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Parental transfer of titanium dioxide nanoparticle aggravated MCLR- induced developmental toxicity in zebrafish offspring

机译:二氧化钛纳米粒子的父母转移加剧了斑马鱼后代的MCLR-诱导的发育毒性

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摘要

This work focuses on the transgenerational effects of titanium dioxide nanoparticles (n-TiO2) and microcystin-LR (MCLR) on the development of F1 zebrafish offspring. Wild-type adult zebrafish (4 months old) were exposed to various MCLR concentrations (0, 0.5, 4, and 32 g L-1) with and without n-TiO2 (100 g L-1) for 45 days. F1 zebrafish embryos from the above-mentioned parents were collected and cultured in clean water for 120 hours post-fertilization (hpf). Our results showed that n-TiO2 could potentially be transferred from parents to offspring, which further led to the increase in the accumulation of MCLR content in F1 zebrafish embryos. Hypoactivity and indistinct retinal layers in F1 larvae were observed, and the presence of n-TiO2 intensified these adverse effects in co-exposure groups. The parental transfer of MCLR and n-TiO2 further increased the formation of reactive oxygen species (ROS) in F1 larvae, which contributed to more apoptotic cells in and around the eyes of F1 larvae. Furthermore, we detected altered gene expression (p53, Bax, Bid, Bcl-2, puma, and Apaf-1), protein expression (P53, Bax, Bcl-2, and cytochrome c) and enzyme activities (caspase-3, caspase-8, and caspase-9), indicating that parental transfer of n-TiO2 could aggravate MCLR-induced apoptosis in F1 offspring through the mitochondria-mediated apoptosis pathway. In summary, this research studied the bioaccumulation, parental transfer, and developmental toxicity of MCLR and n-TiO2 to examine their interactions, revealing that the health risks of co-exposure should not be ignored.
机译:这项工作侧重于二氧化钛纳米颗粒(N-TiO2)和微囊藻醇-1R(MCLR)对F1斑马鱼后代发育的转基因作用。野生型成人斑马鱼(4个月大)暴露于各种MCLR浓度(0,0.5,4和32g L-1),无需N-TiO 2(100g L-1),45天。从上述父母的F1斑马鱼胚胎被收集并在清洁水中培养120小时,后施用120小时(HPF)。我们的研究结果表明,N-TiO2可能会从父母转移到后代,这进一步导致F1斑马鱼胚胎中MCLR含量的积累增加。观察到F1幼虫中的脱催化和霉菌视网膜层,N-TiO2的存在加剧了在共曝光基团中的这些不利影响。 MCLR和N-TiO2的亲本转移进一步增加了F1幼虫中的活性氧物质(ROS)的形成,这导致了F1幼虫的眼中和周围的更多凋亡细胞。此外,我们检测到改变的基因表达(P53,BAX,BID,BCL-2,PUMA和APAF-1),蛋白表达(P53,BAX,BCL-2和细胞色素C)和酶活性(Caspase-3,Caspase -8和Caspase-9),表明N-TiO2的父母转移可以通过线粒体介导的凋亡途径加剧F1后代的MCLR诱导的细胞凋亡。总之,本研究研究了MCLR和N-TiO2的生物累积,父母转移和发育毒性,以检查其相互作用,揭示了共同暴露的健康风险不容忽视。

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  • 来源
    《Environmental Science: Nano》 |2018年第12期|共14页
  • 作者单位

    Huazhong Agr Univ Coll Fisheries Wuhan 430070 Hubei Peoples R China;

    Hubei Acad Agr Sci Inst Agr Qual Stand &

    Testing Technol Wuhan 430064 Hubei Peoples R China;

    Huazhong Agr Univ Coll Fisheries Wuhan 430070 Hubei Peoples R China;

    Univ Calif Davis Dept Biol &

    Agr Engn Davis CA 95616 USA;

    Huazhong Agr Univ Coll Fisheries Wuhan 430070 Hubei Peoples R China;

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  • 正文语种 eng
  • 中图分类 环境科学、安全科学;
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