during early developmental stages.
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基本信息:
DOI：10.19926/j.cnki.issn.1674-232X.2025.02.171
中图分类号:X171.5
引用信息:
[1]于梓辰,朱莉亚,刘春生.CdCl_2对斑马鱼早期发育和脂代谢的影响[J].杭州师范大学学报(自然科学版),2026,25(01):35-46.DOI:10.19926/j.cnki.issn.1674-232X.2025.02.171.
基金信息:
国家重点研发计划项目(2022YFA0806602,2024YFC3712004)
2026-01-30
2026-01-30